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].

[1] B. Alberts, A. Johnson, J. Lewis et al. Molecular Biology of the Cell. 4th edition. New York. Garland Science, 2002. 
[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.

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Axon ID Name Description From price
2141 ABT 199 Potent, orally bioavailable BCL-2-selective inhibitor €135.00
1985 AT 406 Antagonist of Inhibitor of apoptosis proteins (IAPs) €145.00
2185 BAM 7 Selective small-molecule activator of proapoptotic BAX €105.00
1828 BH3I 1 Inhibitor of Bcl-2 family protein €125.00
2334 BT2 Allosteric inhibitor of BCKDC kinase (BDK) and Mcl-1 inhibitor €95.00
2293 Ferrostatin 1 Potent inhibitor of erastin-induced ferroptosis €85.00
2007 HA 14-1 Bcl-2 inhibitor and apoptosis inducer of tumor cells €75.00
2165 S 12 Survivin inhibitor €105.00
2300 TIC 10 active isomer Small molecule that transcriptionally induces TRAIL €125.00
1639 YM 155 Survivin suppressant €95.00

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