Apopotosis why and how ?
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Apoptosis is a pathway of cell death in which cells activate enzymes that degrade the cells and its organelles
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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
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, or programmed cell death, is an internally controlled suicide program where cells are removed with minimal disruption of surrounding tissue. It plays important roles in development, tissue homeostasis, and defense against infection and cancer. There are two main apoptotic pathways - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. Both pathways activate caspases, cysteine proteases that cleave proteins to execute the cell death program through processes like DNA fragmentation and formation of apoptotic bodies. Deregulation of apoptosis contributes to cancer development by allowing damaged or unnecessary cells to survive. Targeting the apoptotic pathway is a strategy for cancer treatment.
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 vs necrosis
1) The document discusses apoptosis and necrosis, two types of cell death. Apoptosis is programmed cell death where cells shrink and fragment in an orderly process. Necrosis is unprogrammed cell death caused by external injury or damage where cells swell and leak.
2) Apoptosis can be triggered internally through mitochondrial pathways or externally through death receptor pathways and leads to caspase activation and cell fragmentation. Cancer cells develop ways to avoid apoptosis like inhibiting proteins in these pathways.
3) Necrosis occurs when cells are damaged by external factors like toxins and involves cell and organelle swelling without fragmentation. Cancer cells and viruses can interfere with apoptosis to allow cancer progression.
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.
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, cell death, and proliferation
This document provides an overview and introduction to cell death (apoptosis and necrosis) and cell proliferation. It discusses the differences between necrosis and apoptosis, the major apoptotic pathways involving death receptors, mitochondria and caspases. Different assays for measuring cell death and proliferation are described, along with their advantages and disadvantages. The document aims to help researchers decide which assays are best suited for measuring cell death or proliferation for their particular purposes.
Recommended
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
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, or programmed cell death, is an internally controlled suicide program where cells are removed with minimal disruption of surrounding tissue. It plays important roles in development, tissue homeostasis, and defense against infection and cancer. There are two main apoptotic pathways - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. Both pathways activate caspases, cysteine proteases that cleave proteins to execute the cell death program through processes like DNA fragmentation and formation of apoptotic bodies. Deregulation of apoptosis contributes to cancer development by allowing damaged or unnecessary cells to survive. Targeting the apoptotic pathway is a strategy for cancer treatment.
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 vs necrosis
1) The document discusses apoptosis and necrosis, two types of cell death. Apoptosis is programmed cell death where cells shrink and fragment in an orderly process. Necrosis is unprogrammed cell death caused by external injury or damage where cells swell and leak.
2) Apoptosis can be triggered internally through mitochondrial pathways or externally through death receptor pathways and leads to caspase activation and cell fragmentation. Cancer cells develop ways to avoid apoptosis like inhibiting proteins in these pathways.
3) Necrosis occurs when cells are damaged by external factors like toxins and involves cell and organelle swelling without fragmentation. Cancer cells and viruses can interfere with apoptosis to allow cancer progression.
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.
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, cell death, and proliferation
This document provides an overview and introduction to cell death (apoptosis and necrosis) and cell proliferation. It discusses the differences between necrosis and apoptosis, the major apoptotic pathways involving death receptors, mitochondria and caspases. Different assays for measuring cell death and proliferation are described, along with their advantages and disadvantages. The document aims to help researchers decide which assays are best suited for measuring cell death or proliferation for their particular purposes.
Apoptosis
Apoptosis is a tightly regulated form of programmed cell death that is controlled by specific genes. During apoptosis, cells fragment their DNA and nuclei and form apoptotic bodies that are phagocytosed by other cells without causing inflammation. This process removes damaged or unnecessary cells in a controlled manner. Apoptosis can be triggered by physiologic processes like development or pathologic conditions like radiation, viral infections, or accumulation of misfolded proteins. It occurs through either the intrinsic mitochondrial pathway involving cytochrome c release or the extrinsic death receptor pathway. Precise genetic control of apoptosis is important for tissue homeostasis and manipulation of these pathways may help treat diseases like cancer.
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 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
Apoptosis, or programmed cell death, is an important process by which cells self-destruct in a regulated manner. During development, apoptosis sculpted structures like fingers and toes by killing cells between them. Apoptosis also causes tissues like the tail to disappear at metamorphosis. The process is mediated by caspase proteases and regulated by Bcl-2 family proteins, with Bax and Bak activating caspases. Cells undergo apoptosis to maintain tissue homeostasis, avoid harming neighbors, and be removed by macrophages.
