This document provides an overview of the cell cycle, including its phases, regulation, checkpoints, and deregulation in cancer. Key points include:
- The cell cycle consists of the G1, S, G2, and M phases, during which the cell grows and divides. Cyclins and cyclin-dependent kinases (CDKs) drive progression through the phases.
- CDK activity is regulated by cyclins, CDK inhibitors, phosphorylation, and ubiquitin-mediated degradation. The retinoblastoma protein (Rb) and E2F transcription factors also regulate the cell cycle.
- Checkpoints like G1/S, intra-S, and G2/M ensure DNA
The document discusses regulation of the cell cycle. It explains that the cell cycle is regulated through checkpoints and cyclin-dependent protein kinases (Cdks) and cyclins. There are three main checkpoints - at the ends of G1 and G2 phases, and during metaphase. These checkpoints ensure DNA integrity and replication, and proper chromosome attachment before progression to the next phase. Cdks drive progression when activated by binding with cyclins, which are synthesized and degraded throughout the cycle in response to cellular signals.
Cell fusion experiments in 1970 showed that the cytoplasm of mitotic cells contained diffusible factors that could induce mitosis in non-mitotic cells, suggesting cell cycle transition from G2 to M phase is under positive control. Cyclin-dependent kinases and cyclins play key roles in cell cycle regulation, with cyclins activating CDKs and undergoing regulated synthesis and degradation. Cell cycle checkpoints at G1/S, G2/M, and metaphase ensure fidelity of cell division by verifying completion of each phase before progression.
The document summarizes key aspects of the cell cycle. It discusses that the cell cycle is a series of events that a cell passes through from the time it is formed until it replicates. There are two main periods - interphase and mitosis. Interphase consists of G1, S, and G2 phases where the cell grows and duplicates its DNA. Mitosis is where the cell nucleus and cytoplasm divide. The cell cycle is tightly regulated by checkpoints and cyclins/CDKs to ensure DNA is properly replicated and divided between daughter cells. Dysregulation of cell cycle controls can lead to cancer if cells continue dividing uncontrollably.
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
The document discusses the normal cell cycle and how cancer disrupts it. In the normal cell cycle, DNA replication is checked carefully. Chemical signals tell cells when to divide and neighboring cells communicate to prevent overcrowding. In cancer, mutations in DNA replication cause cells to ignore signals and crowd together to form tumors. Causes of DNA mutations include radiation, smoking, pollution and viruses. Cancer treatments target the unchecked cell division caused by these mutations.
The document summarizes the cell cycle and its checkpoints. It describes the different phases of the cell cycle including interphase consisting of G1, S, and G2 phases and the mitotic phase. Checkpoints ensure the cell cycle processes are accurately completed before progression including the G1, G2, and metaphase checkpoints. The cell cycle is regulated by cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors that act as positive and negative regulators.
Molecular event during Cell cycle By KK Sahu SirKAUSHAL SAHU
WHAT IS CELL?
WHAT IS CELL DIVISION OR CELL CYCLE?
WHY DO CELL DIVIDE?
HISTORY
CELL CYCLE
INTERPHASE
M-PHASE
MOLECULAR EVENT DURING CELL CYCLE AND CELL REGULATION
TYPES OF CELL DIVISION
IMPORTANCE OF CELL DIVISION
ABNORMALTIES OF CELL CYCLE
REFRENCES
This slideshow contains various stages of cell cycle regulation, cell cycle checkpoints and their proteins involved in regulation. Cell cycle checkpoints transition phases.
The document discusses regulation of the cell cycle. It explains that the cell cycle is regulated through checkpoints and cyclin-dependent protein kinases (Cdks) and cyclins. There are three main checkpoints - at the ends of G1 and G2 phases, and during metaphase. These checkpoints ensure DNA integrity and replication, and proper chromosome attachment before progression to the next phase. Cdks drive progression when activated by binding with cyclins, which are synthesized and degraded throughout the cycle in response to cellular signals.
Cell fusion experiments in 1970 showed that the cytoplasm of mitotic cells contained diffusible factors that could induce mitosis in non-mitotic cells, suggesting cell cycle transition from G2 to M phase is under positive control. Cyclin-dependent kinases and cyclins play key roles in cell cycle regulation, with cyclins activating CDKs and undergoing regulated synthesis and degradation. Cell cycle checkpoints at G1/S, G2/M, and metaphase ensure fidelity of cell division by verifying completion of each phase before progression.
The document summarizes key aspects of the cell cycle. It discusses that the cell cycle is a series of events that a cell passes through from the time it is formed until it replicates. There are two main periods - interphase and mitosis. Interphase consists of G1, S, and G2 phases where the cell grows and duplicates its DNA. Mitosis is where the cell nucleus and cytoplasm divide. The cell cycle is tightly regulated by checkpoints and cyclins/CDKs to ensure DNA is properly replicated and divided between daughter cells. Dysregulation of cell cycle controls can lead to cancer if cells continue dividing uncontrollably.
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
The document discusses the normal cell cycle and how cancer disrupts it. In the normal cell cycle, DNA replication is checked carefully. Chemical signals tell cells when to divide and neighboring cells communicate to prevent overcrowding. In cancer, mutations in DNA replication cause cells to ignore signals and crowd together to form tumors. Causes of DNA mutations include radiation, smoking, pollution and viruses. Cancer treatments target the unchecked cell division caused by these mutations.
The document summarizes the cell cycle and its checkpoints. It describes the different phases of the cell cycle including interphase consisting of G1, S, and G2 phases and the mitotic phase. Checkpoints ensure the cell cycle processes are accurately completed before progression including the G1, G2, and metaphase checkpoints. The cell cycle is regulated by cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors that act as positive and negative regulators.
Molecular event during Cell cycle By KK Sahu SirKAUSHAL SAHU
WHAT IS CELL?
WHAT IS CELL DIVISION OR CELL CYCLE?
WHY DO CELL DIVIDE?
HISTORY
CELL CYCLE
INTERPHASE
M-PHASE
MOLECULAR EVENT DURING CELL CYCLE AND CELL REGULATION
TYPES OF CELL DIVISION
IMPORTANCE OF CELL DIVISION
ABNORMALTIES OF CELL CYCLE
REFRENCES
This slideshow contains various stages of cell cycle regulation, cell cycle checkpoints and their proteins involved in regulation. Cell cycle checkpoints transition phases.
This presentation on "Cell Cycle regulation" takes you to the cell cycle describing the stages and checkpoints involved providing some of the evidences of cell cycle regulation. Then we will move to cyclins and cyclin dependent kinases and the mechanism they follow.
This journey in regulation of cell cycle will take a halt after a general discussion of positive and negative cell cycle regulators.
Thankyou.
cell cycle and its check points and regulationSayanti Sau
This document provides an overview of the cell cycle and its checkpoints. It defines the cell cycle as the series of events that a cell undergoes from the time it is formed until it replicates itself. The cell cycle consists of interphase, which includes G1, S, and G2 phases, and the mitotic (M) phase. Checkpoints ensure DNA replication and cell division occur accurately. The G1 checkpoint determines if conditions allow cell division. The G2 checkpoint verifies DNA replication is complete before mitosis. The metaphase checkpoint confirms proper chromosome alignment before anaphase. Growth factors and cyclin-CDK complexes regulate progression through the cell cycle phases and checkpoints.
The document discusses cell cycle regulation and its importance in cell division, DNA replication, and cell growth. It describes the main phases of the cell cycle - interphase (consisting of G1, S, and G2 phases) and the M phase. Key events in each phase are outlined. The cell cycle is tightly regulated by cyclins and cyclin-dependent kinases (Cdks) that control progression through the cycle. Extracellular factors like growth factors and mitogens also influence cell cycle regulation through cell surface receptors and intracellular signaling pathways.
The document discusses the cell cycle and its control. It describes the cell cycle as consisting of interphase (which includes G1, S, and G2 phases) and mitosis (M phase). Interphase involves cell growth and DNA replication, while mitosis involves the division of the cell into two daughter cells. Transition between phases is regulated by cyclins and cyclin-dependent kinases (Cdks). Key checkpoints ensure replication and division occur accurately. The centromere and chromatids are also described along with their behavior in the different mitotic phases.
