Molecular aspects of pharmacology, Apoptosis
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Apoptosis is a form of programmed cell death that is important for normal development and physiology. It removes cells in an orderly way that is different from necrosis. Apoptosis plays a key role in development by removing cells like the tadpole tail and in maintaining balance by eliminating infected or damaged cells. The process is carefully coordinated and involves cell collapse, protein degradation, DNA fragmentation, and engulfment of the corpse by neighboring cells. Apoptosis can be initiated through either extrinsic pathways involving death ligands and receptors or intrinsic pathways involving mitochondria and DNA damage. This leads to activation of initiator and effector caspases that carry out the process of cell death.
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Apoptosis
Avhijit Roy, a 3rd year B.Pharm student, is researching apoptosis for his project. Apoptosis is a form of programmed cell death that was first introduced in 1972 and plays a role in many physiologic and pathologic processes. It involves biochemical changes like proteolysis and appearance of glycoproteins, as well as molecular mechanisms including initiators that are transmembranous, intracellular or extracellular, activation of caspases and cell death receptors, and growth controlling genes leading to phagocytosis without inflammation.
Apoptosis
This document discusses apoptosis, or programmed cell death. It describes how apoptosis is important in physiological and pathological processes. Physiologically, apoptosis helps sculpt tissues during embryo development and replaces intestinal epithelium cells. Pathologically, apoptosis causes cell death in tumors exposed to chemotherapy, viral infections, and organ atrophy from stimulus withdrawal. Biochemically, apoptosis involves proteolysis, protein cross-linkages, nuclear pyknosis, and phosphatidylserine exposure. Initiation can occur via transmembrane, intracellular, or extracellular signals. The process involves caspase activation, death receptor activation, and growth gene regulation, ultimately leading to cell death and non-inflammatory phagocytosis.
Apoptosis
Apoptosis is an orderly process in which the cell's contents are packaged into small packets of membrane for “garbage collection” by immune cells. Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.
Apoptosis, program cell death
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed...
1. Apoptosis and necrosis are two main types of cell death. Apoptosis is programmed cell death that plays an important role in development and maintaining tissue homeostasis, while necrosis is unregulated cell death caused by external factors like injury.
2. Cancer develops due to mutations in genes that regulate cell growth, allowing cells to proliferate uncontrollably. Cancer cells evade apoptosis and are able to metastasize, or spread to other parts of the body. Abnormalities in apoptosis may contribute to diseases like cancer, neurodegeneration, and autoimmune disorders.
Apoptosis ppt.
Dr. Shabnam N Shah presents information on apoptosis or programmed cell death. Apoptosis is a genetically controlled process important for development and tissue homeostasis. It occurs through the extrinsic pathway initiated by death receptors, the intrinsic pathway involving mitochondria, or the granzyme pathway using perforin and granzymes. Apoptosis is essential for physiological processes but pathological disturbances can also induce cell death.
Apoptosis
A unit that was created for a lesson that would correspond with the caps learning document but what is not in the document
Apoptosis(program cell death)
Apoptosis is a tightly regulated and controlled process of programmed cell death. It is essential for normal development and maintenance of tissues as it removes unnecessary or damaged cells. During apoptosis, cells activate enzymes to degrade their own DNA and proteins. Apoptosis is initiated through either the extrinsic or intrinsic pathway which involve death ligands/receptors or mitochondrial signaling, respectively, ultimately activating caspase enzymes that kill the cell in a controlled manner. Apoptosis is important for development, the immune system, and removing pre-cancerous or infected cells, while deficiencies can lead to cancer or autoimmune disorders.
Recommended
Apoptosis
Avhijit Roy, a 3rd year B.Pharm student, is researching apoptosis for his project. Apoptosis is a form of programmed cell death that was first introduced in 1972 and plays a role in many physiologic and pathologic processes. It involves biochemical changes like proteolysis and appearance of glycoproteins, as well as molecular mechanisms including initiators that are transmembranous, intracellular or extracellular, activation of caspases and cell death receptors, and growth controlling genes leading to phagocytosis without inflammation.
