Abstract

Apoptosis or programmed cell death is a regulatory process in a multicellular organism that involves aspartate specific cysteine rich protease called caspase are members of the interleukin-1β-converting enzyme family. Apoptosis is induced via two main routes involving either the mitochondria (the intrinsic pathway) or the activation of death receptors (the extrinsic pathway). Both pathways converge to induce the activation of caspases the final executioners of cell death, although, it should be noted that caspase-independent forms of apoptosis have been reported. Ultimately, apoptotic cells are ingested by neighboring cells and phagocytes, preventing inflammation and tissue damage that might ensue upon cell-lysis. The activation and function of caspases, involved in the delicate caspase-cascade system, are regulated by various kinds of molecules, such as the inhibitor of apoptosis protein, Bcl-2 family proteins, calpain and calcium.

Highlights

  • Programmed cell death, or apoptosis, is an important regulatory process that is required to maintain the integrity and homeostasis of both developing and adult multicellular organisms 28

  • Deciphering the precise role of caspases in diverse physiological and pathological conditions is of fundamental importance

  • Apoptosis is a major form of cell death, characterized by a series of distinct morphological and biochemical alterations .Apoptotic cell death occurs in two phases: first a commitment to cell death, followed by an execution phase characterized by dramatic stereotypic morphological changes in cell structure, suggesting the presence in different cells of common execution machinery

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Summary

INTRODUCTION

Programmed cell death, or apoptosis, is an important regulatory process that is required to maintain the integrity and homeostasis of both developing and adult multicellular organisms 28. The diverse developmental and pathological stimuli that can induce apoptosis, including receptor-signaling, DNA-damage, growth factor deprivation and several stress signals, all converge on common effector mechanisms in which the key component is the activation of the cell-suicide proteases, the caspases. These enzymes mediate highly specific cleavage of cellular substrates, which results in a series of characteristic morphological changes and the subsequent demise of the IJBR2[7][2011]422‐431 apoptotic cell. The destruction of cell is induced by enzymes executors of proteins they belong to a group of enzymes known as cysteine proteases and exist within the cell as inactive pro-forms or zymogens These zymogens can be cleaved to form active enzymes following the induction of apoptosis. These caspases are responsible for the cleavage of the key cellular proteins, such as cytoskeletal proteins, that leads to the IJBR2[7][2011]422‐431 typical morphological changes observed in cells undergoing apoptosis

CASPASES CHROMATIN BREAKDOWN
TYPES OF CELL DEATH
PROPERTIES
HOW CELL DEATH OCCURS THROUGH CASPASES?
THE APOPTOSOME
DOWNSTREAM SUBSTRATE
11. ROLE OF CASPASE-2
13. IMPORTANCE
14. CONCLUSION
15. ACKNOWLEDGEMENT
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