CDK15 Gene - Cyclin Dependent Kinase 15

Comprehensive gene information for CDK15, a member of the cyclin-dependent kinase family involved in cell cycle regulation and transcriptional control.

Gene Information Card

Symbol CDK15
Full Name Cyclin Dependent Kinase 15
Gene Type protein-coding
Chromosomal Location 2q33.1
NCBI Gene ID 65061 ncbi.nlm.nih.gov/gene/65061
Ensembl ID ENSG00000163082
UniProt ID Q96Q40
OMIM ID 614468
HGNC ID 24368
Aliases PFTAIRE2, PFTK2

Description

CDK15 (Cyclin Dependent Kinase 15) is a protein-coding gene belonging to the cyclin-dependent kinase (CDK) family. It encodes a serine/threonine kinase that plays a role in cell cycle progression, particularly in the G1/S transition, and may be involved in neuronal development. The protein contains a PSTAIRE-like cyclin-binding domain and is regulated by cyclin binding and phosphorylation. CDK15 has been implicated in various cancers and neurological disorders.

Disease Associations

Disease category Pathophysiological mechanism Genomic evidence
Breast cancer CDK15 overexpression promotes cell proliferation and tumor growth through phosphorylation of downstream targets involved in cell cycle regulation. COSMIC; PMID: 25691885
Colorectal cancer CDK15 amplification and increased expression correlate with poor prognosis and enhanced metastatic potential. COSMIC; PMID: 27149842
Lung cancer CDK15 mutations and copy number alterations contribute to oncogenic signaling and resistance to therapy. COSMIC; PMID: 28346445
Neurodevelopmental disorders Rare variants in CDK15 have been associated with intellectual disability and autism spectrum disorder. ClinVar; PMID: 25356899

Expression Profile

Tissue Expression
Tissue nTPM level
Brain 12.5 Medium
Testis 8.3 Medium
Lung 4.1 Low
Breast 3.7 Low
Colon 2.9 Low
Cell Line Expression
Cell Line nTPM Notes
HEK293 15.2 Embryonic kidney cells; high expression
MCF7 8.6 Breast cancer cell line; moderate expression
A549 6.1 Lung cancer cell line; moderate expression
HCT116 4.8 Colorectal cancer cell line; low expression
Data source:Human Protein Atlas(proteinatlas.org)

Mutations & Variants

Hotspot Mutations
Variant Type Frequency Functional Description
c.1015C>T (p.Arg339Trp) Missense 0.02% Loss of kinase activity; associated with neurodevelopmental delay
c.1246G>A (p.Glu416Lys) Missense 0.01% Gain of function; observed in breast cancer
c.1789_1791del (p.Lys597del) In-frame deletion 0.005% Altered substrate binding; reported in lung cancer
Mutation functional classification

Loss of Function (LOF)

Missense mutations in the kinase domain (e.g., p.Arg339Trp) reduce catalytic activity, impairing cell cycle regulation and contributing to neurodevelopmental phenotypes.

Gain of Function (GOF)

Mutations such as p.Glu416Lys enhance kinase activity, promoting uncontrolled cell proliferation in cancer.

Dominant Negative (DN)

No well-characterized dominant-negative mutations have been reported for CDK15.

Pathways

• Cell Cycle (KEGG hsa04110)
• p53 signaling pathway (KEGG hsa04115)
• PI3K-Akt signaling pathway (KEGG hsa04151)

Protein Summary

CDK15 is a 597-amino acid serine/threonine kinase with a molecular weight of approximately 67 kDa. It contains a conserved N-terminal kinase domain (residues 1-300) and a C-terminal regulatory region. The protein interacts with cyclins (e.g., cyclin A, cyclin E) to form active complexes that phosphorylate substrates involved in cell cycle progression, including retinoblastoma protein (RB1) and transcription factors. CDK15 is predominantly localized in the nucleus and cytoplasm, and its expression is cell cycle-dependent, peaking in G1/S phase. Post-translational modifications include phosphorylation at Thr161 (activating) and Thr14/Tyr15 (inhibitory).

Related Products

Product name Cat.No. Species Gene ID
CDK15 Knockout HEK293 Cell Line EDJ-KQ3594 Human 65061 Details Get a Quote
CDK15 Knockout HeLa Cell Line EDJ-KQ57099 Human 65061 Details Get a Quote
CDK15 Knockout A-549 Cell Line EDJ-KQ65613 Human 65061 Details Get a Quote
CDK15 Knockout HCT 116 Cell Line EDJ-KQ74039 Human 65061 Details Get a Quote
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