The document summarizes key aspects of the cell cycle and its control mechanisms. It describes the main phases of the eukaryotic cell cycle - G1, S, G2, and M phase. It explains that cyclins and cyclin-dependent kinases (CDKs) control progression between phases by promoting specific events like DNA replication and mitosis. CDK activity is regulated by binding with cyclins and proteolytic degradation of cyclins by the anaphase promoting complex. Checkpoints in the cell cycle arrest progression under negative intracellular signals to ensure DNA replication and chromosome separation are properly completed.
Basic Cell cycle regulation suitable for undergraduate students.
This presentation has been started from the basics to enable easy understanding. It covers all the details of cell cycle regulation in yeast as well as higher eukaryotes.
CELL CYCLE , MITOSIS ,MEIOSIS AND CELL REGULATIONLIFE SCIENCES
The document discusses the cell cycle and its regulation. It describes the main phases of the cell cycle including interphase with G1, S, and G2 phases, and mitosis. It also covers meiosis and the key differences between mitosis and meiosis. Cell cycle checkpoints are mentioned which allow the cell cycle to be halted at certain points if conditions are not favorable for progression.
Cell cycle checkpoints, apoptosis and cancerSurender Rawat
1. The document discusses various aspects of the cell cycle, including its key phases and regulating molecules. It notes that the cell cycle includes growth, DNA replication, chromosome separation, and cytokinesis.
2. Major regulatory molecules discussed include cyclins, CDKs, Rb protein, and checkpoints like START that ensure DNA damage is repaired before progression.
3. External factors like nutrients and growth signals regulate the cell cycle at transition points like the G1/S boundary through pathways involving cyclins, CDKs, and Rb.
The cell cycle consists of four phases - G1, S, G2, and M. Progression through the cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). There are checkpoints at G1/S and G2/M to ensure DNA replication is complete before cell division. Apoptosis is a form of programmed cell death involved in development and maintenance of tissue homeostasis. It is executed by caspases and can be triggered through extrinsic and intrinsic pathways that activate initiator and effector caspases leading to DNA fragmentation and formation of apoptotic bodies.
The document summarizes key aspects of cell cycle regulation, including checkpoints and core regulatory proteins. It discusses three important checkpoints - the G1, G2, and spindle checkpoints - and how they ensure DNA integrity before progression. It then explains that core regulators like cyclins, cyclin-dependent kinases (Cdks), and the anaphase promoting complex (APC/C) drive the cell cycle in response to internal and external cues by activating or deactivating target proteins through phosphorylation or ubiquitination.
The extracellular matrix (ECM) provides physical scaffolding and biochemical signals outside cells that are essential for tissue development and homeostasis. The ECM is composed of glycoproteins like collagen and proteoglycans that form a network, as well as glycoproteins like fibronectin that attach cells to the network. Collagen provides tensile strength and there are various types of collagen with different structures and functions. The ECM allows communication between cells through connections like tight junctions, desmosomes, and gap junctions. It also binds growth factors and interacts with cell receptors to regulate gene expression. Disruptions to the ECM can cause diseases like scurvy or emphysema.
The document summarizes key aspects of the cell cycle. It describes the main phases (G1, S, G2, M), as well as checkpoints that regulate progression. Mitosis and cytokinesis are explained. The roles of cyclins, CDKs and CKIs are mentioned. Checkpoints for DNA damage, replication errors and spindle assembly are summarized. The document then briefly discusses how cell cycle dysregulation can lead to cancer, noting examples of proto-oncogenes and tumor suppressor genes that are commonly mutated in cancer.
This document discusses cell adhesion molecules (CAMs), which are glycoproteins located on cell surfaces that help cells stick to each other and their surroundings. CAMs are classified into five major families: cadherins, Ig superfamily CAMs, selectins, integrins, and mucins. Cadherins are calcium-dependent and form connections between cells called desmosomes. Selectins help with inflammation and lymphocyte homing. Integrins facilitate cell-cell and cell-extracellular matrix adhesion and are composed of alpha and beta subunits. Malfunctions in CAMs can lead to conditions like breast cancer and leukocyte adhesion deficiency syndrome.
The document summarizes the cell cycle and its regulation. It describes the main stages of the cell cycle - interphase consisting of G1, S, and G2 phases and the M phase. Key regulators of the cell cycle include cyclins, cyclin-dependent kinases, and checkpoints like G1, G2, and M that ensure fidelity of DNA replication and chromosome segregation. Dysregulation of these processes can lead to genomic instability and cancer.
The cell cycle involves an interphase of growth and DNA replication followed by mitosis, where the cell divides. The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs) that drive progression between phases. CDK activity increases upon binding to cyclins and decreases when cyclins are degraded. Growth hormones like auxins and cytokinins promote cell cycle progression by increasing cyclin and CDK expression, while abscisic acid inhibits the cell cycle. Together, these regulatory mechanisms precisely control cell division.
The document discusses chromosome organization and packaging, as well as the cell cycle and its regulation. It describes the different phases of the cell cycle (G1, S, G2, M) and checkpoints that ensure DNA replication is complete and any damage repaired before the cell divides. Key regulators of the cell cycle include cyclins, CDKs, and CDKIs, which promote or inhibit phase transitions in response to internal and external signals. DNA damage checkpoints in particular arrest the cell cycle to allow repair or induce apoptosis if damage is too severe.
Cell adhesion molecules and matrix proteinsUSmile Ï Ṩṃïlệ
Cell adhesion molecules are proteins located on cell surfaces that are involved in binding between cells or between cells and the extracellular matrix. The three main types are cadherins, integrins, and selectins. Cadherins are calcium-dependent proteins that mediate cell-cell adhesion. Integrins are transmembrane receptors that bind to components of the extracellular matrix and mediate cell-matrix adhesion as well as cell signaling. Selectins mediate the initial capture and rolling of leukocytes along vascular surfaces. Cell adhesion molecules play important physiological roles in processes like leukocyte trafficking, blood coagulation, and morphogenesis. They also have applications as therapeutic targets in areas such as cancer, osteoporosis, and inflammatory diseases.
The document discusses cell cycle checkpoints, which ensure the proper progression of the eukaryotic cell cycle. There are three major checkpoints: the G1 checkpoint allows DNA repair before DNA replication in S phase; the S-phase checkpoint continually monitors DNA integrity during replication to permit repair of damage; the G2 checkpoint prevents mitosis from beginning until DNA replication is complete in S phase. Together these checkpoints verify DNA is intact and repaired at critical points to maintain genomic integrity.
The document discusses the cell cycle and cell division. It describes the main stages of the cell cycle including interphase (G1, S, G2 phases) and the mitotic (M) phase. Interphase involves cell growth and DNA replication, while mitosis involves nuclear division and cytokinesis. The stages of mitosis (prophase, metaphase, anaphase, telophase) and cytokinesis are explained. Control mechanisms ensure the cell cycle proceeds normally and discusses how cancer can occur if this control is disrupted.
This document provides an overview of a course on advanced cell biology. It focuses on the topic of membranes, including their structure and key components. The main points are:
- Biological membranes act as barriers that compartmentalize the cell and contain lipids, integral proteins, and peripheral proteins.
- The fluid mosaic model describes membranes as a fluid bilayer of lipids with integral proteins embedded. Key lipids include phospholipids and sphingolipids. Cholesterol provides rigidity.
- Integral membrane proteins span the membrane and include transmembrane alpha helices. Their structure can be predicted using hydropathy plots.
- Membranes establish gradients using pumps, carriers, and channels. Pumps actively transport ions using ATP.
The document summarizes a tutorial on measuring semantic similarity and relatedness between medical concepts. It introduces different types of measures, including path-based measures, measures using information content that incorporate concept specificity, and measures of relatedness that use definition overlaps or corpus co-occurrence information. The tutorial aims to explain the distinction between similarity and relatedness, describe available measures, and how to evaluate and apply them in clinical natural language processing tasks.
This presentation on "Cell Cycle regulation" takes you to the cell cycle describing the stages and checkpoints involved providing some of the evidences of cell cycle regulation. Then we will move to cyclins and cyclin dependent kinases and the mechanism they follow.
This journey in regulation of cell cycle will take a halt after a general discussion of positive and negative cell cycle regulators.
Thankyou.
cell cycle and its check points and regulationSayanti Sau
This document provides an overview of the cell cycle and its checkpoints. It defines the cell cycle as the series of events that a cell undergoes from the time it is formed until it replicates itself. The cell cycle consists of interphase, which includes G1, S, and G2 phases, and the mitotic (M) phase. Checkpoints ensure DNA replication and cell division occur accurately. The G1 checkpoint determines if conditions allow cell division. The G2 checkpoint verifies DNA replication is complete before mitosis. The metaphase checkpoint confirms proper chromosome alignment before anaphase. Growth factors and cyclin-CDK complexes regulate progression through the cell cycle phases and checkpoints.
