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 24 total

per page
Page:
  1. 1
  2. 2
Axon ID Name Description From price
2166 AT 13148 dihydrochloride ATP-competitive inhibitor of multi-AGC kinases €85.00
5051 Axon Ligands™ Cell signaling and Oncology compound library Axon Ligands™ Cell signaling and Oncology compound library Inquire
5053 Axon Ligands™ Stem cell compound library Axon Ligands™ Stem cell compound library Inquire
2669 AZ13705339 Potent and selective PAK1 inhibitor €125.00
2795 AZD 1208 Pim kinase inhibitor €70.00
2305 CX 6258 hydrochloride Pim kinase inhibitor €99.00
2574 Defactinib Orally available second generation inhibitor of FAK and PYK2 €95.00
2331 FRAX 486 Bioavailable, brain penetrating inhibitor of p21-activated kinases (PAKs) €90.00
2348 GNE 7915 Potent, selective, metabolically stable, and brain-penetrable LRRK2 inhibitor €110.00
2181 GSK 2578215A Potent and highly selective LRRK2 inhibitor €125.00
2713 GSK 2982772 Specific inhibitor of RIP1 kinase €115.00
2608 GSK481 Potent inhibitor of RIP1 kinase and TNF induced inflammation €95.00
2780 KD025 Selective ATP-competitive inhibitor of ROCK2 €95.00
2493 LRRK2-IN-1 Potent, ATP-competitive and selective inhibitor of LRRK2 €85.00
1258 Necrostatin-1 RIP1 inhibitor €95.00

Items 1 to 15 of 24 total

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