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. 

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Axon ID Name Description From price
2141 ABT 199 Potent, orally bioavailable BCL-2-selective inhibitor €120.00
2185 BAM 7 Selective small-molecule activator of proapoptotic BAX €105.00
1828 BH3I 1 Inhibitor of Bcl-2 family protein €125.00
2978 Brigatinib Potent, selective, and orally active anaplastic lymphoma kinase (ALK) inhibitor €80.00
2879 CP 31398 Stabilizer of p53 and inducer of apoptosis €95.00
2007 HA 14-1 Bcl-2 inhibitor and apoptosis inducer of tumor cells €75.00
2349 JSH 23 Inhibitor of NF-κB transcription and nuclear translocation of p65 without affecting IκBα degradation €95.00
2823 ML 311 Potent and selective inhibitor of the protein-protein interaction of Mcl-1 and Bim €95.00
1871 Pifithrin-α hydrobromide Inhibitor of p53 protein €95.00
2627 SMER 28 Small molecule enhancer of rapamycin that enhances autophagy €80.00
2385 WZ 4003 Specific dual inhibitor of NUAK1 (ARK5) and NUAK2 (SNARK) €90.00

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