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CDK7
CDK7 Full Name
cyclin-dependent kinase 7
CDK7 Introduction
Cdk7, or cyclin-dependent kinase 7, is a dual-function serine/threonine kinase that plays a central regulatory role in both transcription and the cell cycle. As part of the CDK-activating kinase (CAK) complex—along with cyclin H and MAT1—Cdk7 phosphorylates and activates other CDKs, enabling orderly progression through key cell-cycle checkpoints. In addition to its role in cell-cycle control, Cdk7 acts as a core component of the transcription factor TFIIH, where it phosphorylates the C-terminal domain of RNA polymerase II to initiate transcription. This unique positioning at the intersection of cell division and gene expression gives Cdk7 broad influence over cellular homeostasis.
Figure 1.CDK7 is a critical regulator of transcription.(Sources: Song X, et al.; 2024)
Functionally, Cdk7 operates as a master regulatory switch coordinating the timing and fidelity of essential biological processes. By activating CDKs such as Cdk1, Cdk2, Cdk4, and Cdk6, Cdk7 ensures proper DNA replication, mitotic entry, and cell-cycle transitions. Through its TFIIH-associated activity, it regulates transcription initiation, promoter clearance, and early elongation. Cdk7 also participates in DNA repair pathways by supporting TFIIH's role in nucleotide excision repair, linking transcriptional control with genome integrity. Experimental studies show that disruption of Cdk7 function results in defective transcription, stalled cell-cycle progression, impaired DNA repair, and heightened cellular stress, highlighting its indispensable regulatory capacity.
Clinically, dysregulation of Cdk7 has been implicated in a variety of cancers and proliferative disorders. Elevated Cdk7 expression or hyperactivation is frequently observed in tumors with high transcriptional demand, including breast, ovarian, lung, and colorectal cancers, and often correlates with poor prognosis. Cancer cells reliant on transcriptional addiction or aberrant CDK signaling are particularly sensitive to Cdk7 inhibition, making it an attractive therapeutic target. Selective Cdk7 inhibitors are currently under investigation for their potential to suppress oncogenic transcription programs and halt tumor growth. Beyond oncology, defects in Cdk7–TFIIH function contribute to disorders characterized by impaired DNA repair and transcriptional dysfunction, underscoring the kinase's importance in maintaining genomic stability and normal cellular function.
Alternate Names for CDK7
CDK7; cyclin-dependent kinase 7; CAK1; HCAK; MO15; STK1; CDKN7; p39MO15; CAK; p39 Mo15
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