Apoptosis
This document discusses apoptosis, or programmed cell death. It describes how apoptosis is important in physiological and pathological processes. Physiologically, apoptosis helps sculpt tissues during embryo development and replaces intestinal epithelium cells. Pathologically, apoptosis causes cell death in tumors exposed to chemotherapy, viral infections, and organ atrophy from stimulus withdrawal. Biochemically, apoptosis involves proteolysis, protein cross-linkages, nuclear pyknosis, and phosphatidylserine exposure. Initiation can occur via transmembrane, intracellular, or extracellular signals. The process involves caspase activation, death receptor activation, and growth gene regulation, ultimately leading to cell death and non-inflammatory phagocytosis.
Apoptosis
Apoptosis is an orderly process in which the cell's contents are packaged into small packets of membrane for “garbage collection” by immune cells. Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.
Apoptosis, program cell death
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed...
1. Apoptosis and necrosis are two main types of cell death. Apoptosis is programmed cell death that plays an important role in development and maintaining tissue homeostasis, while necrosis is unregulated cell death caused by external factors like injury.
2. Cancer develops due to mutations in genes that regulate cell growth, allowing cells to proliferate uncontrollably. Cancer cells evade apoptosis and are able to metastasize, or spread to other parts of the body. Abnormalities in apoptosis may contribute to diseases like cancer, neurodegeneration, and autoimmune disorders.
Apoptosis ppt.
Dr. Shabnam N Shah presents information on apoptosis or programmed cell death. Apoptosis is a genetically controlled process important for development and tissue homeostasis. It occurs through the extrinsic pathway initiated by death receptors, the intrinsic pathway involving mitochondria, or the granzyme pathway using perforin and granzymes. Apoptosis is essential for physiological processes but pathological disturbances can also induce cell death.
Apoptosis
A unit that was created for a lesson that would correspond with the caps learning document but what is not in the document
Apoptosis(program cell death)
Apoptosis is a tightly regulated and controlled process of programmed cell death. It is essential for normal development and maintenance of tissues as it removes unnecessary or damaged cells. During apoptosis, cells activate enzymes to degrade their own DNA and proteins. Apoptosis is initiated through either the extrinsic or intrinsic pathway which involve death ligands/receptors or mitochondrial signaling, respectively, ultimately activating caspase enzymes that kill the cell in a controlled manner. Apoptosis is important for development, the immune system, and removing pre-cancerous or infected cells, while deficiencies can lead to cancer or autoimmune disorders.
Apoptosis
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
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
Apoptosis(from the Greek words apo=from and ptosis=falling,)is a highly regulated biochemical mechanism of programmed cell death.
Between 50 -70 billion cells die each day due to apoptosis in the average human adult. For an average child between the age of 8-15 approximately 20-30 billion cells die a day.
German scientist Carl Vogt was first to describe the principle of apoptosis in 1842.
In 1972 Ker first introduced the term apoptosis in a publication.
The 2002 Nobel prize in medicine was awarded to Syndeney Brenner,Horvitz and John E.Sulstone for their work identifiying genes that control apoptosis.The gene were identified by studies in the Nematode C. elegans(CED4) and these same genes function in humans(APAF) for apoptosis.
There is a alignment between the nucleotide sequence of C.elegans and APAF.
Apoptosis can be normally noticed during embryogenesis,metamorphosis and aging.For example,the differentiation of human fingers in a developing embryo requires the cells between the fingers to initiate apoptosis so that the fingers could separate.
Apoptosis is needed to destroy cells infected with viruses, cells with damage DNA.
Caspase dependent apoptosis is inititate either by exrtinsc or intrinsic factors.
There are two main caspase dependent apoptotic pathway
The extrinsic or death receptor pathway
The intrinsic or mitochondrial pathway
Extra cellular signal molecules bind with cell surface receptors(termed death receptors).One typical example is a Fas receptor(FasR),a member of and FasRTNF receptor family.Its ligand is Fasl(Fatty acid synthetase ligand) expressed in cytotoxic t-lymphocytes and natural killer cells.
FasL binds FasR on the surface of a cell recruits the adptor protein, FADD(Fas-associated death domain).This occurs through interaction between the death domain of FADD and FasR.
