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 31 to 45 of 389 total

per page
Page:
  1. 1
  2. 2
  3. 3
  4. 4
  5. 5
Axon ID Name Description From price
2179 ASK1 Inhibitor 10 Potent, selective, and orally bioavailable ASK1 inhibitor €125.00
2166 AT 13148 dihydrochloride ATP-competitive inhibitor of multi-AGC kinases €70.00
1985 AT 406 Antagonist of Inhibitor of apoptosis proteins (IAPs) €145.00
1539 AT 7519 mesylate CDK inhibitor €80.00
5051 Axon Ligands™ Cell signaling and Oncology compound library Axon Ligands™ Cell signaling and Oncology compound library Inquire
5052 Axon Ligands™ Epigenetic compound library Axon Ligands™ Epigenetic compound library Inquire
5053 Axon Ligands™ Stem cell compound library Axon Ligands™ Stem cell compound library Inquire
2345 AZ 20 Potent, orally active and selective inhibitor of ATR protein kinase €105.00
1778 AZ 960 JAK2 inhibitor €95.00
2669 AZ13705339 Potent and selective PAK1 inhibitor €125.00
2795 AZD 1208 Pim kinase inhibitor €70.00
3134 AZD6738 Potent, selective, orally active and bioavailable ATR kinase inhibitor €110.00
2981 B106 Potent and selective PKC-δ inhibitor €135.00
2185 BAM 7 Selective small-molecule activator of proapoptotic BAX €90.00
2918 BAY 1895344 Potent, orally available and highly selective inhibitor of ATR protein kinase €100.00

Items 31 to 45 of 389 total

per page
Page:
  1. 1
  2. 2
  3. 3
  4. 4
  5. 5
Please wait...