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Apoptosis (from Ancient Greek: ἀπόπτωσις, romanized: apóptōsis, lit. 'falling off') is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast. [1]
Apoptosis is the process of programmed cell death (PCD) that may occur in multicellular organisms. [12] Biochemical events lead to characteristic cell changes and death.. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentat
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
[6] [7] It was the first apoptosis regulator identified in any organism. [ 8 ] Bcl-2 derives its name from B-cell lymphoma 2 , as it is the second member of a range of proteins initially described in chromosomal translocations involving chromosomes 14 and 18 in follicular lymphomas .
Apoptosis is the process of programmed cell death. From its early conceptual beginnings in the 1950s, it has exploded as an area of research within the life sciences community. From its early conceptual beginnings in the 1950s, it has exploded as an area of research within the life sciences community.
Apoptosis is a form of programmed cell death where the cell undergoes morphological changes, to minimize its effect on surrounding cells to avoid inducing an immune response. The cell shrinks and condenses - the cytoskeleton will collapse, and the nuclear envelope disassembles the DNA fragments up.
Apoptosis Inducing Factor (AIF) is a protein that triggers chromatin condensation and DNA fragmentation in a cell in order to induce programmed cell death. The mitochondrial AIF protein was found to be a caspase -independent death effector that can allow independent nuclei to undergo apoptotic changes.
CARDs were originally characterized based on their involvement in the regulation of caspase activation and apoptosis. [2] The basic six-helix structure of the domain appears to be conserved as far back as the ced-3 and ced-4 genes in C. elegans, the organism in which several components of the apoptotic machinery were first characterized.