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
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.
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
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 is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis (Intrinsic And Extrinsic Pathway with assays)227777222an
- 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, 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.
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.
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
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.
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
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 is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis (Intrinsic And Extrinsic Pathway with assays)227777222an
- 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, 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.
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.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
The Ras pathway allows cells to respond to external signals by controlling processes like proliferation, survival, and apoptosis. When growth factors bind to receptor tyrosine kinases, it activates Ras which can then activate the MAPK, PI3K, and other pathways to regulate gene expression and cell behavior. Mutations that cause Ras to be constantly active are implicated in many cancers. Inhibiting Ras function through drugs like farnesyltransferase inhibitors may block its ability to drive uncontrolled cell growth.
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 also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
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
1. Programmed cell death, also known as apoptosis, is essential for proper development and for destroying harmful cells.
2. Apoptosis is regulated by caspases, which are cysteine-dependent aspartate specific proteases. Caspases activate a proteolytic cascade that leads to cell death.
3. There are three main apoptotic pathways: the extrinsic pathway which involves death receptors, the intrinsic pathway which involves the mitochondria, and the granzyme pathway which uses granzymes from cytotoxic T cells and natural killer cells.
This document provides an introduction to apoptosis, or programmed cell death. It discusses how apoptosis is important for homeostasis and shaping tissues during development. Apoptosis is a highly regulated process where cells self-degrade through molecular machinery like caspases. The document outlines the molecular pathways of apoptosis, including the extrinsic, intrinsic, and execution pathways. It also discusses apoptosis in animals, plants, and the roles of autophagy and caspase enzymes.
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.
iPS cells, or induced pluripotent stem cells, are adult cells that have been artificially reprogrammed to an embryonic stem cell-like state through the expression of specific genes. Nobel Prize winner Shinya Yamanaka conducted research demonstrating that mouse fibroblasts could be reprogrammed into iPS cells through the use of transcription factors. While iPS cells show promise for regenerative medicine applications, current research is focused on addressing issues such as variability in gene expression and DNA methylation between iPS cell lines as well as developing methods to create iPS cells without integrating vectors that could cause mutations.
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
Apoptosis 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.
Add MTT reagent and incubate. Mitochondrial enzymes in viable cells convert MTT into an insoluble purple formazan product. Lyse cells and solubilize formazan with solvent. Measure absorbance which is directly proportional to number of viable cells. The more viable cells, the higher the absorbance. MTT assay is a sensitive, quantitative and reliable colorimetric method to measure cell viability and proliferation.
This document discusses stem cell niches and their therapeutic applications. It defines a stem cell niche as the microenvironment where stem cells reside, and notes that niches consist of niche cells, stem cells, signals and extracellular matrix that regulate stem cell behavior. Different types of niches are described for blood, cartilage, bone, neural and skin stem cells. The roles of various signaling pathways in maintaining the stem cell niche are also outlined. Finally, the document discusses current and potential future therapeutic applications of stem cells for treating various diseases.
Autophagy plays multifaceted roles in both the innate and adaptive immune system. In innate immunity, autophagy aids in the recognition of pathogens by pattern recognition receptors like TLRs, NLRs, and RLRs. It also facilitates the handling and destruction of intracellular bacteria by phagocytosis and lysosomal fusion. Autophagy regulates the production of cytokines as well. In adaptive immunity, autophagy contributes to antigen presentation on MHC class I and II molecules and is important for the homeostasis and functions of lymphocytes like T cells and B cells. However, the precise mechanisms in some cases require further clarification.
Autophagy is a cellular process where cytoplasmic components are engulfed and degraded in the lysosome or vacuole. There are three main types of autophagy: chaperone-mediated autophagy, macroautophagy, and microautophagy. Macroautophagy involves the formation of a double-membrane vesicle called the autophagosome that delivers cytoplasmic cargo to the lysosome. Autophagy plays an important role in cellular homeostasis and survival during starvation. Defects in autophagy are associated with cancer, neurodegenerative diseases, and other disorders. While autophagy generally promotes survival, excessive autophagy may lead
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
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.