The death effector domain(DED) of FADD active the caspase-8 from procaspase-8.
Caspase 8 activates execuitor caspases which cleave substrates within the cell.Nucleases are activated, chromosomal DNA is degraded and cell dies by apoptosis.
Apoptosis
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
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.
My 1st ppt apoptosis
This document discusses apoptosis, or programmed cell death. It begins by introducing apoptosis and explaining that it is important for eliminating unwanted or dysfunctional cells. It then discusses the significance of apoptosis in maintaining normal tissue development and removing damaged cells. The document outlines two main apoptosis pathways - the extrinsic pathway initiated by death receptors and the intrinsic pathway involving mitochondria. It concludes that apoptosis is a fundamental biological process in organisms that is characterized by specific morphological and biochemical changes in cells undergoing programmed cell death.
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
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
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.
Programmed cell death in plants by shivanand b. koppad
This document discusses programmed cell death (PCD) in plants. It provides definitions of PCD and necrosis, and describes the differences between the two processes. PCD, also called apoptosis, is an actively controlled and genetically regulated process while necrosis is unregulated cell death in response to external stressors. The document outlines the history of studying PCD/apoptosis and discusses PCD pathways, regulators like caspases, and importance in plant development and response to the environment. It also provides a case study on PCD in tomato fruit in response to heat stress.
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 my ppt
This document summarizes apoptosis, or programmed cell death. Apoptosis occurs through a regulated process that eliminates cells without releasing harmful substances. It is caused by physiologic situations like hormone-dependent tissue involution or pathogenic conditions such as DNA damage. The process involves intrinsic and extrinsic pathways that activate caspase enzymes to execute cell death. Examples where apoptosis is important include growth factor deprivation, DNA damage, misfolded protein accumulation in the endoplasmic reticulum, and removal of self-reactive lymphocytes to prevent autoimmunity.
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
Every cell has a natural life cycle involving birth and death. There are two main types of cell death: necrosis and apoptosis. Necrosis is accidental cell death due to external injury, while apoptosis is a carefully regulated process in which cells play an active role in their own death. During apoptosis, cells shrink, break into fragments, and are phagocytosed without causing inflammation. Precisely regulated apoptosis is important for normal development, immune function, and homeostasis, while defects can lead to diseases. Many cancer therapies aim to trigger the apoptosis pathway in tumor cells.
Apoptosis (programmed cell death)
Apoptosis
Its purpose
What if apoptosis stop?
Necrosis vs Apoptosis
Morphology of Apoptosis
Pathways of Apoptosis
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.
Apoptosis (presentation)
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
APOPTOSIS PATHOLOGY
Apoptosis, or programmed cell death, occurs normally during development and throughout adulthood. There are two pathways for caspase activation in apoptosis: the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. The intrinsic pathway involves pro-apoptotic BAX and BAK oligomerizing in the mitochondrial membrane, allowing cytochrome-C and other proteins to leak out and activate caspase-9. The extrinsic pathway occurs when cell death receptors like Fas and FasL bind, activating caspase-8 and -10. Both pathways activate executioner caspases like caspase-3 and -6, leading to nuclear fragmentation, apoptotic body formation, and phagocytosis of cell remnants.
Apoptosis
Apoptosis is the programmed cell death. Aim of cancer therapy is to destroy the invading cells. Cancerous cells can be destroyed by increasing apoptosis.
it can occur in both physiological and pathological conditions. It is different from necrosis. In necrosis, the cell contents leak out and lead to inflammation. But in apoptosis there is no cellular leakage, only apoptotic bodies are formed. They are then engulfed by macrophages.
Intrinsic 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
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
The document discusses apoptosis, or programmed cell death. It defines apoptosis as a tightly regulated suicidal program in cells that activates enzymes to degrade the cell's own DNA and proteins. Apoptosis is important for normal development and tissue homeostasis by removing unwanted cells. The mechanisms of apoptosis involve both intrinsic pathways related to mitochondrial damage and extrinsic pathways activated by death receptors. Key regulators and effectors of apoptosis like caspases, Bcl-2 family proteins, and cytochrome c are discussed. Disorders related to too much or too little apoptosis can lead to conditions like neurodegeneration or cancer.