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
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 (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
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.
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
Apoptosis is a programmed cell death process that occurs in multicellular organisms. During apoptosis, cells undergo changes such as blebbing, shrinkage, and nuclear fragmentation. Between 50-70 billion cells die per day in the human body through apoptosis. Defects in apoptotic processes can lead to diseases such as cancer by allowing non-functional cells to continue proliferating. Apoptosis involves signaling pathways, regulation of mitochondria, caspase activation, and removal of dead cells.
Apoptosis
1) The document discusses apoptosis or programmed cell death in platelets and summarizes several models where apoptosis in platelets has been induced, such as by calcium ionophores or aging of platelets in storage.
2) It describes some apoptotic changes seen in platelet morphology, including shrinkage, condensation of cytoplasm, and membrane blebbing.
3) The document also notes that platelets express mRNA for death ligands and receptors involved in apoptosis, but not Fas ligand or receptor, and that mitochondrial membrane potential breaks down in platelets undergoing 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
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.
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.
PROGRAMMED CELL DEATH (APOPTOSIS )
The document summarizes programmed cell death or apoptosis. It describes apoptosis as a naturally occurring, genetically programmed process where a cell undergoes an organized breakdown. During apoptosis, cells shrink, break into membrane-bound fragments called apoptotic bodies, and are removed by phagocytes without causing inflammation. The document outlines the major pathways of apoptosis, including the intrinsic mitochondrial pathway and extrinsic death receptor pathway, and discusses the roles of caspase proteases and Bcl-2 family proteins in apoptosis signaling and regulation.
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.
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
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 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.
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.
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 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)
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What's hot
Apoptosis
Apoptosis is a tightly regulated form of programmed cell death that is controlled by specific genes. During apoptosis, cells fragment their DNA and nuclei and form apoptotic bodies that are phagocytosed by other cells without causing inflammation. This process removes damaged or unnecessary cells in a controlled manner. Apoptosis can be triggered by physiologic processes like development or pathologic conditions like radiation, viral infections, or accumulation of misfolded proteins. It occurs through either the intrinsic mitochondrial pathway involving cytochrome c release or the extrinsic death receptor pathway. Precise genetic control of apoptosis is important for tissue homeostasis and manipulation of these pathways may help treat diseases like cancer.
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 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
Apoptosis, or programmed cell death, is an important process by which cells self-destruct in a regulated manner. During development, apoptosis sculpted structures like fingers and toes by killing cells between them. Apoptosis also causes tissues like the tail to disappear at metamorphosis. The process is mediated by caspase proteases and regulated by Bcl-2 family proteins, with Bax and Bak activating caspases. Cells undergo apoptosis to maintain tissue homeostasis, avoid harming neighbors, and be removed by macrophages.
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
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 (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
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.
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
Apoptosis is a programmed cell death process that occurs in multicellular organisms. During apoptosis, cells undergo changes such as blebbing, shrinkage, and nuclear fragmentation. Between 50-70 billion cells die per day in the human body through apoptosis. Defects in apoptotic processes can lead to diseases such as cancer by allowing non-functional cells to continue proliferating. Apoptosis involves signaling pathways, regulation of mitochondria, caspase activation, and removal of dead cells.
Apoptosis
1) The document discusses apoptosis or programmed cell death in platelets and summarizes several models where apoptosis in platelets has been induced, such as by calcium ionophores or aging of platelets in storage.
2) It describes some apoptotic changes seen in platelet morphology, including shrinkage, condensation of cytoplasm, and membrane blebbing.
3) The document also notes that platelets express mRNA for death ligands and receptors involved in apoptosis, but not Fas ligand or receptor, and that mitochondrial membrane potential breaks down in platelets undergoing 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
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.
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.
PROGRAMMED CELL DEATH (APOPTOSIS )
The document summarizes programmed cell death or apoptosis. It describes apoptosis as a naturally occurring, genetically programmed process where a cell undergoes an organized breakdown. During apoptosis, cells shrink, break into membrane-bound fragments called apoptotic bodies, and are removed by phagocytes without causing inflammation. The document outlines the major pathways of apoptosis, including the intrinsic mitochondrial pathway and extrinsic death receptor pathway, and discusses the roles of caspase proteases and Bcl-2 family proteins in apoptosis signaling and regulation.
