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v-Abl利用多种机制来驱动成纤维细胞中的G1/S期进程。

v-Abl utilizes multiple mechanisms to drive G1/S progression in fibroblasts.

作者信息

Coutts M, Zou X, Calame K

机构信息

Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.

出版信息

Oncogene. 2000 Feb 10;19(6):801-9. doi: 10.1038/sj.onc.1203398.

DOI:10.1038/sj.onc.1203398
PMID:10698498
Abstract

Transformation of 3T3 fibroblasts by the v-Abl tyrosine kinase replaces mitogenic and adhesion signals normally required for cell cycle progression. A 3T3 cell line conditionally transformed with v-Abl has been used to study v-Abl's effects on cell cycle in the context of either serum depletion or absence of adhesion signals. We show that E2F-dependent mRNAs, encoding proteins required for cell cycle progression, are induced by v-Abl. In addition, we identify two previously unknown targets of v-Abl signaling: (1) cyclin D1 and D2 mRNAs are induced upon v-Abl activation; and (2) the CDK inhibitor p27 is decreased upon v-Abl activation.

摘要

v-Abl酪氨酸激酶对3T3成纤维细胞的转化取代了细胞周期进程中正常所需的促有丝分裂和黏附信号。一种用v-Abl进行条件性转化的3T3细胞系已被用于研究在血清缺乏或缺乏黏附信号的情况下v-Abl对细胞周期的影响。我们发现,v-Abl可诱导依赖E2F的mRNA,这些mRNA编码细胞周期进程所需的蛋白质。此外,我们确定了v-Abl信号传导的两个先前未知的靶点:(1)v-Abl激活后可诱导细胞周期蛋白D1和D2的mRNA;(2)v-Abl激活后CDK抑制剂p27减少。

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NF-kappaB1 can inhibit v-Abl-induced lymphoid transformation by functioning as a negative regulator of cyclin D1 expression.核因子κB1可通过作为细胞周期蛋白D1表达的负调节因子来抑制v-Abl诱导的淋巴细胞转化。
Mol Cell Biol. 2002 Aug;22(15):5563-74. doi: 10.1128/MCB.22.15.5563-5574.2002.