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Apoptosis
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
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
Apoptosis(from the Greek words apo=from and ptosis=falling,)is a highly regulated biochemical mechanism of programmed cell death.
Between 50 -70 billion cells die each day due to apoptosis in the average human adult. For an average child between the age of 8-15 approximately 20-30 billion cells die a day.
German scientist Carl Vogt was first to describe the principle of apoptosis in 1842.
In 1972 Ker first introduced the term apoptosis in a publication.
The 2002 Nobel prize in medicine was awarded to Syndeney Brenner,Horvitz and John E.Sulstone for their work identifiying genes that control apoptosis.The gene were identified by studies in the Nematode C. elegans(CED4) and these same genes function in humans(APAF) for apoptosis.
There is a alignment between the nucleotide sequence of C.elegans and APAF.
Apoptosis can be normally noticed during embryogenesis,metamorphosis and aging.For example,the differentiation of human fingers in a developing embryo requires the cells between the fingers to initiate apoptosis so that the fingers could separate.
Apoptosis is needed to destroy cells infected with viruses, cells with damage DNA.
Caspase dependent apoptosis is inititate either by exrtinsc or intrinsic factors.
There are two main caspase dependent apoptotic pathway
The extrinsic or death receptor pathway
The intrinsic or mitochondrial pathway
Extra cellular signal molecules bind with cell surface receptors(termed death receptors).One typical example is a Fas receptor(FasR),a member of and FasRTNF receptor family.Its ligand is Fasl(Fatty acid synthetase ligand) expressed in cytotoxic t-lymphocytes and natural killer cells.
FasL binds FasR on the surface of a cell recruits the adptor protein, FADD(Fas-associated death domain).This occurs through interaction between the death domain of FADD and FasR.
The death effector domain(DED) of FADD active the caspase-8 from procaspase-8.
Caspase 8 activates execuitor caspases which cleave substrates within the cell.Nucleases are activated, chromosomal DNA is degraded and cell dies by apoptosis.
Apoptosis
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
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.
My 1st ppt apoptosis
This document discusses apoptosis, or programmed cell death. It begins by introducing apoptosis and explaining that it is important for eliminating unwanted or dysfunctional cells. It then discusses the significance of apoptosis in maintaining normal tissue development and removing damaged cells. The document outlines two main apoptosis pathways - the extrinsic pathway initiated by death receptors and the intrinsic pathway involving mitochondria. It concludes that apoptosis is a fundamental biological process in organisms that is characterized by specific morphological and biochemical changes in cells undergoing programmed cell death.
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
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
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.
Programmed cell death in plants by shivanand b. koppad
This document discusses programmed cell death (PCD) in plants. It provides definitions of PCD and necrosis, and describes the differences between the two processes. PCD, also called apoptosis, is an actively controlled and genetically regulated process while necrosis is unregulated cell death in response to external stressors. The document outlines the history of studying PCD/apoptosis and discusses PCD pathways, regulators like caspases, and importance in plant development and response to the environment. It also provides a case study on PCD in tomato fruit in response to heat stress.
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 my ppt
This document summarizes apoptosis, or programmed cell death. Apoptosis occurs through a regulated process that eliminates cells without releasing harmful substances. It is caused by physiologic situations like hormone-dependent tissue involution or pathogenic conditions such as DNA damage. The process involves intrinsic and extrinsic pathways that activate caspase enzymes to execute cell death. Examples where apoptosis is important include growth factor deprivation, DNA damage, misfolded protein accumulation in the endoplasmic reticulum, and removal of self-reactive lymphocytes to prevent autoimmunity.
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
Every cell has a natural life cycle involving birth and death. There are two main types of cell death: necrosis and apoptosis. Necrosis is accidental cell death due to external injury, while apoptosis is a carefully regulated process in which cells play an active role in their own death. During apoptosis, cells shrink, break into fragments, and are phagocytosed without causing inflammation. Precisely regulated apoptosis is important for normal development, immune function, and homeostasis, while defects can lead to diseases. Many cancer therapies aim to trigger the apoptosis pathway in tumor cells.
