Apoptosis
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The document summarizes apoptosis, or programmed cell death. It describes apoptosis as an energy-dependent process for removing unwanted cells, distinguishing it from necrosis. The two main pathways of apoptosis, the extrinsic and intrinsic pathways, are outlined. The extrinsic pathway involves death receptors and ligands that activate initiator caspases like caspase 8. The intrinsic pathway involves signals within the cell that cause changes in mitochondria, activating initiator caspase 9. Both pathways activate effector caspases like caspase 3 that carry out the destruction of the cell. Apoptosis plays important roles in development, the immune system, and preventing diseases like cancer.
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Apoptosis in health and diseases
This document provides an overview of apoptosis in health and disease. It begins with definitions of apoptosis and its key characteristics. It then discusses the intrinsic and extrinsic pathways of apoptosis, involving proteins like caspases, Bcl-2 family members, cytochrome c, and death receptors. The document outlines the morphological changes seen in apoptotic cells and methods to detect apoptosis. It discusses the significance of apoptosis in physiological conditions like development and tissue homeostasis. Finally, it examines how dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative conditions.
Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,n...
Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,n...Bahaudin zakriya university multan pakistan
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimuleIntrinsic and Extrinsic Pathway of Apoptosis
This document provides an overview of apoptosis (programmed cell death) at the cellular level. It discusses how apoptosis can be initiated through either the intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell like mitochondrial membrane permeability, while the extrinsic pathway involves death receptors on the cell surface and their ligands. Key proteins and complexes involved in each pathway are caspase enzymes and the apoptosome. Research on apoptosis has increased understanding of diseases like cancer that involve deregulated cell proliferation and death.
Apoptosis
Apoptosis is a form of programmed cell death that eliminates unwanted cells through activation of intracellular gene products. It occurs physiologically during embryogenesis and in adult tissues, and pathologically to remove cells damaged beyond repair. The key events of apoptosis include activation of caspase enzymes, DNA fragmentation, and recognition of dead cells by phagocytes. Apoptosis occurs via intrinsic and extrinsic pathways, both activating executioner caspases that break down nuclear and cellular components, leading to removal of dead cells without inflammation.
Apoptosis
The document provides an overview of apoptosis, or programmed cell death. It describes the three main pathways that can trigger apoptosis: the extrinsic or death receptor pathway, the intrinsic or mitochondrial pathway, and the perforin/granzyme pathway. The pathways activate initiator caspases that go on to activate executioner caspases, leading to characteristic cell changes like nuclear fragmentation and membrane blebbing. Apoptotic cells are then phagocytosed to prevent inflammation.
Apoptosis
Apoptosis is a normal and controlled form of cell death that plays an important role in multicellular organisms. It occurs through either an intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell such as mitochondrial or endoplasmic reticulum damage, while the extrinsic pathway involves death receptors on the cell surface that activate caspases when bound by ligands. Apoptosis helps shape tissues and organs during development, eliminates unnecessary or harmful cells, and prevents diseases like cancer from developing.
Apoptosis extrinsic mechanism
The extrinsic apoptosis pathway begins outside the cell when death ligands bind to death receptors on the cell surface. This causes the receptors to cluster and form a death-inducing signaling complex (DISC) which activates initiator caspases. The initiator caspases then activate effector caspases that execute the cell's apoptosis by degrading cellular proteins and organelles. Key events in this pathway include DISC formation, caspase activation, and the eventual phagocytosis of the cell fragments.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
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Apoptosis in health and diseases
This document provides an overview of apoptosis in health and disease. It begins with definitions of apoptosis and its key characteristics. It then discusses the intrinsic and extrinsic pathways of apoptosis, involving proteins like caspases, Bcl-2 family members, cytochrome c, and death receptors. The document outlines the morphological changes seen in apoptotic cells and methods to detect apoptosis. It discusses the significance of apoptosis in physiological conditions like development and tissue homeostasis. Finally, it examines how dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative conditions.
Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,n...
Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,n...Bahaudin zakriya university multan pakistan
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimuleIntrinsic and Extrinsic Pathway of Apoptosis
This document provides an overview of apoptosis (programmed cell death) at the cellular level. It discusses how apoptosis can be initiated through either the intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell like mitochondrial membrane permeability, while the extrinsic pathway involves death receptors on the cell surface and their ligands. Key proteins and complexes involved in each pathway are caspase enzymes and the apoptosome. Research on apoptosis has increased understanding of diseases like cancer that involve deregulated cell proliferation and death.
