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Apoptosis

Sino Biological offers a series of reagents for research on apoptosis, including active proteins, antibodies and cDNA clones.

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    Apoptosis Background

    Apoptosis is the process of programmed cell death that is a normal component of the development of multicellular organisms. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion. This makes apoptosis distinct from another form of cell death called necrosis in which uncontrolled cell death leads to lysis of cells, inflammatory responses and, potentially, to serious damage to organism. Apoptosis, by contrast, is a process in which cells play an active role in their own death. Therefore, apoptosis is often referred to as cell suicide.

    Apoptosis is needed to destroy cells that represent a threat to the integrity of the organism. These cells may be infected with viruses, with DNA damage, or cancer cells. Apoptotic cells display distinctive morphology during the apoptotic process. These changes include cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. Apoptosis can be induced in cells through a number of mechanisms, which may originate either extracellularly or intracellularly. Extrinsic signals may be the binding of death inducing ligands to cell surface receptors called death receptors, as well as hormones, growth factors, nitric oxide or cytokines. Apoptosis can be initiated following intrinsic signals that are produced following cellular stress, including heat, radiation, nutrient deprivation, viral infection, and so on. The sensitivity of cells to any of these stimuli can vary depending on a number of factors such as the expression of pro- and anti-apoptotic proteins (e.g. the Bcl-2 proteins or the inhibitor of apoptosis proteins), the severity of the stimulus and the stage of the cell cycle.

    Apoptosis References

      1. Everett, H., et al. (1999) Apoptosis: an innate immune response to virus infection. Trends Microbiol 7(4):160-5.
      2. Popov SG., et al. (2002) Lethal toxin of Bacillus anthracis causes apoptosis of macrophages. Biochem. Biophys. Res. Commun. 293(1):349-55.
      3. Shore GC. (2009) Apoptosis: it's BAK to VDAC. EMBO Rep. 10(12):1311-3.
      4. Speidel D. (2010) Transcription-independent p53 apoptosis: an alternative route to death. Trends Cell Biol. 20(1):14-24.