The document discusses cell cycle regulation and its importance in cell division, DNA replication, and cell growth. It describes the main phases of the cell cycle - interphase (consisting of G1, S, and G2 phases) and the M phase. Key events in each phase are outlined. The cell cycle is tightly regulated by cyclins and cyclin-dependent kinases (Cdks) that control progression through the cycle. Extracellular factors like growth factors and mitogens also influence cell cycle regulation through cell surface receptors and intracellular signaling pathways.
The document discusses the cell cycle and its control. It describes the cell cycle as consisting of interphase (which includes G1, S, and G2 phases) and mitosis (M phase). Interphase involves cell growth and DNA replication, while mitosis involves the division of the cell into two daughter cells. Transition between phases is regulated by cyclins and cyclin-dependent kinases (Cdks). Key checkpoints ensure replication and division occur accurately. The centromere and chromatids are also described along with their behavior in the different mitotic phases.
The document summarizes key aspects of the cell cycle and its control mechanisms. It describes the main phases of the eukaryotic cell cycle - G1, S, G2, and M phase. It explains that cyclins and cyclin-dependent kinases (CDKs) control progression between phases by promoting specific events like DNA replication and mitosis. CDK activity is regulated by binding with cyclins and proteolytic degradation of cyclins by the anaphase promoting complex. Checkpoints in the cell cycle arrest progression under negative intracellular signals to ensure DNA replication and chromosome separation are properly completed.
Basic Cell cycle regulation suitable for undergraduate students.
This presentation has been started from the basics to enable easy understanding. It covers all the details of cell cycle regulation in yeast as well as higher eukaryotes.
CELL CYCLE , MITOSIS ,MEIOSIS AND CELL REGULATIONLIFE SCIENCES
The document discusses the cell cycle and its regulation. It describes the main phases of the cell cycle including interphase with G1, S, and G2 phases, and mitosis. It also covers meiosis and the key differences between mitosis and meiosis. Cell cycle checkpoints are mentioned which allow the cell cycle to be halted at certain points if conditions are not favorable for progression.
Cell cycle checkpoints, apoptosis and cancerSurender Rawat
1. The document discusses various aspects of the cell cycle, including its key phases and regulating molecules. It notes that the cell cycle includes growth, DNA replication, chromosome separation, and cytokinesis.
2. Major regulatory molecules discussed include cyclins, CDKs, Rb protein, and checkpoints like START that ensure DNA damage is repaired before progression.
3. External factors like nutrients and growth signals regulate the cell cycle at transition points like the G1/S boundary through pathways involving cyclins, CDKs, and Rb.
The cell cycle consists of four phases - G1, S, G2, and M. Progression through the cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). There are checkpoints at G1/S and G2/M to ensure DNA replication is complete before cell division. Apoptosis is a form of programmed cell death involved in development and maintenance of tissue homeostasis. It is executed by caspases and can be triggered through extrinsic and intrinsic pathways that activate initiator and effector caspases leading to DNA fragmentation and formation of apoptotic bodies.
The document summarizes key aspects of cell cycle regulation, including checkpoints and core regulatory proteins. It discusses three important checkpoints - the G1, G2, and spindle checkpoints - and how they ensure DNA integrity before progression. It then explains that core regulators like cyclins, cyclin-dependent kinases (Cdks), and the anaphase promoting complex (APC/C) drive the cell cycle in response to internal and external cues by activating or deactivating target proteins through phosphorylation or ubiquitination.
The extracellular matrix (ECM) provides physical scaffolding and biochemical signals outside cells that are essential for tissue development and homeostasis. The ECM is composed of glycoproteins like collagen and proteoglycans that form a network, as well as glycoproteins like fibronectin that attach cells to the network. Collagen provides tensile strength and there are various types of collagen with different structures and functions. The ECM allows communication between cells through connections like tight junctions, desmosomes, and gap junctions. It also binds growth factors and interacts with cell receptors to regulate gene expression. Disruptions to the ECM can cause diseases like scurvy or emphysema.
The document summarizes key aspects of the cell cycle. It describes the main phases (G1, S, G2, M), as well as checkpoints that regulate progression. Mitosis and cytokinesis are explained. The roles of cyclins, CDKs and CKIs are mentioned. Checkpoints for DNA damage, replication errors and spindle assembly are summarized. The document then briefly discusses how cell cycle dysregulation can lead to cancer, noting examples of proto-oncogenes and tumor suppressor genes that are commonly mutated in cancer.
This document discusses cell adhesion molecules (CAMs), which are glycoproteins located on cell surfaces that help cells stick to each other and their surroundings. CAMs are classified into five major families: cadherins, Ig superfamily CAMs, selectins, integrins, and mucins. Cadherins are calcium-dependent and form connections between cells called desmosomes. Selectins help with inflammation and lymphocyte homing. Integrins facilitate cell-cell and cell-extracellular matrix adhesion and are composed of alpha and beta subunits. Malfunctions in CAMs can lead to conditions like breast cancer and leukocyte adhesion deficiency syndrome.
The document summarizes the cell cycle and its regulation. It describes the main stages of the cell cycle - interphase consisting of G1, S, and G2 phases and the M phase. Key regulators of the cell cycle include cyclins, cyclin-dependent kinases, and checkpoints like G1, G2, and M that ensure fidelity of DNA replication and chromosome segregation. Dysregulation of these processes can lead to genomic instability and cancer.
The cell cycle involves an interphase of growth and DNA replication followed by mitosis, where the cell divides. The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs) that drive progression between phases. CDK activity increases upon binding to cyclins and decreases when cyclins are degraded. Growth hormones like auxins and cytokinins promote cell cycle progression by increasing cyclin and CDK expression, while abscisic acid inhibits the cell cycle. Together, these regulatory mechanisms precisely control cell division.
The document discusses chromosome organization and packaging, as well as the cell cycle and its regulation. It describes the different phases of the cell cycle (G1, S, G2, M) and checkpoints that ensure DNA replication is complete and any damage repaired before the cell divides. Key regulators of the cell cycle include cyclins, CDKs, and CDKIs, which promote or inhibit phase transitions in response to internal and external signals. DNA damage checkpoints in particular arrest the cell cycle to allow repair or induce apoptosis if damage is too severe.
Cell adhesion molecules and matrix proteinsUSmile Ï Ṩṃïlệ
Cell adhesion molecules are proteins located on cell surfaces that are involved in binding between cells or between cells and the extracellular matrix. The three main types are cadherins, integrins, and selectins. Cadherins are calcium-dependent proteins that mediate cell-cell adhesion. Integrins are transmembrane receptors that bind to components of the extracellular matrix and mediate cell-matrix adhesion as well as cell signaling. Selectins mediate the initial capture and rolling of leukocytes along vascular surfaces. Cell adhesion molecules play important physiological roles in processes like leukocyte trafficking, blood coagulation, and morphogenesis. They also have applications as therapeutic targets in areas such as cancer, osteoporosis, and inflammatory diseases.
The document discusses cell cycle checkpoints, which ensure the proper progression of the eukaryotic cell cycle. There are three major checkpoints: the G1 checkpoint allows DNA repair before DNA replication in S phase; the S-phase checkpoint continually monitors DNA integrity during replication to permit repair of damage; the G2 checkpoint prevents mitosis from beginning until DNA replication is complete in S phase. Together these checkpoints verify DNA is intact and repaired at critical points to maintain genomic integrity.
The document discusses the cell cycle and cell division. It describes the main stages of the cell cycle including interphase (G1, S, G2 phases) and the mitotic (M) phase. Interphase involves cell growth and DNA replication, while mitosis involves nuclear division and cytokinesis. The stages of mitosis (prophase, metaphase, anaphase, telophase) and cytokinesis are explained. Control mechanisms ensure the cell cycle proceeds normally and discusses how cancer can occur if this control is disrupted.
This document provides an overview of a course on advanced cell biology. It focuses on the topic of membranes, including their structure and key components. The main points are:
- Biological membranes act as barriers that compartmentalize the cell and contain lipids, integral proteins, and peripheral proteins.
- The fluid mosaic model describes membranes as a fluid bilayer of lipids with integral proteins embedded. Key lipids include phospholipids and sphingolipids. Cholesterol provides rigidity.
