Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16INK4A Contributes to Cell Cycle Regulation

Eiji Nishiwaki; Saralinda L. Turner; Susanna Harju; Shiro Miyazaki; Masahide Kashiwagi; James Koh

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Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16INK4A Contributes to Cell Cycle Regulation

机译：肿瘤抑制因子p16INK4A对CDK7-羧基末端结构域激酶活性的调控有助于细胞周期调控

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The eukaryotic cell cycle is regulated by cyclin-dependent kinases (CDKs). CDK4 and CDK6, which are activated by D-type cyclins during the G₁ phase of the cell cycle, are thought to be responsible for phosphorylation of the retinoblastoma gene product (pRb). The tumor suppressor p16INK4A inhibits phosphorylation of pRb by CDK4 and CDK6 and can thereby block cell cycle progression at the G₁/S boundary. Phosphorylation of the carboxyl-terminal domain (CTD) of the large subunit of RNA polymerase II by general transcription factor TFIIH is believed to be an important regulatory event in transcription. TFIIH contains a CDK7 kinase subunit and phosphorylates the CTD. We have previously shown that p16INK4A inhibits phosphorylation of the CTD by TFIIH. Here we report that the ability of p16INK4A to inhibit CDK7-CTD kinase contributes to the capacity to induce cell cycle arrest. These results suggest that p16INK4A may regulate cell cycle progression by inhibiting not only CDK4-pRb kinase activity but also by modulating CDK7-CTD kinase activity. Regulation of CDK7-CTD kinase activity by p16INK4A thus may represent an alternative pathway for controlling cell cycle progression.

机译：真核细胞周期由细胞周期蛋白依赖性激酶（CDKs）调节。 CDK4和CDK6在细胞周期的G _{1 期被D型细胞周期蛋白激活，被认为是视网膜母细胞瘤基因产物（pRb）磷酸化的原因。肿瘤抑制因子p16 INK4A 抑制CDK4和CDK6磷酸化pRb，从而阻止G _{1 / S边界的细胞周期进程。一般认为转录因子TFIIH对RNA聚合酶II大亚基的羧基末端结构域（CTD）进行磷酸化是转录过程中的重要调控事件。 TFIIH包含CDK7激酶亚基，并使CTD磷酸化。先前我们已经证明p16 INK4A 抑制TFIIH的CTD磷酸化。在这里，我们报道p16 INK4A 抑制CDK7-CTD激酶的能力有助于诱导细胞周期停滞。这些结果表明，p16 INK4A 可能不仅通过抑制CDK4-pRb激酶活性，而且通过调节CDK7-CTD激酶活性来调节细胞周期进程。因此，p16 INK4A 对CDK7-CTD激酶活性的调节可能是控制细胞周期进程的另一种途径。}}

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《Molecular and Cellular Biology》 |2000年第20期|共9页
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Eiji Nishiwaki; Saralinda L. Turner; Susanna Harju; Shiro Miyazaki; Masahide Kashiwagi; James Koh;
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中图分类细胞生物学;
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1. Tumor suppressor BLU inhibits proliferation of nasopharyngeal carcinoma cells by regulation of cell cycle, c-Jun N-terminal kinase and the cyclin D1 promoter [J] . Xiangning Zhang, Hui Liu, Binbin Li, BMC Cancer . 2012,第1期

机译：肿瘤抑制因子BLU通过调节细胞周期，c-Jun N端激酶和细胞周期蛋白D1启动子来抑制鼻咽癌细胞的增殖
2. Tumor suppressor in lung cancer 1 (TSLC1), a novel tumor suppressor gene, is implicated in the regulation of proliferation, invasion, cell cycle, apoptosis, and tumorigenicity in cutaneous squamous cell carcinoma [J] . LiuD., FengX., WuX., Tumour biology : . 2013,第6期

机译：肺癌1（TSLC1）的肿瘤抑制基因是一种新型的肿瘤抑制基因，与皮肤鳞状细胞癌的增殖，侵袭，细胞周期，细胞凋亡和致瘤性有关。
3. Increased phosphorylation of the carboxyl-terminal domain of RNA polymerase II and loading of polyadenylation and cotranscriptional factors contribute to regulation of the ig heavy chain mRNA in plasma cells. [J] . Shell SA, Martincic K, Tran J, The Journal of Immunology: Official Journal of the American Association of Immunologists . 2007,第11期

机译：RNA聚合酶II的羧基末端结构域的磷酸化增加以及聚腺苷酸化和共转录因子的负载有助于调节浆细胞中ig重链mRNA。
4. The Tumor Suppressor Gene PTEN Plays a Role in Cell Cycle Regulation and Apoptosis in Prostate Cancer Cell Lines [C] . Alice Hlobilkova, Michaela Svachova, Jana Knillova, International Symposium on Hormonal Carcinogenesis . 2005

机译：肿瘤抑制基因PTEN在前列腺癌细胞系中的细胞周期调节和细胞凋亡中起着作用
5. Regulation of the tumor suppressor pRB by protein kinase Cepsilon in human prostate cancer cells. [D] . Foreman, Tonia Lee. 2003

机译：蛋白激酶Cepsilon在人前列腺癌细胞中对抑癌基因pRB的调节。
6. Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16INK4A Contributes to Cell Cycle Regulation [O] . Eiji Nishiwaki, Saralinda L. Turner, Susanna Harju, 2000

机译：肿瘤抑制因子p16INK4A对CDK7-羧基末端结构域激酶活性的调控有助于细胞周期调控
7. Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16 INK4A Contributes to Cell Cycle Regulation [O] . Eiji Nishiwaki, Saralinda L. Turner, Susanna Harju, 2000

机译：肿瘤抑制器P16 Ink4a的CDK7-羧基 - 末端域激酶活性的调节有助于细胞周期调节

Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16INK4A Contributes to Cell Cycle Regulation

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