| 1994 |
PISSLRE (CDK10) encodes a CDC2-related serine/threonine protein kinase with a PSTAIRE-like motif (PISSLRE), containing all structural elements of cyclin-dependent kinases including regulatory Tyr and Thr residues, with a predicted molecular weight of ~35.8 kDa. |
PCR-based cDNA cloning and amino acid sequence analysis |
Oncogene |
Medium |
8084611 8208557
|
| 1995 |
CDK10 (PISSLRE) is essential for cell growth and acts in G2/M phase; dominant-negative and antisense constructs of PISSLRE overexpressed in U2OS cells suppress growth and halt cell cycle progression at G2-M. |
Antisense and dominant-negative mutant overexpression in U2OS cells with cell cycle analysis |
Cancer research |
Medium |
7664269
|
| 2000 |
CDK10 exists as multiple isoforms with different translation initiation sites and different subcellular distributions due to an alternatively spliced nuclear localization signal; isoform levels do not vary during the cell cycle except when cells enter the cell cycle. |
RT-PCR isoform analysis, subcellular fractionation |
Biochemical and biophysical research communications |
Medium |
11006117
|
| 2001 |
CDK10 interacts with the N-terminus (Pointed domain and transactivation domain) of the ETS2 transcription factor both in vitro and in vivo, requiring an intact Pointed domain in ETS2, and inhibits ETS2 transactivation activity in mammalian cells; CDK10 does not bind ETS1 in the same assay. |
Yeast two-hybrid, in vitro binding assay, co-immunoprecipitation in mammalian cells, transactivation reporter assay |
Oncogene |
High |
11313931
|
| 2006 |
Murine CDK10 binds ETS2 transcription factor in vitro but does not show direct involvement in G2/M transition in the mouse system and does not affect proliferation rate of analyzed cell lines. |
In vitro binding assay, cell proliferation analysis |
Journal of cellular biochemistry |
Medium |
16741970
|
| 2008 |
CDK10 silencing increases ETS2-driven transcription of c-RAF, resulting in MAPK pathway activation and loss of tumor cell reliance on estrogen signaling, thereby conferring resistance to tamoxifen in breast cancer cells. |
RNAi screen, gene silencing, reporter assays, MAPK pathway analysis |
Cancer cell |
High |
18242510
|
| 2013 |
CDK10 is activated by Cyclin M (product of FAM58A) as its cognate cyclin; the CDK10/Cyclin M complex phosphorylates ETS2 in vitro, and in cells it promotes ETS2 degradation by the proteasome; STAR syndrome-associated Cyclin M mutants cannot interact with CDK10; Cyclin M silencing phenocopies CDK10 silencing in increasing c-Raf and conferring tamoxifen resistance. |
Co-immunoprecipitation, in vitro kinase assay with recombinant proteins, proteasome inhibitor experiments, genetic complementation, cell-based ETS2 protein level measurement in STAR patient cells |
Proceedings of the National Academy of Sciences of the United States of America |
High |
24218572
|
| 2016 |
CDK10/Cyclin M phosphorylates PKN2 on threonines 121 and 124 within PKN2's RhoA-binding domain; this phosphorylation stabilizes RhoA protein and the actin network architecture, thereby suppressing primary cilia assembly and elongation; CDK10/CycM deficiency promotes ciliogenesis; ectopic RhoA expression overrides CDK10/CycM knockdown-induced ciliogenesis. |
Unbiased kinase substrate screen, in vitro kinase assay with phosphosite mapping, co-immunoprecipitation, RhoA rescue experiments, cilia length/number measurements, patient kidney tissue analysis |
Cell cycle (Georgetown, Tex.) |
High |
27104747
|
| 2017 |