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis & it’s significance in oral diseases.pptxDr Palak borade
This document summarizes a review article on apoptosis and its significance in oral diseases. It defines apoptosis as programmed cell death and discusses the intrinsic and extrinsic pathways that trigger apoptosis. It describes how apoptosis is regulated by pro-apoptotic and anti-apoptotic proteins. The document then examines the role of apoptosis in oral diseases like pyogenic granuloma, central giant cell granuloma, recurrent aphthous ulcers, periodontitis, oral lichen planus, and systemic conditions like lupus erythematosus. Apoptosis is implicated in both the pathogenesis and resolution of inflammatory and immune-mediated oral diseases.
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.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
The Ras pathway allows cells to respond to external signals by controlling processes like proliferation, survival, and apoptosis. When growth factors bind to receptor tyrosine kinases, it activates Ras which can then activate the MAPK, PI3K, and other pathways to regulate gene expression and cell behavior. Mutations that cause Ras to be constantly active are implicated in many cancers. Inhibiting Ras function through drugs like farnesyltransferase inhibitors may block its ability to drive uncontrolled cell growth.
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 also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
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
1. Programmed cell death, also known as apoptosis, is essential for proper development and for destroying harmful cells.
2. Apoptosis is regulated by caspases, which are cysteine-dependent aspartate specific proteases. Caspases activate a proteolytic cascade that leads to cell death.
3. There are three main apoptotic pathways: the extrinsic pathway which involves death receptors, the intrinsic pathway which involves the mitochondria, and the granzyme pathway which uses granzymes from cytotoxic T cells and natural killer cells.
This document provides an introduction to apoptosis, or programmed cell death. It discusses how apoptosis is important for homeostasis and shaping tissues during development. Apoptosis is a highly regulated process where cells self-degrade through molecular machinery like caspases. The document outlines the molecular pathways of apoptosis, including the extrinsic, intrinsic, and execution pathways. It also discusses apoptosis in animals, plants, and the roles of autophagy and caspase enzymes.
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.
iPS cells, or induced pluripotent stem cells, are adult cells that have been artificially reprogrammed to an embryonic stem cell-like state through the expression of specific genes. Nobel Prize winner Shinya Yamanaka conducted research demonstrating that mouse fibroblasts could be reprogrammed into iPS cells through the use of transcription factors. While iPS cells show promise for regenerative medicine applications, current research is focused on addressing issues such as variability in gene expression and DNA methylation between iPS cell lines as well as developing methods to create iPS cells without integrating vectors that could cause mutations.
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
Apoptosis 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.
Add MTT reagent and incubate. Mitochondrial enzymes in viable cells convert MTT into an insoluble purple formazan product. Lyse cells and solubilize formazan with solvent. Measure absorbance which is directly proportional to number of viable cells. The more viable cells, the higher the absorbance. MTT assay is a sensitive, quantitative and reliable colorimetric method to measure cell viability and proliferation.
This document discusses stem cell niches and their therapeutic applications. It defines a stem cell niche as the microenvironment where stem cells reside, and notes that niches consist of niche cells, stem cells, signals and extracellular matrix that regulate stem cell behavior. Different types of niches are described for blood, cartilage, bone, neural and skin stem cells. The roles of various signaling pathways in maintaining the stem cell niche are also outlined. Finally, the document discusses current and potential future therapeutic applications of stem cells for treating various diseases.
Autophagy plays multifaceted roles in both the innate and adaptive immune system. In innate immunity, autophagy aids in the recognition of pathogens by pattern recognition receptors like TLRs, NLRs, and RLRs. It also facilitates the handling and destruction of intracellular bacteria by phagocytosis and lysosomal fusion. Autophagy regulates the production of cytokines as well. In adaptive immunity, autophagy contributes to antigen presentation on MHC class I and II molecules and is important for the homeostasis and functions of lymphocytes like T cells and B cells. However, the precise mechanisms in some cases require further clarification.
Autophagy is a cellular process where cytoplasmic components are engulfed and degraded in the lysosome or vacuole. There are three main types of autophagy: chaperone-mediated autophagy, macroautophagy, and microautophagy. Macroautophagy involves the formation of a double-membrane vesicle called the autophagosome that delivers cytoplasmic cargo to the lysosome. Autophagy plays an important role in cellular homeostasis and survival during starvation. Defects in autophagy are associated with cancer, neurodegenerative diseases, and other disorders. While autophagy generally promotes survival, excessive autophagy may lead
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
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.
