Apoptosis

The number of cells in multicellular organism is tightly regulated. Not simply by controlling the rate of cell division, but also by controlling the rate of cell death. If cells are no longer needed, they commit suicide by activating an intracellular death program. This process is therefore called programmed cell death or apoptosis (from a Greek word meaning “falling off,” as leaves from a tree). The intrinsic apoptotic pathway occurs by the release of cytochrome c from mitochondria. The extrinsic apoptotic pathway is caused by the binding of death ligands, such as TNF (tumor necrosis factor), Fas, and TRAIL (TNF-related-apoptosis-inducing ligand), to their corresponding receptors. Although programmed cell death is involved in a number of key biological phenomena, aberrant apoptosis results in diverse human diseases [1]
The amount of apoptosis that occurs in developing and adult animal tissues is surprisingly large. In the developing vertebrate nervous system up to half or more of the nerve cells normally die soon after they are formed. In a healthy adult human, billions of cells die in the bone marrow and intestine every hour. Although this process seems remarkably wasteful -especially as the vast majority are perfectly healthy at the time they kill themselves- programmed cell death plays an important role during embryonic development, as hands and feet, for example, are sculpted by apoptosis: they start out as spadelike structures, and the individual digits separate only as the cells between them die. In other cases, cells die when the structure they form is no longer needed. When a tadpole changes into a frog, the cells in the tail die, and the tail, which is not needed in the frog, disappears. In many other cases, cell death helps regulate cell numbers. In the developing nervous system, for example, cell death adjusts the number of nerve cells to match the number of target cells that require innervation. In all these cases, the cells die by apoptosis as well[2].


[2] D.R. Williams et al. An apoptosis-inducing small molecule that binds to heat shock protein 70. Angew. Chem. Int. Ed. Engl. 2008, 47, 7466-7469.
[1] B. Alberts, A. Johnson, J. Lewis et al. Molecular Biology of the Cell. 4th edition. New York. Garland Science, 2002. 

Items 1 to 15 of 34 total

per page
Page:
  1. 1
  2. 2
  3. 3
Axon ID Name Description From price
2222 10058-F4 c-Myc inhibitor inducing cell-cycle arrest at G0/G1 phase €80.00
1902 4μ8C IRE1α inhibitor €105.00
2839 AS 1842856 Inhibitor of the Forkhead box protein O1 (FOXO1) €95.00
2841 COTI-2 Reactivator of mutant p53 €125.00
1495 CP 466722 ATM inhibitor €80.00
2391 CS1 TOPO IIα inhibitor with broad-spectrum in vitro antitumor effects €135.00
2885 GeA-69 Selective allosteric and cell-active PARP14 MD2 inhibitor €95.00
2198 Genz 644282 Topo I inhibitor lacking MDR1 and BCRP affinity €95.00
2390 HAMNO Novel protein interaction inhibitor of replication protein A (RPA) €85.00
1687 Homocamptothecin, (±)-E- Potent topoisomerase I (Topo 1) inhibitor €135.00
1656 Irestatin 9389 IRE1 inhibitor; UPR inhibitor €125.00
2597 KPT 335 XPO1 inhibitor; selective inhibitor of nuclear export (SINE) €105.00
2538 KRIBB11 HSF1 inhibitor that blocks the induction of HSP27 and HSP70 €125.00
2001 KU 0058948 hydrochloride Potent and specific PARP1 inhibitor €135.00
1367 KU 55933 ATM inhibitor €125.00

Items 1 to 15 of 34 total

per page
Page:
  1. 1
  2. 2
  3. 3
Please wait...