CDK7&CCNH&MNAT1 蛋白, Human (sf9, His)

CDK7, along with regulatory partners CCNH and MNAT1, operates as a crucial serine/threonine kinase in cell cycle regulation and RNA polymerase II-mediated transcription. As the catalytic subunit of the CDK-activating kinase (CAK) complex, CDK7 plays a pivotal role in activating CDK1/cyclin-B and CDK2/cyclins during cell cycle transitions. It phosphorylates key targets, including SPT5/SUPT5H and POLR2A. CDK7, in complex with TFIIH, activates RNA polymerase II for transcript elongation. Its consistent expression and activity contribute to DNA-bound peptide-mediated transcription and cellular growth regulation. CDK7&CCNH&MNAT1 Protein, Human (sf9, His) is the recombinant heterotrimer protein (consiting of CDK7, CCNH, MNAT1), expressed by Sf9 insect cells, with N-His labeled tag. CDK7&CCNH&MNAT1 Protein, Human (sf9, His), has molecular weight of ~25 & 38 & 44 kDa, respectively.

CDK7 与其调节伙伴 CCNH 和 MNAT1 一起，充当丝氨酸/苏氨酸激酶，在细胞周期调节和 RNA 聚合酶 II 介导的转录中发挥关键作用。作为 CDK 激活激酶 (CAK) 复合物的催化亚基，CDK7 在 G2-M 转变期间的 CDK1/细胞周期蛋白-B 和 G1-S 转变期间的 CDK2/细胞周期蛋白的激活和形成中发挥着关键作用。其磷酸化靶标包括 SPT5/SUPT5H、SF1/NR5A1、POLR2A、p53/TP53、CDK1、CDK2、CDK4、CDK6 和 CDK11B/CDK11。通过苏氨酸磷酸化，CAK 激活细胞周期蛋白相关激酶，从而调节细胞周期进程。此外，当 CDK7 与核心 TFIIH 基础转录因子复合时，通过其大亚基 (POLR2A) 的 C 端结构域 (CTD) 丝氨酸磷酸化促进 RNA 聚合酶 II 激活。这种激活使 RNA 聚合酶 II 能够逃脱启动子并启动转录物延伸。CDK7 在整个细胞周期中的一致表达和活性有助于其参与 DNA 结合肽介导的转录和细胞生长抑制。此外，作为对 DNA 损伤的反应，CDK7 触发 p53/TP53 的激活，形成反馈环，其中 p53/TP53 随后可以使 CDK7 失活，可能导致细胞周期停滞、转录关闭和细胞恢复或凋亡。

Human

Sf9 insect cells

N-His

P50613 (A2-F346)&P51946 (Y2-L323)&P51948 (D2-S309)

1022  [NCBI]&902  [NCBI]&4331  [NCBI]

Approximately 25&38&44 kDa

Greater than 85% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.