Apoptosis
Apoptosis is a form of programmed cell death that eliminates unwanted cells through activation of intracellular gene products. It occurs physiologically during embryogenesis and in adult tissues, and pathologically to remove cells damaged beyond repair. The key events of apoptosis include activation of caspase enzymes, DNA fragmentation, and recognition of dead cells by phagocytes. Apoptosis occurs via intrinsic and extrinsic pathways, both activating executioner caspases that break down nuclear and cellular components, leading to removal of dead cells without inflammation.
Apoptosis
The document provides an overview of apoptosis, or programmed cell death. It describes the three main pathways that can trigger apoptosis: the extrinsic or death receptor pathway, the intrinsic or mitochondrial pathway, and the perforin/granzyme pathway. The pathways activate initiator caspases that go on to activate executioner caspases, leading to characteristic cell changes like nuclear fragmentation and membrane blebbing. Apoptotic cells are then phagocytosed to prevent inflammation.
Apoptosis
Apoptosis is a normal and controlled form of cell death that plays an important role in multicellular organisms. It occurs through either an intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell such as mitochondrial or endoplasmic reticulum damage, while the extrinsic pathway involves death receptors on the cell surface that activate caspases when bound by ligands. Apoptosis helps shape tissues and organs during development, eliminates unnecessary or harmful cells, and prevents diseases like cancer from developing.
Apoptosis extrinsic mechanism
The extrinsic apoptosis pathway begins outside the cell when death ligands bind to death receptors on the cell surface. This causes the receptors to cluster and form a death-inducing signaling complex (DISC) which activates initiator caspases. The initiator caspases then activate effector caspases that execute the cell's apoptosis by degrading cellular proteins and organelles. Key events in this pathway include DISC formation, caspase activation, and the eventual phagocytosis of the cell fragments.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Advances in apoptotic pathways
1. Apoptosis is a tightly regulated form of programmed cell death that plays an important role in development, tissue homeostasis, and the immune system. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
2. The process of apoptosis involves initiator caspases that activate executioner caspases, leading to degradation of nuclear and cytoplasmic components. Mitochondria also play a key role by releasing pro-apoptotic factors. Various proteins regulate apoptosis, including Bcl-2 family members and inhibitors of apoptosis (IAPs).
3. Dysregulation of apoptosis contributes to diseases like cancer, neurodegeneration, and HIV/AIDS. Detection of
Apaptosis
This document discusses apoptosis in cardiovascular disorders. It provides an overview of apoptotic pathways and diseases in the cardiovascular system where apoptosis plays a role. It discusses imaging techniques to study apoptosis and potential therapeutic options to modulate apoptosis. It defines key terms related to apoptosis and describes the intrinsic and extrinsic apoptotic pathways. It also compares necrosis and apoptosis and discusses the role of apoptosis in cardiac development and heart failure.
Programmed Cell death or Apoptosis
Three studies on programmed cell death in plants are summarized:
1. A study showed that heat-induced cell death in cucumber cotyledons resulted in DNA fragmentation and the release of cytochrome c from mitochondria into the cytosol, demonstrating conserved mechanisms with animal apoptosis.
2. A study found that caspase-specific peptide inhibitors effectively inhibited chemically-induced cell death in tomato cells, indicating caspase-like proteases mediate plant apoptotic pathways.
3. A study showed that anthocyanins from black soybeans protected human skin cells from UVB-induced reactive oxygen species, apoptosis, and caspase activation by preventing pro-apoptotic signaling.
Apoptosis
This document discusses apoptosis, or programmed cell death. It defines apoptosis as the demise of cells through programmed cell death and describes it as being characterized by well-orchestrated events. It notes there are two pathways that can initiate apoptosis - the intrinsic pathway, which is triggered by internal stimuli like DNA damage, and the extrinsic pathway, which is triggered by external death signals binding to cell surface death receptors. Both pathways ultimately lead to activation of caspases and the execution phase of apoptosis.