- Integral membrane proteins span the membrane and include transmembrane alpha helices. Their structure can be predicted using hydropathy plots.
- Membranes establish gradients using pumps, carriers, and channels. Pumps actively transport ions using ATP.
The document summarizes a tutorial on measuring semantic similarity and relatedness between medical concepts. It introduces different types of measures, including path-based measures, measures using information content that incorporate concept specificity, and measures of relatedness that use definition overlaps or corpus co-occurrence information. The tutorial aims to explain the distinction between similarity and relatedness, describe available measures, and how to evaluate and apply them in clinical natural language processing tasks.
Cloroplastos são organelas nas células vegetais onde a fotossíntese ocorre. A fotossíntese usa a luz do sol, água, dióxido de carbono e clorofila nos cloroplastos para produzir açúcares, oxigênio e energia. A fotossíntese tem duas fases, a fase clara que usa a luz para quebrar moléculas de água e produzir oxigênio, ATP e NADPH, e a fase escura que usa esses produtos para
Diseases can be caused by defects in the endoplasmic reticulum (ER) and Golgi apparatus. Some diseases are due to a lack of signal sequences that direct proteins to the ER, while others are caused by the ER's inability to properly fold proteins or defects in glycosylation. Vesicles are sacs that transport substances within the cell; different types include exosomes, endosomes, lysosomes, and vacuoles. A centrifuge can separate cell components - at 50,000g it can separate mitochondria and chloroplasts but not smaller organelles or ribosomes.
This is a compilation of the Yeast genome project from the different databases and sources.
By:
Nazish Nehal,
M. Tech (Biotechnology),
University School of Biotechnology (USBT),
Guru Gobind Singh Indraprastha University (GGSIPU),
New Delhi (INDIA)
The cell membrane, also called the plasma membrane, is a biological membrane that separates the interior of a cell from the outside environment. It is composed primarily of lipids and proteins arranged in a fluid mosaic structure. The lipid bilayer that forms the foundation of the cell membrane is made up of phospholipids with hydrophilic heads and hydrophobic tails. Embedded within this bilayer are transmembrane and peripheral proteins that perform important functions like selective transport, cell signaling, and providing anchoring sites. The fluid mosaic model proposed by Singer and Nicolson in 1972 is widely accepted as it accounts for the fluid and dynamic nature of the cell membrane.
The plasma membrane acts as a gatekeeper that regulates what enters and exits the cell. It uses both passive and active transport. Passive transport relies on diffusion and moves substances along concentration gradients, while active transport requires energy and can move substances against concentration gradients using mechanisms like the sodium-potassium pump. The plasma membrane is a lipid bilayer with embedded proteins that gives cells structure and allows for selective permeability and transport of molecules in and out of the cell.
O documento resume a origem e estrutura das mitocôndrias e cloroplastos de acordo com a teoria da endossimbiose. As mitocôndrias e cloroplastos teriam se originado de bactérias primitivas que foram englobadas por células eucarióticas, estabelecendo uma relação de endossimbiose. Ambas possuem DNA e ribossomos próprios, características típicas de organismos ancestrais.
Prokaryotic cells like E. coli have a simple structure without membrane-bound organelles. They have a cell wall, plasma membrane, cytoplasm, pili, flagella, ribosomes, and a nucleoid region containing naked DNA. Each of these structures serves important functions - the cell wall provides structure, the plasma membrane controls substance transfer, pili allow adhesion, flagella provide locomotion, ribosomes synthesize proteins, and the nucleoid stores genetic information. Prokaryotes reproduce through binary fission, where one cell divides into two identical daughter cells.
The document summarizes the structure and functions of the plasma membrane. It describes the fluid mosaic model of the plasma membrane, which consists of a phospholipid bilayer with integral and peripheral proteins floating within. Various proteins embedded in the membrane act as channels, carriers, receptors and enzymes. The membrane is selectively permeable and can transport molecules via passive diffusion, osmosis, and active transport using carrier proteins and membrane-assisted mechanisms like exocytosis. The cell surface is also modified by junctions between cells and an extracellular matrix.
The Amazing World Of Fungus And ProtistsTia Hohler
The document provides an overview of protists and fungi, describing their characteristics, types, and roles. It explains that protists are eukaryotic organisms that are not classified as animals, plants or fungi, and describes three main types of protists - animal-like protists (protozoa), plant-like protists (algae), and fungus-like protists. It also discusses the four main types of fungi and their structures and life cycles, as well as commercial and disease-causing fungi.
The document summarizes key parts of eukaryotic cells. It describes the cell membrane, cell wall, nucleus, and cytoplasm. The nucleus contains DNA and directs cell activities. Organelles like mitochondria and chloroplasts provide energy for cells. The endomembrane system transports materials through the cell using structures like the endoplasmic reticulum and Golgi apparatus. Lysosomes digest waste and the cytoskeleton provides cell structure and movement.
Organelles are distinct structures within cells that carry out specific functions. In prokaryotes, organelles are not surrounded by membranes, while in eukaryotes they are. Prokaryotic cells have a cell membrane, cell wall, cytoplasm, and genetic material stored in a nucleoid. They may also contain features like pili, flagella, and a mesosome for cellular respiration. Ribosomes in prokaryotic cells are found freely in the cytoplasm.
The document summarizes key concepts about how genetic information flows from DNA to protein. It discusses how genes specify proteins through transcription and translation. Transcription involves RNA polymerase making an RNA copy of a gene. This RNA then undergoes processing in eukaryotes before being translated into a protein by ribosomes. The genetic code was discovered to be a triplet code of nucleotides that specifies which amino acid will be added during translation.
This document provides an overview of antifungal agents including their classification, mechanisms of action, indications, and adverse effects. It discusses several classes of antifungals such as azoles, polyenes, and echinocandins. Azoles like ketoconazole and fluconazole inhibit ergosterol synthesis, while polyenes like amphotericin B bind to ergosterol in the fungal cell membrane. Echinocandins target glucan synthesis. The document reviews specific drugs, their dosages, mechanisms, and side effects in treating superficial and systemic fungal infections. Future antifungal agents that may be effective for resistant fungal strains are also mentioned.
The document summarizes key aspects of cell membranes and transport across membranes. It describes the fluid mosaic model of membrane structure, including the roles of phospholipids, cholesterol, glycolipids, proteins, and glycoproteins. It also outlines various processes of transport across membranes, including diffusion, facilitated diffusion, osmosis, active transport, endocytosis, and exocytosis.
The yeast two-hybrid system is used to identify protein-protein interactions. It involves fusing two interacting proteins to a DNA-binding domain and transcriptional activation domain. If the proteins interact, it brings the domains together and activates a reporter gene. This allows identification of novel interactions and domains involved. Some advantages are it occurs in vivo, can find weak interactions, and doesn't require purified proteins. Disadvantages include false positives and some proteins may not fold correctly in yeast.
Fungi are eukaryotic organisms that differ from bacteria in having true nuclei and organelles. Most fungi are multicellular and have cell walls containing chitin. Fungi can be classified based on their morphology and reproductive structures. Important characteristics include whether they are molds, yeasts, or dimorphic. Laboratory identification of fungi involves microscopic examination of stained smears and cultures as well as culture characteristics. Direct visualization with KOH preparations and histopathology are used to diagnose fungal infections.
General overview of Plasma/ Cell membrane.
Definition of Plasma/ Cell membrane
Structure of Plasma membrane
1. Sandwitch model ORDanielli- Davson Model
2. Fluid mosaic model
Plasma Membrane Proteins
Chemical Composition of Plasma/ Cell Membrane
Movement across the Cell Membrane
Channels through cell membrane
1. Cells are the basic unit of all living things. Robert Hooke first observed cells in 1665 using a microscope. The cell theory states that all living things are made of cells, cells come only from pre-existing cells, and cells contain the basic components necessary for life.
2. Cells vary in size but have limitations based on their surface area to volume ratio. As cells increase in size, their ability to exchange materials decreases. Multicellular organisms overcome this through specialized tissues, organs and circulatory systems.
3. Cells carry out the basic functions of life including metabolism, reproduction, homeostasis, growth, response to stimuli, waste removal and nutrition. Unicellular organisms carry out all life functions
- The cell cycle consists of four main phases - G1, S, G2, and M. The G1, S, and G2 phases make up interphase.
- The cell cycle is tightly regulated by cyclins and cyclin-dependent kinases (CDKs). Different cyclin-CDK complexes control progression through the different cell cycle phases.