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis & it’s significance in oral diseases.pptxDr Palak borade
This document summarizes a review article on apoptosis and its significance in oral diseases. It defines apoptosis as programmed cell death and discusses the intrinsic and extrinsic pathways that trigger apoptosis. It describes how apoptosis is regulated by pro-apoptotic and anti-apoptotic proteins. The document then examines the role of apoptosis in oral diseases like pyogenic granuloma, central giant cell granuloma, recurrent aphthous ulcers, periodontitis, oral lichen planus, and systemic conditions like lupus erythematosus. Apoptosis is implicated in both the pathogenesis and resolution of inflammatory and immune-mediated oral diseases.
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.
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.
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.
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)
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.
Cell death, also known as programmed cell death (PCD), is an important process in multicellular organisms whereby cells undergo an regulated death process. There are three main types of cell death - apoptosis, necrosis, and autophagy. Apoptosis is a tightly regulated form of cell death that plays a key role in development and homeostasis. Necrosis is unregulated cell death that results in inflammation. PCD is important in plants for processes like formation of xylem vessels, senescence, and the hypersensitive response to pathogens. Many pathogens have evolved ways to suppress PCD to promote infection.
Caspases are cysteine-dependent aspartate specific proteases that cleave target proteins after aspartic acid residues. They exist as inactive zymogens called procaspases in cells and initiate a proteolytic cascade when activated. This leads to cleavage of key proteins and characteristic apoptosis morphology. The Bcl-2 family of proteins regulate apoptosis at the mitochondrial membrane, with pro-apoptotic proteins like Bax activating apoptosis and anti-apoptotic proteins like Bcl-2 inhibiting apoptosis. Many cancers acquire mutations in genes encoding proteins that regulate apoptosis, allowing cancer cells to evade cell death signals and continue uncontrolled proliferation. Targeting apoptosis pathways is a promising strategy for cancer treatment.
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, or programmed cell death, is regulated by intrinsic and extrinsic pathways. The intrinsic pathway involves mitochondria releasing cytochrome c which activates caspase proteases, leading to DNA fragmentation and cell death. The extrinsic pathway involves death receptors activating caspase-8 through adaptor proteins. Caspases are cysteine proteases that cleave other proteins and dismantle the cell in apoptosis. The Bcl-2 family and inhibitor of apoptosis (IAP) proteins also regulate apoptosis. Dysregulation of apoptosis contributes to diseases like cancer and neurodegeneration.
Apoptosis 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 is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment, but it is also involved in a wide range of pathological processes, including cancer. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer by acting in the extrinsic/intrinsic pathway. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. In particular, this review provides references concerning the apoptotic molecules, their interactions, the mechanisms involved in apoptosis resistance, and also the modulation of apoptosis for the treatment of cancer. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies.
1. Apoptosis is a tightly regulated form of programmed cell death that plays an important role in development, tissue homeostasis, and the immune system. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
2. The process of apoptosis involves initiator caspases that activate executioner caspases, leading to degradation of nuclear and cytoplasmic components. Mitochondria also play a key role by releasing pro-apoptotic factors. Various proteins regulate apoptosis, including Bcl-2 family members and inhibitors of apoptosis (IAPs).
3. Dysregulation of apoptosis contributes to diseases like cancer, neurodegeneration, and HIV/AIDS. Detection of
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 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.
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.
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.
This presentation illustrates the various pathways of development of AD ,including the recent molecular pathways , and their implication in early diagnosis and therapy .
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
Assessment and Planning in Educational technology.pptxKavitha Krishnan
In an education system, it is understood that assessment is only for the students, but on the other hand, the Assessment of teachers is also an important aspect of the education system that ensures teachers are providing high-quality instruction to students. The assessment process can be used to provide feedback and support for professional development, to inform decisions about teacher retention or promotion, or to evaluate teacher effectiveness for accountability purposes.
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Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
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Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
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তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
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This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
Dive into the world of AI! Experts Jon Hill and Tareq Monaur will guide you through AI's role in enhancing nonprofit websites and basic marketing strategies, making it easy to understand and apply.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
3. Normal cell: homeostasis
Maintenance of the integrity of cell membrane
Aerobic respiration
Synthesis of functional and structural proteins
Preservation of genetic apparatus of the cell
4. Irreversible form of cell injury
in the form of:
Necrosis
Apoptosis,
Autophagy,
some other alternative ways -
Necroptosis,
Anoikis,
Entosis,
Cornification.