Apoptosis
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis (Programm of cell death)
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. During apoptosis, cells exhibit characteristic changes such as blebbing, shrinkage, nuclear fragmentation, and chromosomal DNA fragmentation. Between 50-70 billion cells die each day in the human body through apoptosis. Apoptosis is important for development and shaping of embryos, as well as for destroying infected, cancerous, or damaged cells. Caspases are a family of cysteine proteases that play essential roles in apoptosis. There are intrinsic and extrinsic pathways of caspase activation - the intrinsic pathway involves mitochondria and the extrinsic involves death receptors. Inhibitor of apoptosis proteins can block apoptosis and lead to conditions like cancer if unregulated.
Apoptosis
The document discusses apoptosis, or programmed cell death. It defines apoptosis as a process where cells undergo changes like nuclear fragmentation, cell shrinkage, and blebbing of the plasma membrane. This results in the formation of apoptotic bodies containing nuclear and cytoplasmic material. The document notes that apoptosis is initiated by caspase activation and mitochondrial changes, and that it involves DNA fragmentation and membrane alterations during cell death.
6. apoptosis mdzah- sp sinhasan
Apoptosis is a tightly regulated form of programmed cell death that occurs through activation of intracellular enzymes. It plays an important role in physiological processes like embryogenesis and pathological conditions like viral infections. During apoptosis, cells shrink and their chromatin condenses. This leads to formation of apoptotic bodies that are phagocytosed by macrophages. The process is controlled through signaling pathways and mitochondrial permeability, which activate caspase enzymes that degrade DNA and proteins, cross-link proteins, and mark the cell for phagocytosis. Understanding apoptosis provides insights into development, disease mechanisms, and potential therapies.
Apoptosis seminar f
Apoptosis, or programmed cell death, plays an important role in development, immunity, and maintenance of genomic integrity. Disruption of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative diseases. The document discusses the key stages and molecular mechanisms of apoptosis, including the roles of caspases, Bcl-2 family proteins, and death receptors. It also covers the importance of apoptosis in processes like immune system development, tissue remodeling, and response to DNA damage. Therapeutic strategies aim to either inhibit inappropriate apoptosis or induce apoptosis in conditions like cancer.
Mechanism cell deaths
This document summarizes various mechanisms of cell death, including apoptosis and necrosis. Apoptosis, or programmed cell death, involves activation of caspases through intrinsic or extrinsic pathways, leading to controlled cell death without inflammation. Necrosis occurs due to external factors causing cell membrane rupture and inflammatory cell death. Other mechanisms discussed include autophagy, which involves lysosomal degradation of cellular components, and entosis, where one cell crawls inside another to die.
Apoptosis
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
Apoptosis
Apoptosis is a programmed cell death process that occurs in multicellular organisms. It is an important physiological process that helps remove damaged or unnecessary cells. During apoptosis, cells shrink, condense and fragment into apoptotic bodies that are then phagocytosed and removed without triggering inflammation. Apoptosis is regulated by a network of pro- and anti-apoptotic genes and proteins and occurs through intrinsic and extrinsic pathways that activate caspase enzymes and lead to cell death. Apoptosis plays a key role in development, homeostasis, and protection against unhealthy cells.
Apoptosis basics + microphotographs
Apoptosis is a
-pathway of cell death that is
-induced by an internally regulated program
-in which cells destined to die activate intrinsic enzymes that --degrade the cells’ own nuclear DNA and also nuclear and cytoplasmic proteins
-With minimal host reaction.
APOPTOSIS : The programmed cell death
Apoptosis and necrosis are two types of cell death. Apoptosis is a regulated process where cells actively cause their own death, minimizing harm to surrounding cells and tissue. It occurs normally during development and to remove damaged cells, and is controlled through caspase activation via intrinsic and extrinsic pathways. In contrast, necrosis is unregulated cell death caused by external factors like toxins or trauma. Apoptosis plays important roles in development, tissue homeostasis, and diseases like cancer when its regulation is disrupted. The cell cycle and checkpoints also interact with apoptosis to control cell proliferation and death.
Apoptosis
Apoptosis, or programmed cell death, is regulated by intrinsic and extrinsic pathways. The intrinsic pathway involves mitochondria releasing cytochrome c which activates caspase proteases, leading to DNA fragmentation and cell death. The extrinsic pathway involves death receptors activating caspase-8 through adaptor proteins. Caspases are cysteine proteases that cleave other proteins and dismantle the cell in apoptosis. The Bcl-2 family and inhibitor of apoptosis (IAP) proteins also regulate apoptosis. Dysregulation of apoptosis contributes to diseases like cancer and neurodegeneration.