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.
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
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 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.
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.
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Similar to Apopotosis why and how ?
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 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 by rasheed.pptx
Cell death occurs through two main forms: apoptosis and necrosis. Apoptosis is programmed cell death where cells undergo changes like DNA fragmentation and shrinkage in a way that avoids damaging nearby cells. Necrosis is unprogrammed cell death due to external factors like injury or internal issues. During necrosis, cells lose metabolic function and membrane integrity, organelles swell, and cell contents may leak out. Necrosis can occur through several types including coagulative, liquefactive, and gangrenous necrosis. Autophagy is a process where cells digest damaged organelles through the formation and fusion of vesicles to maintain cellular homeostasis.
Cell injury apoptosis
Apoptosis is a tightly regulated form of programmed cell death that occurs both during normal development and in disease states. It is characterized by cell shrinkage, chromatin condensation, and fragmentation of the cell into membrane-bound vesicles that are phagocytosed without eliciting inflammation. Apoptosis is mediated by caspases, cysteine proteases that exist as inactive proenzymes and become activated through either the intrinsic mitochondrial pathway or extrinsic death receptor pathway. In the mitochondrial pathway, signals alter the balance of pro- and anti-apoptotic BCL2 family proteins, allowing mitochondrial outer membrane permeabilization and cytochrome c release, leading to caspase activation and cell death.
Apoptosis.pdf
Apoptosis is a tightly regulated form of programmed cell death that involves the activation of caspases. There are intrinsic and extrinsic pathways of apoptosis. The intrinsic pathway involves signals within the cell such as DNA damage, causing mitochondrial membrane permeabilization and cytochrome c release. This forms the apoptosome and activates caspase-9 and caspase-3. The extrinsic pathway involves death receptors and activates caspase-8. Caspases cleave cellular proteins leading to cell death. Phagocytes then engulf and degrade the apoptotic bodies. Other forms of regulated cell death include necroptosis, pyroptosis and ferroptosis.
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 process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis
Apoptosis, or programmed cell death, is an important physiological process that eliminates unwanted or damaged cells. There are two main pathways that trigger apoptosis - the extrinsic or death receptor pathway, and the intrinsic or mitochondrial pathway. The extrinsic pathway involves death receptors and ligands that activate caspase enzymes. The intrinsic pathway occurs in response to cellular stress and involves mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. This forms the apoptosome complex and activates caspase-9 and caspase-3, leading to apoptosis. Apoptosis is a highly regulated process involving Bcl-2 family proteins, caspase enzymes, and characteristic morphological changes including cell shrinkage, nuclear fragmentation, and membrane blebbing. Assays to detect
Cell death
Cell death can occur through two main processes: apoptosis and necrosis. Apoptosis is programmed cell death that occurs under normal physiological conditions, triggered by intracellular signals. The cell shrinks and fragments into apoptotic bodies that are phagocytosed, avoiding inflammation. Necrosis is accidental cell death due to external factors like trauma or toxins, where the cell lyses and releases intracellular contents, potentially causing tissue damage and inflammation. Both processes are important for development, tissue homeostasis, and removal of damaged cells.
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Pathology
There are two main types of cell death: necrosis and apoptosis. Necrosis is accidental cell death due to external factors like trauma or toxins. It is characterized by cellular contents leaking out and causing inflammation. Apoptosis is programmed cell death that occurs as part of normal development and tissue homeostasis. It is triggered through internal signals or external death ligands binding to receptors. This activates a caspase cascade that breaks down the cell in a controlled, non-inflammatory way. Dysregulation of apoptosis can lead to cancer, autoimmune disease, or neurodegeneration.
Apoptosis
Apoptosis is a tightly regulated and genetically programmed process of cell death. It involves the activation of intracellular enzymes that break down nuclear DNA and proteins, breaking the cell into fragments called apoptotic bodies. There are two main pathways that trigger apoptosis - the mitochondrial pathway, which involves the release of death proteins from mitochondria, and the death receptor pathway, initiated by ligands binding to receptors on the cell surface. Both pathways activate caspases that dismantle the cell in an orderly manner, after which phagocytes remove the cellular debris.