- Checkpoints exist to monitor DNA damage before progression into S phase and M phase. These checkpoints are regulated by proteins like ATM, ATR, Chk1, Chk2, and p53.
- Dysregulation of cell cycle control and checkpoint pathways contributes to uncontrolled cell proliferation in cancer. Both oncogenes and tumor
The phenomenon of signal transduction, also known as cell signaling, pertains to the intricate mechanisms that facilitate the transfer of biological information between cells. The effective coordination of diverse specialized cell types in various tissues and organs is a prerequisite for the proper functioning of complex multicellular organisms, necessitating intercellular communication. This communication must be continuous and dynamic to maintain coordination. Additionally, cell signaling pathways play a crucial role in the mechanisms of action of numerous drugs, including both local and general anesthetics. Consequently, a fundamental understanding of cell signaling mechanisms is imperative for comprehending various pathophysiologic and pharmacologic mechanisms.
The document provides an overview of the cell cycle, including its key phases (interphase consisting of G1, S, and G2 phases and the M phase), events that occur during each phase such as DNA replication in S phase, and control mechanisms. It discusses critical cell cycle regulators like cyclins and CDKs that form complexes to drive the cell cycle forward, as well as checkpoints that monitor cell growth and DNA integrity to ensure cells are ready to progress through the cycle. The cell cycle is tightly regulated by both intrinsic factors including cyclins and CDKs, and extrinsic factors like growth factors that influence division.
Why do different cell types' rates of the cell cycle differ?
The cell cycle is swiftly completed by injured or lost cell types to produce replacements.
Adult skin and digestive tract cells go through the cell cycle quite fast, whereas nervous system cells divide very seldom.
Cells divide regularly during embryonic development, perhaps as frequently as once or twice an hour, moving through the cell cycle very quickly.
What is the cell cycle?
The regular sequence of activities that cells go through as they develop and divide is known as the cell cycle. Prokaryotic cells go through a rapid cycle of cell division, DNA replication, and expansion. In prokaryotes, cell division occurs in a single stage known as binary fission (shown right).Compared to prokaryotic cells, eukaryotic cells have a more complicated cell cycle.
How is the eukaryotic cell cycle divided?
Interphase is the period between cell divisions. Depending on the kind of cell, the interphase might be shorter or longer.
The three stages or phases of the eukaryotic interphase are G1, S, and G2.
The M phase of the cell cycle is when eukaryotic cells divide. Mitosis and cytokinesis are the two stages that make up the M phase.
What happens during each phase of eukaryotic interphase?
G1: Cells do most of their growing during this phase. It begins when mitosis is complete and ends when DNA replication begins.
S: DNA is synthesized as chromosomes are replicated.
G2: Many of the molecules and cell structures required for cell division are produced; usually the shortest phase of the cell cycle.
What happens during the M phase of the eukaryotic cell cycle?
The M phase is usually much shorter than interphase and results in two daughter cells.
The first step of the M phase is mitosis. The cell’s nucleus divides during mitosis.
The second step of the M phase is cytokinesis, during which the cell’s cytoplasm is divided.
What are the steps of mitosis?
Mitosis consists of four steps: prophase, metaphase, anaphase, and telophase.
Prophase: nuclear envelope breaks down, DNA condenses, spindle begins to form.
Metaphase: replicated chromosomes, which appear as paired sister chromatids, line up across the center of the cell and attach to spindle.
Anaphase: sister chromatids separate and move toward ends of the cell.
Telophase: chromosomes disperse, nuclear envelope reforms.
What completes the M phase of the cell cycle?
Cytokinesis completes the M phase of the cell cycle. It may begin while telophase is still taking place.
During cytokinesis, the cytoplasm (which includes all of the contents of a eukaryotic cell outside the nucleus) draws inward, eventually pinching off into two nearly equal parts. Each part contains a nucleus.
In plant cells and other eukaryotic cells that have a cell wall, a cell plate forms halfway between the divided nuclei. It gradually develops into cell membranes and forms a complete cell wall surrounding each daughter cell.
Upon the completion of cytokinesis and the M phase, a
This presentation on "Cell Cycle regulation" takes you to the cell cycle describing the stages and checkpoints involved providing some of the evidences of cell cycle regulation. Then we will move to cyclins and cyclin dependent kinases and the mechanism they follow.
This journey in regulation of cell cycle will take a halt after a general discussion of positive and negative cell cycle regulators.
Thankyou.
The document summarizes key aspects of the cell cycle and its implications for cancer therapy. It describes the cell cycle clock and checkpoints that regulate progression through the different phases. Dysregulation of cyclins, CDKs, and CDK inhibitors can disrupt normal cell cycle control and lead to uncontrolled proliferation. Tumor suppressor genes and oncogenes play important roles in cancer by influencing the cell cycle. Chemotherapy and radiation therapy target rapidly dividing cancer cells, aiming to push them through checkpoints where they are most vulnerable. CDK4 inhibitors show promise for breast cancer treatment by decreasing the proliferation marker Ki67.
New Microsoft Office PowerPoint Presentation-1.pptxShounakKamat1
The cell cycle is a precisely programmed series of events that enables a cell to duplicate its contents and divide into two daughter cells. It consists of interphase (G1, S, G2 phases) and mitosis (M phase). Progression through the cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). CDK activity is controlled by association with cyclins, CDK inhibitors, and phosphorylation. Checkpoint pathways like the G1/S, G2, and spindle assembly checkpoints ensure replication and division errors are corrected before progression. Deregulation of these checkpoint pathways can lead to genomic instability and carcinogenesis.
The cell cycle is regulated by cyclin-dependent kinases (Cdks) whose activity oscillates throughout the cycle. Cdks form complexes with cyclins, which activate the Cdks and determine which phase of the cycle they control. The cyclin-Cdk complexes phosphorylate target proteins to promote replication and mitosis. Progression through the cell cycle is also controlled by ubiquitin ligases and phosphorylation/dephosphorylation events. The cycle operates through a series of switches that trigger irreversible events, keeping it tightly regulated and coordinated.
This document provides information on human cell cycle checkpoints and regulation. It discusses the three main cell cycle checkpoints - G1/S, G2/M, and M checkpoints. Each checkpoint verifies processes are completed before progression to the next phase. Key regulators of the cell cycle discussed include cyclins, CDKs, CDKIs, Rb protein, and p53 protein. Cyclins and CDKs control progression through different cell cycle phases, while CDKIs inhibit CDKs to arrest the cell cycle. Rb and p53 are important tumor suppressor proteins that also regulate the cell cycle.
This document provides an overview of the cell cycle and its regulation. It describes the main phases of the cell cycle (G1, S, G2, M) and key regulatory molecules like cyclins and cyclin-dependent kinases (CDKs). Cyclin-CDK complexes drive progression through the cell cycle by phosphorylating target proteins. There are three major checkpoints (G1, G2/M, metaphase) that ensure cellular conditions are suitable before progressing to the next phase. The document discusses these checkpoints and their control mechanisms in detail.
Cell Cycle_ Usman.pptx sasgdgdb vdf g g rg gmunshi5
The cell cycle is regulated by cyclins, cyclin-dependent kinases (CDKs), and tumor suppressors. The M phase is the shortest phase and includes mitosis and cytokinesis. G1 phase duration is variable. CDKs must bind to cyclins to transition between phases and are inhibited by CDK inhibitors in the presence of errors. The Cyclin D/Cdk4 complex initiates DNA replication by phosphorylating the retinoblastoma protein (pRb). The p53 tumor suppressor inhibits DNA replication through activating pRb and initiating apoptosis in cells with irreparable DNA damage.
Cell cycle and regulation in eukaryotesBhanu Krishan
The document summarizes key aspects of the cell cycle and its regulation in human cells. It describes the main phases of the cell cycle - interphase (which includes G1, S, and G2 phases) and mitotic phase. It also discusses the roles of cyclins and cyclin-dependent kinases (CDKs) in controlling progression through the cell cycle. CDK-cyclin complexes form to phosphorylate target proteins and drive progression between phases. Different CDK-cyclin pairs function to regulate DNA replication and chromosome segregation during cell division.
The document summarizes regulation of DNA replication in eukaryotes. It explains that eukaryotic genomes are divided into replicons that are each activated once per cell cycle. This is achieved through licensing factors that load onto origins of replication in G1 phase, but are removed or inactivated during DNA replication, preventing re-replication. The key licensing factors are the origin recognition complex (ORC) and proteins Cdc6 and Cdt1, which load the MCM complex onto DNA.