Apoptosis
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
Apoptosis
Apoptosis is a coordinated programmed cell death process. It involves the single or group of cells shrinking in size and forming apoptotic bodies which are then phagocytosed without causing inflammation. There are two main pathways that initiate apoptosis - the extrinsic death receptor pathway and the intrinsic mitochondrial pathway. These pathways involve a cascade of molecular events culminating in the activation of caspases. The execution phase is carried out by caspase-8, caspase-9 and caspase-3/6 which leads to the formation of apoptotic bodies and concludes with phagocytosis.
Apoptosis
Cell death is the basic process. Various genes are related to it along with two basic pathways. Apoptosis is needed to avoid some basic as well as lethal diseases.
Apoptosis
Apoptosis is a programmed cell death process that is essential for maintaining homeostasis. It involves the activation of caspases that trigger cell dismantling. Central regulators include Bcl-2 family proteins like Bax and Bak that induce mitochondrial membrane permeabilization and cytochrome c release upon activation. Cytochrome c then activates caspase-9 through formation of the apoptosome complex, triggering a caspase cascade that leads to apoptosis. Proteins like IAPs inhibit caspase activity and must be neutralized by other proteins like SMAC/Diablo to allow apoptosis to proceed. Together, these events ensure damaged or unnecessary cells are removed in a controlled manner.
Apoptosis seminar
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
Apoptosis
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis Pathway
The document discusses apoptosis, or programmed cell death. It begins by defining apoptosis and explaining that it is a normal physiological process in multicellular organisms for tissue homeostasis and development. Apoptosis is regulated by both pro-apoptotic and anti-apoptotic factors like the Bcl-2 family of proteins. It involves characteristic morphological and biochemical changes in cells, including blebbing, nuclear fragmentation, and DNA fragmentation. Caspases play a central role in apoptosis by activating a cascade of proteolytic enzymes. Apoptosis occurs through both the intrinsic mitochondrial pathway and the extrinsic death receptor pathway.
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1. Apoptosis is a tightly regulated form of programmed cell death that plays an important role in development, tissue homeostasis, and the immune system. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
2. The process of apoptosis involves initiator caspases that activate executioner caspases, leading to degradation of nuclear and cytoplasmic components. Mitochondria also play a key role by releasing pro-apoptotic factors. Various proteins regulate apoptosis, including Bcl-2 family members and inhibitors of apoptosis (IAPs).
3. Dysregulation of apoptosis contributes to diseases like cancer, neurodegeneration, and HIV/AIDS. Detection of
Apaptosis
This document discusses apoptosis in cardiovascular disorders. It provides an overview of apoptotic pathways and diseases in the cardiovascular system where apoptosis plays a role. It discusses imaging techniques to study apoptosis and potential therapeutic options to modulate apoptosis. It defines key terms related to apoptosis and describes the intrinsic and extrinsic apoptotic pathways. It also compares necrosis and apoptosis and discusses the role of apoptosis in cardiac development and heart failure.
Programmed Cell death or Apoptosis
Three studies on programmed cell death in plants are summarized:
1. A study showed that heat-induced cell death in cucumber cotyledons resulted in DNA fragmentation and the release of cytochrome c from mitochondria into the cytosol, demonstrating conserved mechanisms with animal apoptosis.
2. A study found that caspase-specific peptide inhibitors effectively inhibited chemically-induced cell death in tomato cells, indicating caspase-like proteases mediate plant apoptotic pathways.
3. A study showed that anthocyanins from black soybeans protected human skin cells from UVB-induced reactive oxygen species, apoptosis, and caspase activation by preventing pro-apoptotic signaling.
Apoptosis
This document discusses apoptosis, or programmed cell death. It defines apoptosis as the demise of cells through programmed cell death and describes it as being characterized by well-orchestrated events. It notes there are two pathways that can initiate apoptosis - the intrinsic pathway, which is triggered by internal stimuli like DNA damage, and the extrinsic pathway, which is triggered by external death signals binding to cell surface death receptors. Both pathways ultimately lead to activation of caspases and the execution phase of apoptosis.
