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APOPTOSIS, MORPHOLOGICAL FEATURES OF APOPTOSIS, MECHANISM OF APOPTOSIS,…
APOPTOSIS
- Coordinated and internally programmed cell death
- Not accompanied by inflammation and collateral tissue damage
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MECHANISM OF APOPTOSIS
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- Withdrawal of normal cell survival signals:
eg: absence of hormones,
growth factors,
cytokines
eg: heat, radiation, hypoxia, toxins, radicals
- intrinsic (mitochondrial),
- Cytochrome C is regulated by
pro and anti apoptotic members of
Bcl proteins
- Balance lost between pro and anti apoptotic Bcl proteins
- Pro apoptotic activates Bcl-2 effector Bax, Bak which damage mitochondrial
membranes.
- Cytochrome C leaks into cytoplasm
- Activates caspase cascade
- extrinsic (cell death rececptor initiated).
- Activation of death receptors in cell membrane
- Type 1 tumour necrosis factor receptor (TNF-R1), Transmembreane protein
called Fas (CD95) and its ligand (FasL)
- Binding of Fas and FasL activates Fas associated death domain (FADD)
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FINAL PHASE OF APOPTOSIS
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- Mitochondrial pathway activates caspase 9
- Death receptor activates caspases 8 and 10
- Caspases act on DNAase and nuclear matrix proteins
- Phagocytosis:
phosphatidylserine and thrombospondin
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