Cyclin K

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

Cyclin-K is a protein that in humans is encoded by the CCNK gene.[5][6][7]

Quick facts CCNK, Available structures ...
CCNK
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCCNK, CPR4, Cyclin K, IDDHDF
External IDsOMIM: 603544; MGI: 1276106; HomoloGene: 14748; GeneCards: CCNK; OMA:CCNK - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001099402
NM_003858

NM_009832

RefSeq (protein)

NP_001092872

NP_033962

Location (UCSC)Chr 14: 99.48 – 99.54 MbChr 12: 108.15 – 108.17 Mb
PubMed search[3][4]
Wikidata
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Function

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]

Interactions

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]

References

Further reading

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