Apoptosis (programmed cell death)
Apoptosis
Its purpose
What if apoptosis stop?
Necrosis vs Apoptosis
Morphology of Apoptosis
Pathways of Apoptosis
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.
Apoptosis (presentation)
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
APOPTOSIS PATHOLOGY
Apoptosis, or programmed cell death, occurs normally during development and throughout adulthood. There are two pathways for caspase activation in apoptosis: the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. The intrinsic pathway involves pro-apoptotic BAX and BAK oligomerizing in the mitochondrial membrane, allowing cytochrome-C and other proteins to leak out and activate caspase-9. The extrinsic pathway occurs when cell death receptors like Fas and FasL bind, activating caspase-8 and -10. Both pathways activate executioner caspases like caspase-3 and -6, leading to nuclear fragmentation, apoptotic body formation, and phagocytosis of cell remnants.
Apoptosis
Apoptosis is the programmed cell death. Aim of cancer therapy is to destroy the invading cells. Cancerous cells can be destroyed by increasing apoptosis.
it can occur in both physiological and pathological conditions. It is different from necrosis. In necrosis, the cell contents leak out and lead to inflammation. But in apoptosis there is no cellular leakage, only apoptotic bodies are formed. They are then engulfed by macrophages.
Intrinsic 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.
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Programmed cell death in plants by shivanand b. koppad
Programmed cell death in plants by shivanand b. koppad
Similar to Molecular aspects of pharmacology, Apoptosis
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
The document discusses apoptosis, or programmed cell death. It defines apoptosis as a tightly regulated suicidal program in cells that activates enzymes to degrade the cell's own DNA and proteins. Apoptosis is important for normal development and tissue homeostasis by removing unwanted cells. The mechanisms of apoptosis involve both intrinsic pathways related to mitochondrial damage and extrinsic pathways activated by death receptors. Key regulators and effectors of apoptosis like caspases, Bcl-2 family proteins, and cytochrome c are discussed. Disorders related to too much or too little apoptosis can lead to conditions like neurodegeneration or cancer.
Programmed cell death
This document summarizes programmed cell death or apoptosis. It discusses the distinct modalities of programmed cell death including apoptosis, autophagy and necroptosis. It covers the role of programmed cell death in disease, the mechanisms and molecular regulators involved in different types of cell death, methods to detect programmed cell death, and the therapeutic potential of modulating programmed cell death pathways.
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 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
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 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.
programed cell death
Apoptosis or programmed cell death, is carefully coordinated collapse of cell, protein degradation , DNA fragmentation followed by rapid engulfment of corpses by neighbouring cells.
Cell injury
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
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
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
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.
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.pptx
Programmed cell death, also known as apoptosis, is a naturally occurring process where a cell is directed to die in a controlled manner. During apoptosis, cells shrink and break into fragments that are easily removed by phagocytes without causing inflammation. This process is important for tissue homeostasis, development, the immune system, and removal of damaged cells. Apoptosis is characterized by specific morphological changes like blebbing, nuclear fragmentation, chromatin condensation, and formation of apoptotic bodies. Understanding apoptosis provides insights into cancer development and potential new treatments.
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)
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
Programmed Cell death || Apoptosis || Necrosis || Phagocytosis || Necrosis || Ligands || Receptors|| Genetics || Cell biology || Molecular Biology || Cell types || Cellular types || cell shrinkage || Initiation Caspases || Microbiology || Genetics ||Cell types || Necrosis vs apoptosis
Apoptosis
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
Apoptosis
This document provides an overview of apoptosis, or programmed cell death. It begins by defining apoptosis and necrosis, explaining that apoptosis is normal and programmed cell death while necrosis is accidental cell death. It then discusses the importance of apoptosis in development and homeostasis. The key events and mechanisms of apoptosis are described, including the roles of caspases, Bcl-2 proteins, cytochrome c, death receptors/ligands, and the intrinsic and extrinsic pathways. Differences between apoptosis and necrosis are highlighted. The summary concludes by noting how aberrant cell death can lead to diseases like cancer or neurodegeneration.
