Cyclin D1, cancer progression, and opportunities in cancer treatment.
Cyclin D1, cancer progression, and opportunities in cancer treatment.
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DOI：
10.1007/s00109-016-1475-3
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发表时间：
2016-12
影响因子：
4.7
通讯作者：
Diehl, J. Alan
中科院分区：
文献类型：
--
作者：
Qie, Shuo;Diehl, J. Alan
哺乳动物细胞编码三种D型细胞周期蛋白（D1、D2和D3），它们作为细胞周期蛋白依赖性激酶4和6（CDK 4/CDK 6）的变构调节剂协调地发挥作用，调节细胞周期从G1期到S期的转变。细胞周期蛋白的表达、积累和降解以及CDK 4/CDK 6的组装和活化受生长因子刺激的控制。在人类癌症中，细胞周期蛋白D1比细胞周期蛋白D2或D3更频繁地失调，因此它已被更广泛地表征。细胞周期蛋白D1的过表达导致CDK活性失调，在限制促有丝分裂信号传导的条件下细胞快速生长，绕过关键细胞检查点并最终导致肿瘤生长。本文综述了细胞周期蛋白D1的转录、翻译、翻译后调控及其生物学功能，特别关注导致其在人类癌症中失调的机制。
Mammalian cells encode three D cyclins (D1, D2 and D3) that coordinately function as allosteric regulators of cyclin dependent kinase 4 and 6 (CDK4/CDK6) to regulate cell cycle transition from G1 to S phase. Cyclin expression, accumulation and degradation, as well as assembly and activation of CDK4/CDK6 are governed by growth factor stimulation. Cyclin D1 is more frequently dysregulated than cyclins D2 or D3 in human cancers and as such it has been more extensively characterized. Overexpression of cyclin D1 results in dysregulated CDK activity, rapid cell growth under conditions of restricted mitogenic signaling, bypass of key cellular checkpoints and ultimately neoplastic growth. This review discusses cyclin D1 transcriptional, translational, posttranslational regulation, and its biological function with a particular focus on the mechanisms that result in its dysregulation in human cancers.
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影响因子：
50.3
作者：
Barbash, Olena;Zamfirova, Petia;Lin, Douglas I.;Chen, Xiangmei;Yang, Ke;Nakagawa, Hiroshi;Lu, Fengmin;Rustgi, Anil K.;Diehl, J. Alan
通讯作者：
Diehl, J. Alan
影响因子：
50.3
作者：
Anders L;Ke N;Hydbring P;Choi YJ;Widlund HR;Chick JM;Zhai H;Vidal M;Gygi SP;Braun P;Sicinski P
通讯作者：
Sicinski P
影响因子：
21.3
作者：
Carrano, AC;Eytan, E;Pagano, M
通讯作者：
Pagano, M
DOI：
10.1073/pnas.220247197
发表时间：
2000-11-07
影响因子：
11.1
作者：
Brewer, JW;Diehl, JA
通讯作者：
Diehl, JA
影响因子：
5.3
作者：
Aktas, H;Cai, H;Cooper, GM
通讯作者：
Cooper, GM