11-03-2014, 01:03 PM
ASSIGNMENT ON APOPTOSIS
APOPTOSIS.ppt (Size: 1.11 MB / Downloads: 27)
INTRODUCTION
It is a functional death and it is a good mechanism to eliminate wasted, useless, unwanted, or crippled cells.
Process of programmed cell death that may occur in multicellular organisms
Leads to characteristic changes like cell shrinkage, nuclear fragmentation, chromatin condensation & chromosomal DNA fragmentation
Between 50 & 70 billion cells die each day due to apoptosis in the average human adult.
HISTORY
German scientist Carl Vogt was first to describe the principle of apoptosis in 1842
In 1885, anatomist Walther Flemming delivered a more precise description of the process of programmed cell death.
Kerr received the Paul Ehrlich & Ludwig Darmastedter Prize on March 14, 2000, for his description of apoptosis.
The 2002 Nobel Prize in medicine was awarded to Sydney Brenner, Horvitz and John E. Sulston for their work regarding apoptosis.
What makes a cell decide to commit suicide?
Withdrawal of positive signals
examples :
growth factors for neurons
Interleukin-2 (IL-2)
Receipt of negative signals
examples :
increased levels of oxidants within the cell
damage to DNA by oxidants
death activators :
Tumor necrosis factor alpha (TNF-)
Lymphotoxin (TNF-β)
Fas ligand (FasL)
APOPTOSIS: Role in Disease
Neurons are post-mitotic (cannot replace themselves;
neuronal stem cell replacement is inefficient)
Neuronal death caused by loss of proper connections,
loss of proper growth factors (e.g. NGF), and/or
damage (especially oxidative damage)
Neuronal dysfunction or damage results in loss of synapses
or loss of cell bodies
(synaptosis is reversible; apopsosis is irreversible)
Also plays a major role in Pakinson’s disease, Alzheimer’s disease & Huntington’s disease
FUTURE PERSPECTIVES
The biological roles of newly identified death receptors and ligands need to be studied
Need to know whether defects in these ligands and receptors contribute to disease
CONCLUSION
an important process of cell death
can be initiated extrinsically through death ligands
(e.g. TRAIL, FasL) activating initiator caspase 8 through induced proximity.
can be initiated intrinsically through DNA damage (via cytochrome c) activating initiator caspase 9 through oligomerization.
Initiator caspases 8 and 9 cleave and activate
effector caspase 3, which leads to cell death.