Cyclin-K is a protein that in humans is encoded by the CCNK gene. [5] [6] [7]
Cyclin-K is a protein that in humans is encoded by the CCNK gene. [5] [6] [7]
The protein encoded by this gene is a member of the transcription cyclin family. These cyclins may regulate transcription through their association with and activation of cyclin-dependent kinases (CDKs) through conformational changes. [8] [9] Activation of CDKs through their cyclin partner, creates kinase complexes that will activate target proteins through phosphorylation. Targeted proteins can then ultimately regulate decisions of a cell's progression within the cell cycle to occur. This gene product may be seen to play a dual role in both regulating CDK and RNA polymerase II (RNAP2) activities. [7] Cyclin K only uses RNA recruitment to activate transcription. [10]
Cyclin K has been shown to interact with multiple CDKs including CDK9 and latest CDK12 and CDK13. [6] [9] Roles include helping to phosphorylate C-terminal domains of subunits of RNAP2. [11] Cyclin K is most noted for its associated induction of processive elongation. [8] Also, identified with G1 and S phase cyclin activity, however functions are not deeply understood. [5] [12]
Cyclin K also interacts with HIV nef protein. [13] In the presence of overexpressed Nef protein, Cyclin k and CDK9 binding is induced, inhibiting the positive elongation factor of other CDK9 binding complexes, resulting in an inhibition of specific HIV-1 gene expression. [9] [13] CDK 13 may also be characterized to interact with HIV mRNA splicing, alongside Nef, and the underexpression of Gag and Env related proteins. [12] [10]
Cyclin K is indispensable for Leukemia growth. SETD1A, is also known to bind Cyclin K through its FLOS domain. [14] The interaction is shown to be important to DNA damage response genes and for Leukemia proliferation. [10] [14]
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