Apoptosis
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis (Programm of cell death)
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. During apoptosis, cells exhibit characteristic changes such as blebbing, shrinkage, nuclear fragmentation, and chromosomal DNA fragmentation. Between 50-70 billion cells die each day in the human body through apoptosis. Apoptosis is important for development and shaping of embryos, as well as for destroying infected, cancerous, or damaged cells. Caspases are a family of cysteine proteases that play essential roles in apoptosis. There are intrinsic and extrinsic pathways of caspase activation - the intrinsic pathway involves mitochondria and the extrinsic involves death receptors. Inhibitor of apoptosis proteins can block apoptosis and lead to conditions like cancer if unregulated.
Apoptosis
The document discusses apoptosis, or programmed cell death. It defines apoptosis as a process where cells undergo changes like nuclear fragmentation, cell shrinkage, and blebbing of the plasma membrane. This results in the formation of apoptotic bodies containing nuclear and cytoplasmic material. The document notes that apoptosis is initiated by caspase activation and mitochondrial changes, and that it involves DNA fragmentation and membrane alterations during cell death.
6. apoptosis mdzah- sp sinhasan
Apoptosis is a tightly regulated form of programmed cell death that occurs through activation of intracellular enzymes. It plays an important role in physiological processes like embryogenesis and pathological conditions like viral infections. During apoptosis, cells shrink and their chromatin condenses. This leads to formation of apoptotic bodies that are phagocytosed by macrophages. The process is controlled through signaling pathways and mitochondrial permeability, which activate caspase enzymes that degrade DNA and proteins, cross-link proteins, and mark the cell for phagocytosis. Understanding apoptosis provides insights into development, disease mechanisms, and potential therapies.
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Apoptosis, or programmed cell death, plays an important role in development, immunity, and maintenance of genomic integrity. Disruption of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative diseases. The document discusses the key stages and molecular mechanisms of apoptosis, including the roles of caspases, Bcl-2 family proteins, and death receptors. It also covers the importance of apoptosis in processes like immune system development, tissue remodeling, and response to DNA damage. Therapeutic strategies aim to either inhibit inappropriate apoptosis or induce apoptosis in conditions like cancer.
Mechanism cell deaths
This document summarizes various mechanisms of cell death, including apoptosis and necrosis. Apoptosis, or programmed cell death, involves activation of caspases through intrinsic or extrinsic pathways, leading to controlled cell death without inflammation. Necrosis occurs due to external factors causing cell membrane rupture and inflammatory cell death. Other mechanisms discussed include autophagy, which involves lysosomal degradation of cellular components, and entosis, where one cell crawls inside another to die.
Apoptosis
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
Apoptosis
Apoptosis is a programmed cell death process that occurs in multicellular organisms. It is an important physiological process that helps remove damaged or unnecessary cells. During apoptosis, cells shrink, condense and fragment into apoptotic bodies that are then phagocytosed and removed without triggering inflammation. Apoptosis is regulated by a network of pro- and anti-apoptotic genes and proteins and occurs through intrinsic and extrinsic pathways that activate caspase enzymes and lead to cell death. Apoptosis plays a key role in development, homeostasis, and protection against unhealthy cells.
Apoptosis basics + microphotographs
Apoptosis is a
-pathway of cell death that is
-induced by an internally regulated program
-in which cells destined to die activate intrinsic enzymes that --degrade the cells’ own nuclear DNA and also nuclear and cytoplasmic proteins
-With minimal host reaction.
APOPTOSIS : The programmed cell death
Apoptosis and necrosis are two types of cell death. Apoptosis is a regulated process where cells actively cause their own death, minimizing harm to surrounding cells and tissue. It occurs normally during development and to remove damaged cells, and is controlled through caspase activation via intrinsic and extrinsic pathways. In contrast, necrosis is unregulated cell death caused by external factors like toxins or trauma. Apoptosis plays important roles in development, tissue homeostasis, and diseases like cancer when its regulation is disrupted. The cell cycle and checkpoints also interact with apoptosis to control cell proliferation and death.
Apoptosis
Apoptosis, or programmed cell death, is regulated by intrinsic and extrinsic pathways. The intrinsic pathway involves mitochondria releasing cytochrome c which activates caspase proteases, leading to DNA fragmentation and cell death. The extrinsic pathway involves death receptors activating caspase-8 through adaptor proteins. Caspases are cysteine proteases that cleave other proteins and dismantle the cell in apoptosis. The Bcl-2 family and inhibitor of apoptosis (IAP) proteins also regulate apoptosis. Dysregulation of apoptosis contributes to diseases like cancer and neurodegeneration.
