摘要
细胞周期素依赖性激酶11是转录型CDK亚家族中一个相对被忽视的成员,尽管它可能是这一组中最多才多艺的CDK。已知不同的CDK 11变体在主要的细胞过程中起重要作用,如mRNA转录(CDK11p110)、有丝分裂(CDK11p58)和凋亡(CDK11p46和CDK11p60)。每种cdk 11的目标是一组特定的底物r。与其功能背景有关,但所有的亚型均来自于人类染色体1p36.2中的CDC2L基因复合体。CDK11p110的合成是通过cdk 11 mRNA的正常帽依赖性翻译而得到的。而CDK11p58翻译是通过IRES启动的,只发生在G2和M期。CDK11p46和CDK11p60则是caspase在apop过程中切割较大亚型的产物。下垂。CDK 11的主要合作伙伴是L型细胞周期蛋白,虽然CDK11p58与细胞周期蛋白D3有特异性的相互作用。CDK 11功能障碍与癌症之间的联系早已为人所知,CDK 11在不同癌细胞株的增殖中起关键作用。本文综述了25年来对cdk 11基因和功能方面的研究。
关键词: CDK 11,PITSLRE,RNAPII转录,纺锤体组装,姐妹染色单体内聚力,促凋亡信号。
Current Medicinal Chemistry
Title:The Emerging Picture of CDK11: Genetic, Functional and Medicinal Aspects
Volume: 25 Issue: 8
关键词: CDK 11,PITSLRE,RNAPII转录,纺锤体组装,姐妹染色单体内聚力,促凋亡信号。
摘要: Cyclin-dependent kinase 11 is a relatively neglected member of the transcriptional CDKs subfamily, despite possibly being the most versatile CDK in this group. Different CDK11 variants are known to play essential roles in major cellular processes as mRNA transcription (CDK11p110), mitosis (CDK11p58), and apoptosis (CDK11p46 and CDK11p60). Each CDK11 species targets a particular set of substrates related to its functional background, but all isoforms originate from the CDC2L gene complex in human chromosome 1p36.2. CDK11p110 is synthesized through regular cap-dependent translation of CDK11 mRNA, whereas CDK11p58 translation is initiated through an IRES, and occurs only at G2 and M phases. CDK11p46 and CDK11p60, in turn, are the products of caspase cleavage of the larger isoforms during apoptosis. L-type cyclins are the main partners of CDK11, although CDK11p58 species interacts specifically with cyclin D3. The link between CDK11 dysfunction and cancer has been known for a long time, and critical roles in the proliferation of different cancer cell lines have been assigned to CDK11. This review summarizes more than 25 years of studies that unraveled CDK11 genetic and functional aspects.
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Cite this article as:
The Emerging Picture of CDK11: Genetic, Functional and Medicinal Aspects, Current Medicinal Chemistry 2018; 25 (8) . https://dx.doi.org/10.2174/0929867324666170815102036
DOI https://dx.doi.org/10.2174/0929867324666170815102036 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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