CDK7

CDK7 (Cyclin Dependent Kinase 7) is a Protein Coding gene. Diseases associated with CDK7 include Breast Cancer and Hemophagocytic Lymphohistiocytosis, Familial, 3. Among its related pathways are RNA Polymerase II Transcription Initiation And Promoter Clearance and Formation of HIV elongation complex in the absence of HIV Tat. Gene Ontology (GO) annotations related to this gene include transferase activity, transferring phosphorus-containing groups and protein tyrosine kinase activity. An important paralog of this gene is CDK20.

Cyclin Dependent Kinase 7

Serine/threonine kinase involved in cell cycle control and in RNA polymerase II-mediated RNA transcription. Cyclin-dependent kinases (CDKs) are activated by the binding to a cyclin and mediate the progression through the cell cycle. Each different complex controls a specific transition between 2 subsequent phases in the cell cycle. Required for both activation and complex formation of CDK1/cyclin-B during G2-M transition, and for activation of CDK2/cyclins during G1-S transition (but not complex formation). CDK7 is the catalytic subunit of the CDK-activating kinase (CAK) complex. Phosphorylates SPT5/SUPT5H, SF1/NR5A1, POLR2A, p53/TP53, CDK1, CDK2, CDK4, CDK6 and CDK11B/CDK11. CAK activates the cyclin-associated kinases CDK1, CDK2, CDK4 and CDK6 by threonine phosphorylation, thus regulating cell cycle progression. CAK complexed to the core-TFIIH basal transcription factor activates RNA polymerase II by serine phosphorylation of the repetitive C-terminal domain (CTD) of its large subunit (POLR2A), allowing its escape from the promoter and elongation of the transcripts. Phosphorylation of POLR2A in complex with DNA promotes transcription initiation by triggering dissociation from DNA. Its expression and activity are constant throughout the cell cycle. Upon DNA damage, triggers p53/TP53 activation by phosphorylation, but is inactivated in turn by p53/TP53; this feedback loop may lead to an arrest of the cell cycle and of the transcription, helping in cell recovery, or to apoptosis. Required for DNA-bound peptides-mediated transcription and cellular growth inhibition.

7-methylguanosine mRNA capping Source: Reactome
Cell cycle arrest Source: UniProtKB
Cell division Source: UniProtKB-KW
G1/S transition of mitotic cell cycle Source: Reactome
G2/M transition of mitotic cell cycle Source: Reactome
Nucleotide-excision repair, preincision complex assembly Source: Reactome
Phosphorylation of RNA polymerase II C-terminal domain Source: GO_Central
Positive regulation of transcription by RNA polymerase II Source: GO_Central
Protein phosphorylation Source: GO_Central
Protein stabilization Source: CAFA
Regulation of cyclin-dependent protein serine/threonine kinase activity Source: ProtInc
snRNA transcription by RNA polymerase II Source: Reactome
Termination of RNA polymerase I transcription Source: Reactome
Transcription by RNA polymerase II Source: UniProtKB
Transcription-coupled nucleotide-excision repair Source: Reactome
Transcription elongation from RNA polymerase II promoter Source: Reactome
Transcription initiation from RNA polymerase II promoter Source: ARUK-UCL
Transcription initiation from RNA polymerase I promoter Source: Reactome

Nucleus; Cytoplasm; Perinuclear region. Colocalizes with PRKCI in the cytoplasm and nucleus. Translocates from the nucleus to cytoplasm and perinuclear region in response to DNA-bound peptides.

Phosphorylation of Ser-164 during mitosis inactivates the enzyme. Phosphorylation of Thr-170 is required for activity. Phosphorylated at Ser-164 and Thr-170 by CDK2.