Apoptosis
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
Apoptosis
Apoptosis is a coordinated programmed cell death process. It involves the single or group of cells shrinking in size and forming apoptotic bodies which are then phagocytosed without causing inflammation. There are two main pathways that initiate apoptosis - the extrinsic death receptor pathway and the intrinsic mitochondrial pathway. These pathways involve a cascade of molecular events culminating in the activation of caspases. The execution phase is carried out by caspase-8, caspase-9 and caspase-3/6 which leads to the formation of apoptotic bodies and concludes with phagocytosis.
Apoptosis
Cell death is the basic process. Various genes are related to it along with two basic pathways. Apoptosis is needed to avoid some basic as well as lethal diseases.
Apoptosis
Apoptosis is a programmed cell death process that is essential for maintaining homeostasis. It involves the activation of caspases that trigger cell dismantling. Central regulators include Bcl-2 family proteins like Bax and Bak that induce mitochondrial membrane permeabilization and cytochrome c release upon activation. Cytochrome c then activates caspase-9 through formation of the apoptosome complex, triggering a caspase cascade that leads to apoptosis. Proteins like IAPs inhibit caspase activity and must be neutralized by other proteins like SMAC/Diablo to allow apoptosis to proceed. Together, these events ensure damaged or unnecessary cells are removed in a controlled manner.
Apoptosis seminar
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
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Similar to Apoptosis
Apoptosis
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis Pathway
The document discusses apoptosis, or programmed cell death. It begins by defining apoptosis and explaining that it is a normal physiological process in multicellular organisms for tissue homeostasis and development. Apoptosis is regulated by both pro-apoptotic and anti-apoptotic factors like the Bcl-2 family of proteins. It involves characteristic morphological and biochemical changes in cells, including blebbing, nuclear fragmentation, and DNA fragmentation. Caspases play a central role in apoptosis by activating a cascade of proteolytic enzymes. Apoptosis occurs through both the intrinsic mitochondrial pathway and the extrinsic death receptor pathway.
Apoptosis slide
The intrinsic pathway of apoptosis is triggered by intracellular stress signals like DNA damage or lack of growth factors. The Bcl-2 family of proteins regulate mitochondrial outer membrane permeabilization which leads to the release of cytochrome c from the mitochondria. Cytochrome c binds to Apaf-1 and procaspase-9 to form the apoptosome, activating caspase-9 and the downstream caspase-3, resulting in apoptosis. This pathway does not require death receptors and is instead initiated by internal damage signals within the cell.
Apoptosis (Intrinsic And Extrinsic Pathway with assays)
- Apoptosis is a process of programmed cell death that occurs under normal physiological conditions and involves the active participation of the cell. It is important for development and homeostasis.
- The intrinsic pathway is mitochondria-mediated and does not require receptor activation. It is triggered by intracellular signals like DNA damage or lack of growth factors. This causes changes in mitochondrial permeability and the release of pro-apoptotic factors like cytochrome c.
- Cytochrome c activates caspase-9 through the apoptosome complex, leading to caspase-3 activation and cell death. The process is regulated by Bcl-2 family proteins that control mitochondrial permeability.
Apoptosis
1. Programmed cell death, also known as apoptosis, is essential for proper development and for destroying harmful cells.
2. Apoptosis is regulated by caspases, which are cysteine-dependent aspartate specific proteases. Caspases activate a proteolytic cascade that leads to cell death.
3. There are three main apoptotic pathways: the extrinsic pathway which involves death receptors, the intrinsic pathway which involves the mitochondria, and the granzyme pathway which uses granzymes from cytotoxic T cells and natural killer cells.
Seminar- recent advances in apoptosis
Add MTT reagent and incubate. Mitochondrial enzymes in viable cells convert MTT into an insoluble purple formazan product. Lyse cells and solubilize formazan with solvent. Measure absorbance which is directly proportional to number of viable cells. The more viable cells, the higher the absorbance. MTT assay is a sensitive, quantitative and reliable colorimetric method to measure cell viability and proliferation.
physiology of apoptosis first year mbbs medical.pdf
The document summarizes apoptosis (programmed cell death) through three parts:
Part 1 introduces apoptosis, its history, morphological hallmarks, and provides examples of apoptosis in development including web-footed chickens.
Part 2 describes the key mechanisms and pathways of apoptosis including caspases, the intrinsic mitochondrial pathway involving Bcl-2 proteins and p53, and the extrinsic death receptor pathway.