The cell cycle involves an orderly sequence of events where a cell duplicates its contents and divides into two daughter cells. It consists of interphase, where the cell grows and DNA replicates, and M phase where the cell divides. Key phases of interphase include G1, S, and G2 phases separated by gap phases. The cell cycle is tightly regulated by cyclins and CDKs which form complexes to drive the cell through checkpoints between phases. DNA replication only occurs once per cycle through control of initiation factors. Sister chromatids are held together by cohesin until anaphase.
This document provides a summary of Lecture 23 which covered the cell cycle. It began with an overview of the cell cycle and its key phases. It then discussed checkpoints and regulators like cyclins and cyclin-dependent kinases. A detailed look was taken at the M phase, covering processes in prophase, prometaphase, metaphase, anaphase, telophase and cytokinesis. The lecture concluded with references to quantitative studies of the cell cycle and an outlook on related follow-up courses.
The cell cycle consists of four main phases - G1, S, G2, and M. In G1, cells grow and undergo protein synthesis in preparation for DNA replication. The S phase is when DNA replication occurs. In G2, the cell prepares for mitosis by producing necessary proteins. During mitosis (M phase), the nucleus and cell contents divide to form two daughter cells each with identical DNA. The progression through the cell cycle phases is regulated by cyclins and cyclin-dependent kinases (CDKs). Different cyclins activate specific CDKs to promote the transition between phases, with checkpoints ensuring errors are corrected before progression.
The document summarizes regulation of the cell cycle. It describes how the eukaryotic cell cycle is divided into four phases - M, G1, S, and G2. Key proteins called cyclin-dependent kinases (Cdks) complexed with cyclins regulate progression between phases. Cdk activity is controlled by cyclin accumulation and degradation as well as phosphorylation/dephosphorylation. Distinct cyclin-Cdk complexes trigger events like DNA replication and mitosis. The system incorporates checkpoints and can arrest the cycle in response to errors or conditions.
The cell cycle is tightly regulated and divided into four main phases: G1, S, G2, and M. Progression through the cell cycle is controlled by cyclins and cyclin-dependent kinases (Cdks). Cyclins activate Cdks and direct them to specific protein targets to drive cell cycle events. Key control points include the Start checkpoint in G1, the restriction point, and control of the G2 to M transition. Damage checkpoints and the spindle assembly checkpoint ensure fidelity of DNA replication and chromosome segregation. The anaphase promoting complex/cyclosome (APC/C) triggers the onset of anaphase through ubiquitin-mediated proteolysis.
Mending Clothing to Support Sustainable Fashion_CIMaR 2024.pdfSelcen Ozturkcan
Ozturkcan, S., Berndt, A., & Angelakis, A. (2024). Mending clothing to support sustainable fashion. Presented at the 31st Annual Conference by the Consortium for International Marketing Research (CIMaR), 10-13 Jun 2024, University of Gävle, Sweden.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
The cost of acquiring information by natural selectionCarl Bergstrom
This is a short talk that I gave at the Banff International Research Station workshop on Modeling and Theory in Population Biology. The idea is to try to understand how the burden of natural selection relates to the amount of information that selection puts into the genome.
It's based on the first part of this research paper:
The cost of information acquisition by natural selection
Ryan Seamus McGee, Olivia Kosterlitz, Artem Kaznatcheev, Benjamin Kerr, Carl T. Bergstrom
bioRxiv 2022.07.02.498577; doi: https://doi.org/10.1101/2022.07.02.498577
JAMES WEBB STUDY THE MASSIVE BLACK HOLE SEEDSSérgio Sacani
The pathway(s) to seeding the massive black holes (MBHs) that exist at the heart of galaxies in the present and distant Universe remains an unsolved problem. Here we categorise, describe and quantitatively discuss the formation pathways of both light and heavy seeds. We emphasise that the most recent computational models suggest that rather than a bimodal-like mass spectrum between light and heavy seeds with light at one end and heavy at the other that instead a continuum exists. Light seeds being more ubiquitous and the heavier seeds becoming less and less abundant due the rarer environmental conditions required for their formation. We therefore examine the different mechanisms that give rise to different seed mass spectrums. We show how and why the mechanisms that produce the heaviest seeds are also among the rarest events in the Universe and are hence extremely unlikely to be the seeds for the vast majority of the MBH population. We quantify, within the limits of the current large uncertainties in the seeding processes, the expected number densities of the seed mass spectrum. We argue that light seeds must be at least 103 to 105 times more numerous than heavy seeds to explain the MBH population as a whole. Based on our current understanding of the seed population this makes heavy seeds (Mseed > 103 M⊙) a significantly more likely pathway given that heavy seeds have an abundance pattern than is close to and likely in excess of 10−4 compared to light seeds. Finally, we examine the current state-of-the-art in numerical calculations and recent observations and plot a path forward for near-future advances in both domains.
(June 12, 2024) Webinar: Development of PET theranostics targeting the molecu...Scintica Instrumentation
Targeting Hsp90 and its pathogen Orthologs with Tethered Inhibitors as a Diagnostic and Therapeutic Strategy for cancer and infectious diseases with Dr. Timothy Haystead.
When I was asked to give a companion lecture in support of ‘The Philosophy of Science’ (https://shorturl.at/4pUXz) I decided not to walk through the detail of the many methodologies in order of use. Instead, I chose to employ a long standing, and ongoing, scientific development as an exemplar. And so, I chose the ever evolving story of Thermodynamics as a scientific investigation at its best.
Conducted over a period of >200 years, Thermodynamics R&D, and application, benefitted from the highest levels of professionalism, collaboration, and technical thoroughness. New layers of application, methodology, and practice were made possible by the progressive advance of technology. In turn, this has seen measurement and modelling accuracy continually improved at a micro and macro level.
Perhaps most importantly, Thermodynamics rapidly became a primary tool in the advance of applied science/engineering/technology, spanning micro-tech, to aerospace and cosmology. I can think of no better a story to illustrate the breadth of scientific methodologies and applications at their best.
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...Leonel Morgado
Current descriptions of immersive learning cases are often difficult or impossible to compare. This is due to a myriad of different options on what details to include, which aspects are relevant, and on the descriptive approaches employed. Also, these aspects often combine very specific details with more general guidelines or indicate intents and rationales without clarifying their implementation. In this paper we provide a method to describe immersive learning cases that is structured to enable comparisons, yet flexible enough to allow researchers and practitioners to decide which aspects to include. This method leverages a taxonomy that classifies educational aspects at three levels (uses, practices, and strategies) and then utilizes two frameworks, the Immersive Learning Brain and the Immersion Cube, to enable a structured description and interpretation of immersive learning cases. The method is then demonstrated on a published immersive learning case on training for wind turbine maintenance using virtual reality. Applying the method results in a structured artifact, the Immersive Learning Case Sheet, that tags the case with its proximal uses, practices, and strategies, and refines the free text case description to ensure that matching details are included. This contribution is thus a case description method in support of future comparative research of immersive learning cases. We then discuss how the resulting description and interpretation can be leveraged to change immersion learning cases, by enriching them (considering low-effort changes or additions) or innovating (exploring more challenging avenues of transformation). The method holds significant promise to support better-grounded research in immersive learning.
Sexuality - Issues, Attitude and Behaviour - Applied Social Psychology - Psyc...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Evidence of Jet Activity from the Secondary Black Hole in the OJ 287 Binary S...Sérgio Sacani
Wereport the study of a huge optical intraday flare on 2021 November 12 at 2 a.m. UT in the blazar OJ287. In the binary black hole model, it is associated with an impact of the secondary black hole on the accretion disk of the primary. Our multifrequency observing campaign was set up to search for such a signature of the impact based on a prediction made 8 yr earlier. The first I-band results of the flare have already been reported by Kishore et al. (2024). Here we combine these data with our monitoring in the R-band. There is a big change in the R–I spectral index by 1.0 ±0.1 between the normal background and the flare, suggesting a new component of radiation. The polarization variation during the rise of the flare suggests the same. The limits on the source size place it most reasonably in the jet of the secondary BH. We then ask why we have not seen this phenomenon before. We show that OJ287 was never before observed with sufficient sensitivity on the night when the flare should have happened according to the binary model. We also study the probability that this flare is just an oversized example of intraday variability using the Krakow data set of intense monitoring between 2015 and 2023. We find that the occurrence of a flare of this size and rapidity is unlikely. In machine-readable Tables 1 and 2, we give the full orbit-linked historical light curve of OJ287 as well as the dense monitoring sample of Krakow.