APOPTOSIS.pptx
Cell death, also known as programmed cell death or apoptosis, is a natural and regulated process in multicellular organisms. There are two main types of cell death: programmed cell death (apoptosis) and non-programmed cell death (necrosis). Apoptosis is an actively controlled and regulated process where individual cells commit suicide in response to internal or external signals. It involves the activation of caspases, which trigger a caspase cascade that breaks down proteins and leads to cell death. There are intrinsic and extrinsic pathways that trigger apoptosis through mitochondrial or death receptor mechanisms respectively. Programmed cell death is important for development, tissue homeostasis, and removal of damaged cells.
Cell Death physiology for mbbs, BPT, bds........pdf
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4.pathology apoptosis2016
1. Programmed cell death (PCD) refers to regulated cell death processes that eliminate cells when they are no longer useful or potentially harmful.
2. Apoptosis is a form of PCD characterized by nuclear fragmentation, chromatin condensation, cell shrinkage and blebbing, and formation of apoptotic bodies that are quickly phagocytosed, avoiding inflammation. It relies on caspase activation through the mitochondrial or death receptor pathways.
3. Alternative cell death pathways include necroptosis, pyroptosis and autophagy. Necroptosis resembles necrosis morphologically but is caspase-independent and regulated. Pyroptosis involves caspase-1 and occurs during microbial infection, triggering inflammation. Autophagy
PROGRAMMED CELL DEATH
The document discusses different types of cell death, including programmed cell death mechanisms like apoptosis and autophagy. It notes that cell death is tightly regulated and important for development, health, and eliminating damaged or infected cells. The major types of cell death covered are apoptosis (genetically programmed suicide), autophagy (housekeeping role), necrosis (unprogrammed trauma-induced death), and necroptosis (programmed necrosis).
Cell death
Apoptosis is a genetically programmed form of cell death that is essential for sculpting body structures during development, removing excess or harmful cells, and serving immune system functions. Key morphological changes during apoptosis include membrane blebbing, chromatin condensation, cytoplasmic condensation, DNA fragmentation, and the cell being phagocytosed. Signaling pathways such as TNF, Fas, and TRAIL induce apoptosis through caspase activation and regulation by pro-apoptotic and anti-apoptotic Bcl-2 family members. Apoptosis is important in many clinical contexts like cancer, autoimmune disease, and neurodegeneration.
Apoptosis roohit
Apoptosis is a programmed cell death process that occurs in multicellular organisms. It is characterized by cell shrinkage, nuclear fragmentation, and global mRNA decay. Apoptosis ensures the orderly disposal of cells and occurs during normal cell turnover, development, and aging. It also helps remove infected, damaged or unnecessary cells. There are two main pathways of apoptosis - the intrinsic pathway which is triggered by intracellular signals within the cell, and the extrinsic pathway which is initiated by activation of cell surface death receptors by extracellular ligands. Both pathways activate caspases, a family of cysteine proteases, that trigger the degradation of proteins and DNA fragmentation that leads to cell death. Deregulation of apoptosis can contribute to diseases like cancer
Cell inj apoptosis
Apoptosis, or programmed cell death, is a tightly regulated suicide program where cells activate enzymes to degrade their own DNA and proteins. Apoptosis occurs physiologically during development and pathologically due to DNA damage, hypoxia, radiation, or cytotoxic drugs. Morphologically, apoptotic cells appear rounded, shrunken, and fragmented with condensed chromatin and apoptotic bodies that are phagocytosed without inflammation. Apoptosis is controlled through signaling pathways, regulated by proteins, and executed by caspases through protein and DNA cleavage and removal of apoptotic cells. Dysregulated apoptosis can lead to cancer or neurodegenerative diseases.
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Apopotosis why and how ?
- 1. Why and How? Presented By – Gyanendra Kumar Prajapati 1st year M.Pharm Guided By – Mr.G.S.Prasanna KLE University’s College of Pharmacy, Bengaluru 1
- 2. 1. Definition 2. Causes of apoptosis : Physiological and pathological Conditions 3. Mechanism of apoptosis 4. Pathways of apoptosis 5. Examples of Apoptosis 6. Reference
- 3. Apoptosis is a pathway of cell death in which cells activate enzymes that degrade the cells and its organelles. Plasma membrane remains intact - structure is altered >>> Subsequently apoptotic cell becomes target for phagocytosis.