Robbins Basic pathology
6. Cell injury during ischaemia/hypoxia
Mechanisms –
Depletion of ATP
Mitochondrial Damage
Loss of Calcium Homeostasis
Accumulation of Oxygen-Derived
free radical
Defects in Membrane PermeabilityRobbins Basic pathology
11. 1. Dry gangrene
2. Moist gangrene
3. Gas gangrene
Gangrenous necrosis
• Necrotic tissue invaded by saprophytic bacteria(putrefactive)
Fibrinoid necrosis
Ag-Ab complexes and fibrin accumulate in
arteries or other vessels.
Robbins Basic pathology
12. APOPTOSIS
The name was first introduced by John Kerr in 1972. ( Lockshin., 1964)
Review articles Apoptosis—an introduction Alfons Lawen
It is a form of cell death designed to eliminate unwanted host cells
through activation of a coordinated, internally programmed series of
events effected by dedicated set of gene products.
Apoptosis is needed for proper development
Apoptosis is needed in pathological process
Need of apoptosis
25. TUNEL
Cells with fragmented nuclei can also be visualized by an
assay that labels DNA ends Terminal deoxynucleotidyl
transferase–mediated dUTP Nick End-Labeling
DNA ladder
When a DNA sample from an apoptotic
cells is electrophoresed, the
fragmentation pattern gives rise to a
“DNA ladder
FACS Analysis
Molecular biology of cells,4th edition
TEM
Single-cell electrophoresis
(Comet assay)
26. Cross-talk between different modes of cell death.
Necroptosis
(RIP 1 dependent)
Anoikis(shedding)
Entosis
(cannibalism, cell eating cell)
Cornification
(keratinocytes,caspase14
dependent)
Some other alternative ways of cell death
Yaun,J.,2013
27. Necrosis and apoptosis are main mechanisms of cell death.
Necrosis is accidental, uncontrolled, un-programmed cell death.
Apoptosis can be a physiological and pathological process.
Apoptosis Involve Extrinsic (ligands and receptor mediated),Intrinsic (Cyt.c
mediated) and Cytotoxic T-cells mediated Granzyme pathway.
p53 gene (TP53) is a tumor suppressor gene which on mutation favors
apoptosis.
Over-expression and under-expression of apoptosis both are harmful for
normal homeostasis.
Cell death have clarified many aspects of this fundamental process and
brought to the attention of scientist its role in a large number of different
diseases.
28. Références:
Hotchkiss,R.S.,Strasser,R.et.al.2009.Mechanisms of cell death. The New England Journal
of Médicine,361:1570-83
Bienvenu A. L., Rey E.G. and Picot, S. 2010. Apoptosis induced by parasitic diseases.
Parasites & Vectors. 3:106
Chowdhury, I., Tharakan, B. and Bhat, G. K. 2006. Current concepts in apoptosis: the
physiological suicide program revisited. Cellular & Molecular Biology Letters 11:506 –
525
Woodruff,T.M., Thundyil., et.al. Pathophysiology, treatment and animals and cellular
models of human ischemic stroke. Molecular Degenration,2011,6:11.
1Wang, C. and Youle, R. J. 2009. The Role of Mitochondria in Apoptosis. Annu. Rev.
Genet., 43:95–118
Marcelo, A. and Wanderley, S. D. 2006. Bacteria-induced apoptosis: an approach to
bacterial pathogenesis. Braz. J. Morphol. Sci. 23(1):75-86.
Elmore, S. 2007. Apoptosis: a review of programmed cell death. Toxicol. Pathol. 2007,
35(4): 495–516.
Barcinski, M. A. and DosReis, G. A. 1999. Apoptosis in parasites and parasite-induced
apoptosis in the host immune system: a new approach to parasitic diseases. Braz. J. Med.
Biol. Res., 32(4): 395-401.
Yaun,J. and Kroemer,G. 2013 Alternative cell death mechanisms in development and
beyond.,24:2592-2602.
Gonzalz,A.M.F.et.al.2013.The modulation of apoptosis by oncogenic viruses. Virology
Journal.10:182