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- W4230472246 abstract "This chapter describes various aspects of apoptosis. Apoptosis or programmed cell death is a mechanism by which cells commit suicide. It is characterized by chromatin condensation, internucleosomal fragmentation of DNA by an Mg2+-dependent endonuclease, blebbing of the cell membrane and vesicularization of the cell contents. The product of the BCL2 gene is an important regulator of apoptosis, first identified from its involvement in the most common chromosome translocation in B cell follicular lymphoma. Growth arrest and apoptosis can be induced by a variety of cytokines including the TGFβ family, members of which inhibit the proliferation of a wide variety of cell types that may also undergo concomitant cell death. TGFβ-induced apoptosis is blocked in myeloblastic leukemia cells by BCL2 expressed at a level that does not block but merely delays p53-induced apoptosis. Expression of the tumor suppressor gene p53, which can arrest cell proliferation, may also promote apoptosis. The p53 levels increase in response to a variety of DNA-damaging treatments and, in addition to trans-activating BAX, wild-type p53 can repress BCL2 expression. It is found that the key role of the tumor suppressor gene product pRb in inhibiting cell cycle progression in its hypophosphorylated form is consistent with the observation that Rb−/− mice die prenatally as a consequence of inappropriate DNA synthesis and apoptosis in cells of the nervous system." @default.
- W4230472246 created "2022-05-11" @default.
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- W4230472246 date "1997-01-01" @default.
- W4230472246 modified "2023-09-27" @default.
- W4230472246 title "Apoptosis" @default.
- W4230472246 doi "https://doi.org/10.1016/b978-012344548-3/50007-8" @default.
- W4230472246 hasPublicationYear "1997" @default.
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