2. Introduction
Historic events of cell cycle discovery
Phases of cell cycle
Cell cycle machinery
Steps of cell cycle and its regulation in normal
cells
Check points of cell cycle
Cell cycle in malignant cells
Applied aspects of cell cycle in oncology
Summary
3. • Definition - The cell cycle is the series of events that take place in
a cell leading to its division and duplication (replication) that
produces two daughter cells
• Specific populations retain the ability to proliferate throughout the
adult life span, which is essential for proper tissue homeostasis.
• Quiescent cell — biochemically and functionally active but do not
divide to generate daughter cells.
• Most cells in the adult body are quiescent
• On average, about 2 trillion cell divisions occur in an adult human
every 24 hours (about 25 million per second).
5. Rudolf Carl Virchow
(1855)
“Omnis cellula e cellulae”
(cells only arise from pre- existing
cells)
rejection of the concept of
spontaneous generation by cells
6. Leland Hartwell Paul M. Nurse Timothy Hunt
concept of
“checkpoints”
1970
cyclin-dependent
kinase (CDK)
1976
cyclins
1982
7. The Nobel Prize in Physiology or Medicine 2001 was
awarded jointly to Leland H. Hartwell, Tim Hunt and Sir Paul
M. Nurse "for their discoveries of key regulators of the cell
cycle
9. • Cell moves from the quiescent (also known as G0) state into the first
gap phase, or G1, in which the cell prepares itself for the cell division
process.
• Not surprisingly, this process therefor takes a significant amount of
time (from 8 to 30 hours) and energy.
• Mitogenic growth factors are essential for continued passage
through the G1 phase.
• If growth factors are withdrawn at any point during this phase, the
cell will not divide.
10. • As the cell nears the end of the G1 phase, the cell passes through a
key transition point, called the restriction point, whereupon it
becomes growth factor independent and is fully committed to
undergoing cell division
• Within an hour or two, the cell enters the synthesis phase, or S
phase, in which each of the chromosomes is replicated
• The cell then enters a second gap phase, called G2, which lasts 3 to 5
hours, and then initiates mitosis, or the M phase, a rapid phase
(lasting about 1 hour) in which the chromosomes are segregated.
• Upon completion of mitosis, the daughter cells can enter quiescence
or initiate a second round of cell division, depending on the milieu.
15. • The Cdks are subfamily of kinases that are defined by their
dependence on a regulatory subunit, called a cyclin.
• Cdks act in association with a cyclin subunit that binds within the
kinase.
• The first identified human Cdk was Cdk1 .
• Cdk4 and Cdk6 regulate cell cycle entry
• Cdk2 may have specific roles during the G1-to-S transition and S
phase.
• Cdk1 is essential in the control of G2 and mitosis and also may play
additional roles in earlier stages.
• Four distinct subclasses—D-, E-, A-, and B-type cyclins—are involved
in cell cycle regulation
16.
17.
18. • There are 3 major mechanisms of cyclin-CDK complex regulation.
• Firstly, The kinase activation is dependent on phosphorylation of a
threonine residue that is adjacent to the active site (Thr160 in Cdk2).
• This phosphorylation is catalysed by a kinase, called Cdk-activating
kinase (CAK)
• In mammalian cells, phosphorylation occurs after cyclin binding.
• Although it appears that at least two mammalian CAKs exist, the
major CAK is a tri molecular complex composed of Cdk7, cyclin H, and
Mat1.
19.
20. • Secondly, the cyclin-Cdk complex frequently is subject to inhibitory
phosphorylation of Thr14 and Tyr15 residues within the Cdk’s active
site by the Wee1 (Tyr15) and Myt1 (Thr14 and Tyr15) kinases.
• Activation of the cyclin/Cdk complex is then dependent on the
action of a dual-specificity phosphatase called Cdc25.
• Mammalian cells have three different Cdc25 proteins Cdc25a,
Cdc25b, and Cdc25c, which show some specificity for different
cyclin-Cdk complexes.
21.
22. • Thirdly, Cdks are modulated by a series of CdK inhibitors (CKIs)
• The CKIs can be divided into two distinct families based on their
biological properties.
• The first CKI family is named INK4, based on their roles as Inhibitors
of CDK4.
• The INK4 family has four members called p16INK4a, p15INK4b,
p18INK4c, and p19INK4d
• These INK4 proteins specifically prevent the binding of cyclins to
monomeric Cdk4 and Cdk6 but do not inhibit other Cdks.
• The second CKI family is named Cip/Kip and includes three members:
p21Cip1 , p27Kip1, and p57Kip2
• Cip/Kip proteins do not bind to monomeric Cdks but associate with
and inhibit the activity of cyclin-Cdk complexes already formed.
26. • The retinoblastoma protein (pRb) behaves as a classic tumor
suppressor
• RB1 gene is inactivated in approximately one third of all sporadic
human tumors.
• pRb and the pRb-related proteins p107 and p130 are collectively
known as the pocket proteins
• These are transcriptional repressors whose major function is to
inhibit the expression of cell-cycle related proteins
• This suppressive activity is dependent on the ability to prevent cell
cycle entry through inhibition of the E2F transcription factors
• The E2F proteins regulate the cell cycle dependent transcription of
core components of the cell cycle control
27. pRb regulates E2F through two distinct mechanisms
. Directly associates with E2F
and it is sufficient to block
the transcriptional activity of
E2F
pRb-E2F complex can recruit
histone deacetylases to the
promoters of E2F-responsive
genes and thereby actively
repress their transcription
• As Cell cycle entry requires the phosphorylation of pRb by cyclin-Cdk
complexes and the consequent dissociation of pRb from E2F,above
two mechanisms do not allow cell cycle entry
31. • In eukaryotes, two major complexes, PP1 and PP2A, account for more
than 90% of protein phosphatase activity.
• These protein families cooperate in the dephosphorylation
• PP1 and PP2A are major phosphatases responsible for pRb
dephosphorylation during mitotic exit
• Cell cycle ultimately is regulated by the dynamic equilibrium between
Cdks and phosphatases activity.
• In the absence of Cdk activity, the balance tilts in favor of the
phosphatases.
• When Cdks are activated, phosphatase activity is overtaken.
• Reactivation of PP1 and PP2A phosphatases is a mandatory step for
the exit from mitosis and the transition to interphase
33. • ubiquitin-mediated protein degradation is a major regulatory
mechanism to ensure ordered transition through the different
phases of the cell division cycle.
• SCF and APC/C are the ubiquitin ligases which drive the degradation
of cell cycle regulators to accomplish irreversible cell cycle
transitions
• Once SCF binds its substrate, it transfers a ubiquitin molecule within
the target protein which targets the substrate to the proteasome for
degradation.
• The APC/C is a much larger complex but has similar mechanism of
action
36. 1
• In quiescent cells , E2F-responsive genes recruit pocket
proteins, along with their associated histone
deacetylases, to actively repress their transcription
2
• CKIs normally are expressed in quiescent cells
• D-type cyclins are present at very low levels in most
quiescent cells
3
• Now when mitogenic signal comes,mitogens directly
induce the transcription of D class cyclins
• Transcriptional induction of D-type cyclins promotes cell
cycle entry.
37. D-type cyclins
associate
with Cdk4
and Cdk6
This complex
phosphorylate
pRb, partially
inactivating its
transcriptional
suppressor
function
the D-
type
cyclins
inactivate
CKIs
Entry into the
cell cycle
40. • The DNA replication machinery is to ensure that the genome is
copied once—and only once—in each cell cycle.
• This is achieved through a two-step process
• first it establishes a pre replication complex (pre-RC) at origin of
replication, a process that is frequently referred to as origin licensing
• Subsequently it transforms pre-RCs into the preinitiation complex
(pre- IC) that activates DNA replication
• These two steps occur at distinct stages of the cell cycle to ensure
that origins are only licensed once per cell cycle and re replication
cannot occur.
• Pre-RC formation takes place during G1.
41. • The first step is the recruitment of the multiprotein complex called
the origin recognition complex (ORC) to the origin DNA
• The origin recognition complex recruits additional proteins including
Cdc6, Cdt1, and finally the mini chromosome maintenance (MCM)
complex, a helicase that is required to unwind the DNA strands to
form the pre-RC.