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Molecular aspects of pharmacology, Apoptosis
- 1. TOPIC:- MOLECULAR ASPECTS OF PHARMACOLOGY UBMITTED TO:- Dr. SHIKHA BASKAR SUBMITTED BY:-ISHA RUHELA M. PHARMA 2nd sem.
- 2. History of cell death / apoptosis research 1800s Numerous observation of cell death 1908 Mechnikov wins Nobel prize (phagocytosis) 1964-66 Necrosis & PCD described 1971 Term apoptosis coined 1989-91 Apoptosis genes identified, including bcl-2, fas /apo1 & p53, ced-3 sequenced (Richerd et.al., 2001)
- 3. INTRODUCTION Apoptosis is a form of programmed cell death or “cellular suicide”. It is different from necrosis,in which cells due to injury. •Apoptosis is an orderly process in which the cells contents are packaged into small packets of membrane for “garbage collection” by immune cells. •Apoptosis removes cells during development eliminates potentially cancerous and virus infected cells and maintains balance in the body. •Apoptosis also plays a key role in human development.
- 4. • Example of apoptosis during normal development include the loss of a tadpole’s tail as it turns into a frog and removal of unneeded neurons in as neural circuits in the brain are wired.
- 5. INTRODUCTION Cell death by injury -Mechanical damage -Exposure to toxic chemicals Cell death by suicide -Internal signals -External signals
- 6. Conted….. Apoptosis or programmed cell death, is carefully coordinated collapse of cell, protein degradation , DNA fragmentation followed by rapid engulfment of corpses by neighbouring cells. (Tommi, 2002) Essential part of life for every multicellular organism from worms to humans. (Faddy et al.,1992) Apoptosis plays a major role from embryonic development to senescence.
- 7. Importance of Apoptosis • Important in normal physiology / development – Development: Immune systems maturation, Morphogenesis, Neural development – Adult: Immune privilege, DNA Damage and wound repair. • Excess apoptosis – Neurodegenerative diseases • Deficient apoptosis – Cancer – Autoimmunity
- 8. Why should a cell commit suicide? Apoptosis is needed for proper development Examples: The resorption of the tadpole tail The formation of the fingers and toes of the fetus The sloughing off of the inner lining of the uterus The formation of the proper connections between neurons in the brain Apoptosis is needed to destroy cells Examples: Cells infected with viruses Cells of the immune system Cells with DNA damage Cancer cells
- 9. What makes a cell decide to commit suicide? Withdrawal of positive signals examples : growth factors for neurons Interleukin-2 (IL-2) Receipt of negative signals examples : increased levels of oxidants within the cell damage to DNA by oxidants death activators : Tumor necrosis factor alpha (TNF-α) Lymphotoxin (TNF-β) Fas ligand (FasL)
- 11. membrane blebbing & changes mitochondrial leakage organelle reduction cell shrinkage nuclear fragmentation chromatin condensation APOPTOSIS: Morphological events
- 12. MAJOR PLAYERS IN APOPTOSIS • Caspases • Adaptor proteins • TNF & TNFR family • Bcl-2 family
- 13. Apoptosis: Pathways Death Ligands Effector Caspase 3 Death Receptors Initiator Caspase 8 PCD DNA damage & p53 Mitochondria/ Cytochrome C Initiator Caspase 9 “Extrinsic Pathway” “Intrinsic Pathway”
- 14. Sherman et al., 1997 Induction of apoptosis related genes, signal transduction
- 15. Wilde, 1999
- 16. Ligand-induced cell death Ligand Receptor FasL Fas (CD95) TNF TNF-R TRAIL DR4 (Trail-R)
- 17. an important process of cell death can be initiated extrinsically through death ligands (e.g. TRAIL, FasL) activating initiator caspase 8 through induced proximity. can be initiated intrinsically through DNA damage (via cytochrome c) activating initiator caspase 9 through oligomerization. Initiator caspases 8 and 9 cleave and activate effector caspase 3, which leads to cell death.