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首页> 外文期刊>Molecular and Cellular Biology >Id2 Promotes Apoptosis by a Novel Mechanism Independent of Dimerization to Basic Helix-Loop-Helix Factors
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Id2 Promotes Apoptosis by a Novel Mechanism Independent of Dimerization to Basic Helix-Loop-Helix Factors

机译：Id2通过一种独立于二聚化至基本螺旋-螺旋-螺旋因子的新型机制促进细胞凋亡。

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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 G1/S transition. We have found that Id2 augments apoptosis in both interleukin-3 (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.
机译：Id蛋白质的螺旋-环-螺旋（HLH）家族成员已证明在分化和细胞增殖的调控中发挥作用。 Id蛋白通过与基本HLH转录因子的HLH介导的异二聚作用抑制分化。这阻止了它们与DNA的序列特异性结合以及通常以组织特异性方式表达的靶基因的激活。 Id蛋白还可以充当细胞增殖的正调节剂。提议的Id介导的促进进入S期的不同机制还涉及HLH介导的相互作用，该相互作用影响G 1 / S过渡的调节剂。我们发现Id2增强白介素3（IL-3）依赖的32D.3髓样祖细胞和U2OS骨肉瘤细胞的凋亡。我们无法检测到Id3的类似活动。与Id2对分化和细胞增殖的影响相反，Id2介导的凋亡独立于HLH介导的二聚化。 Id2促进细胞死亡的能力在于其N端区域，并与程序性细胞死亡途径的已知成分即促凋亡基因 BAX 的表达增强有关。

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