- 4. • Initially recognized in 1972 •Greek designation for “falling off” •Eliminate potentially harmful cells •Pathologic event when cells are damaged beyond repairs, especially when the damage affect the cell’s DNA proteins in these situations.
- 5. •Death by apoptosis is a normal phenomenon that serves to eliminate cells that are no longer needed . Example : •The programmed destruction of cells during embryogenesis. •Involution of Hormone dependent tissues •Cell loss in proliferating cell populations •Cell death induced by cytotoxic lymphocytes •Infected and neoplastic cells.
- 6. Department of Pharmacology 6 Apoptosis in bud formation during which many interdigital cells die. They are stained black by a TUNEL method Incomplete differentiation in two toes due to lack of apoptosis
- 7. DNA damage Accumulation of misfolded proteins Cell injury in certain infections Pathological atrophy in parenchymal organs.
- 8. Cell shrinkage Chromatin condensation Nuclear fragmentation Chromosomal DNA fragmentation Formation of cytoplasmic blebs& apoptotic bodies Phagocytosis. Department of Pharmacology 8
- 9. Apoptosis activation of enzyme called caspases Caspases depends on a finely turned balance b/w production of pro and anti-apoptotic proteins. Department of Pharmacology 9 Mitochondrial pathway+ death receptor pathway → caspases
- 10. Department of Pharmacology 10
- 11. Department of Pharmacology 11
- 12. The Mitochondria (Intrinsic) Pathway of Apoptosis Mitochondria contain several proteins that are capable of inducing apoptosis, Include cytochrome C and other proteins that neutralize endogenous inhibitors of apoptosis. Permeability of mitochondria Damage DNA or accumulate unacceptable amounts of misfolded proteins Department of Pharmacology 12
- 13. The death receptor (Extrinsic) Pathway of Apoptosis Many Cells express surface molecules called death receptors that trigger apoptosis. Tumor necrosis factor (TNF) receptor family which contain in their cytoplasmic regions a conserved “death domain” so named it mediates interaction with other proteins in valued in cell death. Department of Pharmacology 13
- 14. The mitochondrial and death receptor pathways lead to the activation of the initiator caspases, activated capases cleave numerous targets activation of nucleases that degrade DNA and nucleus proteins capses Department of Pharmacology 14
- 15. Cells entire phagocytes by producing “eat – me” signals Phosphatidylserine is present on the inner leaflet of plasma membrane Apoptotic cells this phospholipids“flips to the outer leaflet Tissue macrophoages and leads to phogocytosed of the apoptosis Department of Pharmacology 15
- 16. Prompt clearance of the dead cells Secondary membrane damage and release their cellular content Dead cells disappear without leaving trace and inflammation is virtually absent Emphasize that distinctions between necrosis & apoptosis these two from of cells death may co exist. Department of Pharmacology 16
- 17. Cell death in many situations is caused by apoptosis. Illustrate the role two pathways of apoptosis in normal physiology and in disease. Department of Pharmacology 17
- 18. Hormone - sensitive cells deprived of the relevant hormone lymphocytes that are not stimulated by antigens and cytokines that are not stimulated by antigens and neurons deprived of nerve growth factor die by apoptosis. Department of Pharmacology 18
- 19. Chemotherapeutic agents induces DNA damage which is severe may trigger apoptic death DNA is damage the P53 protein accumulates in cells Cell cycle to allows the DNA to be repaired before it is replicated Synthesis of pro-apoptotic members of the certain BCL- 2 family. Department of Pharmacology 19
- 20. Lymphocytes capable of recognizing self antigens Encounter self antigens the cell die by apoptosis Failure of apoptosis of self reactive lymphocytes is one of the causes of autoimmune disease. Department of Pharmacology 20
- 21. Robbins' pathologic basis of disease. R. S. Cotran, V. Kumar and S. L. Robbins. W. B. Saunders, Philadelphia, 1989. No. of pages: 1519. Pharmacology – Rang And Dale of pages: 69 Department of Pharmacology 21
- 22. Department of Pharmacology 22