• Once cells enter S phase, the transformation of the pre-RC to the
pre-IC requires the activity of two kinases: a Cdk and the Ddf4-
dependent kinase
• The transition from pre-RC to pre-IC results in inhibition of Cdt1 by
ubiquitin-mediated degradation and geminin binding.
• Origin licensing cannot occur again until activation of anaphase-
promoting complex/cyclosome (APC/C) at the end of mitosis allows
accumulation of Cdt1.
42. PRE RC COMPLEX
ORC COMPLEX
PRE INITIATION
COMPLEX
ACTS AS A
HELICASE
AND
UNWINDS
DNA
49. G1/S Checkpoint
• In G1 cells, double-stranded DNA breaks (DSBs) are the most
common and most deleterious type of DNA damage.
• The central components of the DNA damage response (DDR) are two
members of the phosphoinositide 3-kinase-related kinase family
Ataxia telangiectasia mutated (ATM) ATM-rad3-related (ATR)
• The DSBs are recognized by the multifunctional Mre11-Rad50-Nbs1
(MRN) complex.
• MRN complex recruits ATM to the site of damage.
• The active ATM recruits proteins modify the
chromatin at the region of the break activate repair and
signaling Signals Chk2
50. Chk2 influences the G1 cell cycle arrest via two mechanisms
Chk2 phosphorylates all three members of the Cdc25 family
Phosphorylation of these cdc25 family proteins
prevent the activation of cyclin dependent kinases
stop the progression of cell cycle
(rapid response & effect within minutes after DNA damage)
Chk2 phosphorylates p53
51. NORMAL CELL
• p53 protein is maintained at
low steady-state levels because
it has a very short half-life.
• This short half-life is a result of
rapid ubiquitination of p53 by
hdm2 (the human ortholog of
murine mdm2 protein)
degradation of p53.
DIVIDING CELL DURING
G1/S CHECKPOINT AND
Chk2 ACTIVITY
• Phosphorylation of p53 by chk2
prevent association hdm2
• leads to an accumulation of p53
• P53 induces cell cycle arrest
• This p53-mediated arrest takes
longer to develop than does the
cdc25 response
• p53 has the capacity to induce
apoptosis
52.
53.
54. Intra-S Phase Checkpoint
• The major goal to prevent the replication of damaged
DNA
• S phase cells must respond virtually instantaneously to DNA damage
to halt initiation of new replication forks throughout the S phase
• In contrast to DSB in G1 cells , where ATM is solely responsible for
checkpoint activation, in S and G2 checkpoints, recruitment of ATR
also occurs.
Replication-linked DSBs
• S PHASE DNA BREAKS
Non replication linked DSBs
55. Replication - linked DSBs
• the presence of single-stranded
DNA (ssDNA) is a hallmark of
the replication process.
• The ssDNA is coated by
replication protein A (RPA) and
bound by ATR even during the
normal replication process.
• In response to DNA damage,
the ATR kinase is activated, and
it then recruits a variety of
complexes that mediate both
repair and checkpoint
activation, including ATM
Non replication-associated
DSBs
• In first step,these recruit and
activate ATM through the MRN-
dependent process described
previously for the G1/S
checkpoint.
• Then through the action of the
MRN endonuclease it is then
bound by RPA and ATR
• ATR contributes to the
checkpoint response as it
activates Chk1, which also can
phosphorylate the Cdc25
proteins and p53
56.
57. G2 Checkpoint
• G1/S and intra-S phase checkpoints prevent cells from unfaithful
replication
• G2 checkpoint is required to prevent the passage of DNA lesions to
the two daughter cells during mitosis
• DSBs are detected exactly as described previously for the S-phase
non replication associated DSBs.
60. The kinetochore is the protein structure on chromatids where the spindle
fibers attach during cell division to pull sister chromatids apart.
61. Spindle Assembly Checkpoint (SAC)
• To ensure appropriate partitioning of the chromosomes occurs
during mitosis.
• Chromosome segregation does not occur until all condensed sister
chromatid pairs are aligned at the metaphase plate with the
appropriate bi orientation
• This process actually is controlled by a signaling network that
constitutes the SAC
• The core components of this checkpoint are Mad1, Mad2, BubR1,
Bub1
• During prometaphase, these proteins localize to the outer
kinetochore and, in the absence of biorientation, prevent the Cdc20
activator from binding to the APC/C. (to promote to anaphase)
62. Lack of tension or lack of attachment at the kinetochore
stable Mad1-Mad2 complexes
This is able to bind to Cdc20
The Mad2-Cdc20 association triggers the recruitment of BubR1-Bub3
into an APC/C-inhibitory complex (the mitotic checkpoint complex
[MCC]).
a single unattached kinetochore is sufficient to form these complexes
and inhibit APC/C-Cdc20 activity.
separase is inhibited by the high levels of securin
cyclin B–Cdk1 complexes, being unable to cleave the centromeric
cohesin
63. When all chromosomes are bi-polar attached to the mitotic spindle
SAC is satisfied
Mad1 : Mad2 complex is removed from the kinetochores
Cdc20 is now released from the MCC complex
activates the APC/C
rapid ubiquitination and degradation of cyclin B and securin
Inactivation of these two proteins
activation of separase cleaves cohesion of chromatids
66. Unscheduled Cell Cycle Entry in Cancer
• Loss or mutation of the prb tumor suppressor – retinoblastoma,
osteosarcoma, small-cell lung cancers
• Overexpression of cyclins - 50% of invasive breast cancers have
elevated cyclin D
• Cdk4 and cdk6 amplification - breast cancers, sarcomas, gliomas, and
melanomas
• CKI - decreased expression of the p57kip2 is found in human bladder
cancers.
• Germline mutations in p16ink4a - predispose to melanoma
• Deletion of p15ink4b and p16ink4a- lymphomas, mesotheliomas
67. Mutations in p53 and Checkpoint Regulators
• The most frequently altered cell cycle
• germline mutations of p53 - Li-Fraumeni syndrome with significantly
increased rates of brain tumors, breast cancers
• Mdm2 gene amplification - resulting in Mdm2 protein
overexpression and subsequent p53 inactivation
• ATM mutations - ataxia-telangiectasia, elevated incidence of
leukemias, lymphomas, and breast cancer
• Chk2 mutations - several cancers, including lung cancer
• Chk1 mutations - human colon and endometrial cancer
68. Aneuploidy and Chromosomal Instability
• Abnormal chromosome number - “aneuploidy” is a frequent feature
of cancer cells
• Estimates suggest that normal cells mis -segregate a chromosome
every hundred cell divisions
• This rate is dramatically increased in cells that display Chromosomal
instability, which missegregate a chromosome in every one to three
cell divisions
• Several regulators such as separase, securin, condensins, Cdc20, or
Aurora kinases, as well as the SAC component Mps1, are included in
the overexpression signature that marks chromosomally unstable
cancers.
74. • Most cells in postnatal tissues are quiescent. Exceptions include
abundant cells of the hematopoietic system, skin, and gastrointestinal
mucosa, as well as other minor progenitor populations in other
tissues.
• Many quiescent cells can re enter into the cell cycle with the
appropriate stimuli, and the control of this process is essential for
tissue homeostasis
• The key challenges for proliferating cells are to make an accurate copy
of the 3 billion bases of DNA (S phase) and to segregate the
duplicated chromosomes equally into daughter cells (mitosis)
• Progression through the cell cycle is dependent on both intrinsic and
extrinsic factors, such as growth factor or cytokine exposure, cell-to-
cell contact, and basement membrane attachments
75. • The internal cell cycle machinery is controlled largely by oscillating
levels of cyclin proteins and by modulation of cyclin-dependent kinase
(Cdk) activity. One way in which growth factors regulate cell cycle
progression is by affecting the levels of the D-type cyclins, Cdk activity,
and the function of the retinoblastoma protein
• Cell cycle checkpoints are surveillance mechanisms that link the rate
of cell cycle transitions to the timely and accurate completion of prior
dependent events. p53 is a checkpoint protein that induces cell cycle
arrest, senescence, or death in response to cellular stress
• Checkpoints minimize replication and segregation of damaged DNA
or the abnormal segregation of chromosomes to daughter cells, thus
protecting cells against genome instability.
• Disruption of cell cycle controls is a hallmark of all malignant cells.
alterations include dysregulation of the core cell cycle machinery,
and/or disruption of cell cycle checkpoint controls