Part 3 outlines the importance of apoptosis in normal physiology and development and consequences of deregulated apoptosis such as neurodegeneration when in excess and cancer when deficient.
Apoptosis
The document summarizes key aspects of apoptosis including:
- The origins and definition of the term apoptosis from Greek meaning "falling leaves".
- The significance of apoptosis in development and maintenance of tissues by removing excess or damaged cells.
- The morphological features of apoptosis including membrane blebbing, nuclear fragmentation, and formation of apoptotic bodies.
- The molecular mechanisms including caspase signaling pathways like the intrinsic pathway involving mitochondria and the extrinsic pathway involving death receptors.
- Regulatory mechanisms involving proteins like Bcl-2 that balance survival and death signals.
- Dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and HIV infection.
APOPTOSIS MBBS.pdf
Apoptosis is a programmed cell death process that occurs in physiological and pathological conditions. It is mediated by caspases and involves two main pathways - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. Both pathways activate initiator and executioner caspases that degrade cellular proteins and lead to characteristic morphological changes including cell shrinkage, nuclear fragmentation, and formation of apoptotic bodies that are phagocytosed without inflammation. Apoptosis is regulated and differs from necrosis in being an energy-dependent process without inflammatory response.
Apoptosis in plant cell
The document discusses various types of programmed cell death (PCD), including apoptosis, autophagy, paraptosis, autoschizis, oncosis, and necrosis. It provides details on the characteristics and mechanisms of apoptosis and autophagy. Apoptosis involves blebbing, cell shrinkage, nuclear fragmentation, and is mediated by caspases through the intrinsic and extrinsic pathways. Autophagy results in autophagosomic-lysosomal degradation of cytoplasmic contents and organelles. The document also discusses some plant-specific features of apoptosis and its role in pollen self-incompatibility.
apopwqgdcbhuredgbcfyhhvhcctosis (1).pptx
This document provides an overview of apoptosis, or programmed cell death. It begins with an introduction defining apoptosis and its importance in development, aging, and disease. It then describes the main types and mechanisms of apoptosis, including the extrinsic and intrinsic pathways. Key features of apoptosis like morphology, assays to detect it, and differences from necrosis are summarized. The document concludes by discussing other forms of programmed cell death and clinical applications of understanding apoptosis.
Apoptosis
Apoptosis is a programmed cell death process that removes unwanted cells. It is mediated by caspase enzymes and leads to cell fragmentation into apoptotic bodies that are phagocytosed. There are two main pathways - the intrinsic mitochondrial pathway, where cellular stress leads to mitochondrial cytochrome c release and caspase activation, and the extrinsic death receptor pathway, where death ligands such as FasL bind receptors and recruit caspase-8. Both pathways activate executioner caspases like caspase-3 to degrade cellular proteins and carry out apoptosis. Disorders can arise from too little apoptosis, allowing abnormal cell survival like in cancer, or excessive apoptosis leading to cell loss in diseases like neurodegeneration.
Cell death,regulators, apoptosis,necrosis,autophagy
The document summarizes different types of cell death including programmed cell death (PCD), apoptosis, necrosis, and autophagy. It describes key aspects of apoptosis such as the intrinsic and extrinsic pathways, the role of caspases and Bcl-2 proteins, mitochondrial involvement, and morphological changes cells undergo during apoptosis. Necrosis is described as unprogrammed cell death caused by external factors like trauma or infection. Autophagy is noted as another form of programmed cell death.
Apoptosis
Apoptosis is a tightly regulated form of programmed cell death that plays an important role in tissue homeostasis, development, and the immune system. It is characterized by fragmentation of DNA and the nucleus. There are two main pathways that trigger apoptosis - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway - which both activate caspases and lead to dismantling of the cell. Apoptosis is important for removing damaged, unneeded, or infected cells, and balancing it with cell proliferation is critical for health.
Apoptosis.pptx
Apoptosis is a tightly regulated and programmed form of cell death that is essential for tissue homeostasis. It is characterized by nuclear fragmentation, membrane blebbing, and phagocytosis of cellular debris without inflammation. The intrinsic pathway is mediated by mitochondria and pro-apoptotic Bcl-2 family proteins, while the extrinsic pathway involves death receptors and caspase activation. Caspases are cysteine proteases that dismantle the cell through cleavage of structural proteins and DNA. Apoptosis must be balanced, as too little can lead to cancer and too much can contribute to diseases.
