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Id2 promotes apoptosis by a novel mechanism independent of dimerization to basic helix-loop-helix factors

Id2 由 Dimerization 的一个新奇机制独立人士把 Apoptosis 提升到基本 Helix-Loop-Helix 因素

作     者:Florio, M Hernandez, MC Yang, H Shu, HK Cleveland, JL Israel, MA 

作者机构:Univ Calif San Francisco Dept Neurosurg Brain Tumor Res Ctr Preuss Lab Mol Neurooncol San Francisco CA 94143 USA St Jude Childrens Res Hosp Dept Biochem Memphis TN 38105 USA Univ Tennessee Dept Biochem Memphis TN 38163 USA 

出 版 物:《MOLECULAR AND CELLULAR BIOLOGY》 (分子生物学与细胞生物学)

年 卷 期:1998年第18卷第9期

页      面:5435-5444页

核心收录:

学科分类:0710[理学-生物学] 071010[理学-生物化学与分子生物学] 07[理学] 

基  金:NCI NIH HHS [CA76379  R01 CA076379  P30 CA021765  CA21765  CA13525] Funding Source: Medline 

主  题:.terminal transcription factors programmed cell progenitors cell proliferation target genes proapoptotic Cell Death brain tumor dimerization regulators basic helix-loop-helix Id proteins Id Promotes HLH-mediated dependent myeloid OS osteosarcoma effects of Id 

摘      要:Members of the helix-loop-helix (HLH) family of Id proteins have demonstrated roles in the regulation of differentiation and cell proliferation. Id proteins inhibit differentiation by HLH-mediated heterodimerization with basic HLH transcription factors. This blocks their sequence-specific binding to DNA and activation of target genes that are often expressed in a tissue-specific manner. Id proteins can also act as positive regulators of cell proliferation. The different mechanisms proposed for Id-mediated promotion of entry into S phase also involve HLH-mediated interactions affecting regulators of the G(1)/S transition. We have found that Id2 augments apoptosis in both interleukin3 (IL-3)-dependent 32D.3 myeloid progenitors and U2OS osteosarcoma cells. We could not detect a similar activity for Id3. In contrast to the effects of Id2 on differentiation and cell proliferation, Id2-mediated apoptosis is independent of HLH-mediated dimerization. The ability of Id2 to promote cell death resides in its N-terminal region and is associated with the enhanced expression of a known component of the programmed cell death pathway, the proapoptotic gene BAX.

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