APOPTOSIS by dr Alfarah.pptx
1) Apoptosis is a tightly regulated form of programmed cell death that occurs as a normal physiological process or in pathological conditions. It is characterized by cell shrinkage, chromatin condensation, DNA fragmentation, and formation of membrane-bound apoptotic bodies that are phagocytosed without inflammation.
2) The intrinsic and extrinsic pathways regulate apoptosis through a cascade of caspase activation. The intrinsic pathway involves mitochondrial permeabilization and cytochrome c release in response to cellular stress. This activates caspase-9 and downstream executioner caspases like caspase-3. The extrinsic pathway is triggered via death receptors engaging caspase-8 and -10. Both pathways converge on caspase activation and cell dismantling.
3)
Apoptosis and CANCER biology 2020.pdf
APOPTOSIS & CANCER
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Apoptosis
Apoptosis is a tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
Apoptosis
This presentation is about Necrosis, Apoptosis and Necroptosis in physiologic and some pathological conditions
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Apoptosis
- 1. By- Nisha Lakra M.Sc 2nd SEMESTER DEPARTMENT OF Applied genetics Brindavan College
- 2. Apoptosis is the process of programmed cell death. The word apoptosis was introduced by Kerr, Wyllie and Currie to describe a form of cell death distinct from necrosis.
- 3. Apoptosis • Chromatin condensation • Cell Shrinkage • Preservation of Organelles and cell membranes • Rapid engulfment by neighboring cells preventing inflammation Necrosis • Nuclear swelling • Cell Swelling • Disruption of Organelles • Rupture of cell and release of cellular contents • Inflammatory response
- 4. Apoptosis is an energy dependent programmed cell death for removal of unwanted individual cells
- 5. Death Ligands Effector Caspase 3 Death Receptors Initiator Caspase 8 Cell death DNA damage & p53 Mitochondria/ Cytochrome C Initiator Caspase 9 “Extrinsic Pathway” “Intrinsic Pathway”
- 6. • They belong to a group of enzymes known as cysteine proteases,Zymogens- inactive forms. • Caspase 8 and 10- initiator (extrinsic) • Caspase 9- initiator (intrinsic) Single chain of pro-enzymes. Contains an N-terminal domain, a small subunit and a large subunit (similar to a ribosome). Apoptotic stimulus Activation Substrate Cleavage Enzyme.
- 7. Inflammatory Caspases: 1, 4, and 5 Initiator Caspases: 2, 8, 9, and 10 Long N-terminal domain Interact with effector caspases Effector Caspases: 3, 6, and 7 Little to no N-terminal domain Initiate cell death
- 8. It involves transmembrane death receptors that are members of the tumor necrosis factor (TNF) receptor gene superfamily. ligands of these receptors are FasL, TNF-alpha, Apo3L, and Apo2L. Corresponding receptors are FasR, TNFR1, DR3, and DR4/DR5, respectively. The signal transduction of the extrinsic pathway involves several caspases which are proteases with specific cellular targets.
- 10. It involves non-receptor–mediated intracellular signals, inducing activities in the mitochondria that initiate apoptosis. Pro-apoptotic proteins activate caspases that mediate the destruction of the cell through many pathways. The regulation of pro-apoptotic events in the mitochondria occurs through activity of members of the Bcl-2 family of proteins and the tumor suppressor protein p53. Members of the Bcl-2 family of proteins may be pro- or anti-apoptotic. The anti-apoptotic proteins are Bcl-2, Bcl- x, Bcl-xL, Bcl-XS, Bcl-w, and BAG. Pro-apoptotic proteins include Bcl-10, Bax, Bak, Bid, Bad, Bim, Bik, and Blk.
- 12. IMPORTANCE OF APOPTOSIS o Important in normal physiology / development – Development: Immune systems maturation, Morphogenesis, Neural development – Adult: Immune privilege, DNA damage and wound repair. o Excess apoptosis – Neurodegenerative diseases o Deficient apoptosis – Cancer – Autoimmunity
- 13. APOPTOSIS: important in embryogenesis Morphogenesis (eliminates excess cells): Selection (eliminates non-functional cells):
- 14. APOPTOSIS: important in embryogenesis Immunity (eliminates dangerous cells): Self antigen recognizing cell Organ size (eliminates excess cells):
- 15. Thank you