CDK10 loss-of-function (knockout) in mice causes postnatal death with severe growth retardation, skeletal defects, and kidney/lung abnormalities; Cdk10-knockout MEFs develop longer cilia, consistent with CDK10 regulating ciliogenesis; CDK10 transduces signals from primary cilia to sustain embryonic and postnatal development. |
Conditional knockout mouse generation, MEF cilia length measurements, transcriptomic analysis |
American journal of human genetics |
High |
28886341
|
| 2017 |
Inactivation of CDK10 kinase domain suppresses apoptosis and promotes tumor growth; kinase-defective CDK10 mutant colorectal cancer cells show exaggerated apoptotic response and reduced proliferative capacity; CDK10 upregulates Bcl-2 expression in a kinase-activity-dependent manner. |
Kinase-defective mutant expression, apoptosis assays, in vivo xenograft model with siRNA |
Molecular cancer therapeutics |
Medium |
28663269
|
| 2020 |
An optimized peptide substrate for CDK10/CycM was identified; known CDK inhibitors including SNS-032, riviciclib, flavopiridol, dinaciclib, AZD4573, AT7519, and NVP-2 potently inhibit CDK10/CycM in vitro kinase assay. |
In vitro kinase assay with peptide substrate optimization, inhibitor profiling |
Frontiers in chemistry |
Medium |
32175313
|
| 2021 |
Recombinant CDK10/CycQ (Cyclin Q, same as CycM) complex phosphorylates RNA pol II CTD, c-MYC, and RB1 in vitro; an analogue-sensitive CDK10 mutant identifies 89 phosphosites on 66 proteins in HEK cells including targets in cell cycle, translation, stress response, growth signalling, and transcriptional regulation; CDK10 is itself phosphorylated in vitro by CDK1 and CDK5 at multiple sites. |
Recombinant protein in vitro kinase assay, analogue-sensitive kinase approach with mass spectrometry phosphoproteomics |
Open biology |
High |
35291876
|
| 2021 |
CDK10 truncated variants associated with Al Kaissi syndrome retain ability to form CDK10/CycM heterodimer; the CycM truncated variant partially activates CDK10 in vitro, while the CDK10 truncated variant remains inactive; both variants are degraded by the proteasome when expressed in human cells. |
Recombinant protein expression in insect cells, in vitro kinase assay, yeast two-hybrid, proteasome inhibitor treatment in human cells |
Molecular genetics & genomic medicine |
Medium |
34369103
|
| 2023 |
CDK10 binds ETS2 and promotes its degradation, thereby inactivating the downstream c-Raf/p-MEK/p-ERK pathway that drives EMT and MMP2/9 expression; the p-MEK/p-ERK pathway also conducts positive feedback regulation on ETS2 expression; CDK10 knockdown promotes metastatic foci formation in a xenograft mouse model. |
Co-immunoprecipitation, protein degradation assays, MAPK pathway analysis, xenograft mouse model |
Molecular carcinogenesis |
Medium |
37737453
|
| 2024 |
RNF115, an E3 ubiquitin ligase, ubiquitinates and degrades CDK10 in thyroid carcinoma cells, thereby activating the Raf-1 pathway and enhancing cancer cell cycle progression. |
Ubiquitination assay, co-immunoprecipitation, overexpression/knockdown experiments, in vivo tumor model |
Cell biology and toxicology |
Medium |
38376606
|
| 2024 |
CDK10 silencing activates the JNK/c-Jun signaling pathway in lung cancer cells, promoting proliferation, migration, and radioresistance; c-Jun depletion reverses the effects of CDK10 knockdown, placing CDK10 upstream of JNK/c-Jun in this context. |
CDK10 siRNA knockdown, pathway inhibition (c-Jun depletion), cell proliferation and radioresistance assays |
BMB reports |
Medium |
38919013
|
| 2026 |
CDK10 can partially compensate for the transcriptional function of CDK11 in RNA Polymerase II elongation regulation in metazoans. |
Functional genetic complementation experiments (context from CDK11 inhibition studies) |
bioRxivpreprint |
Low |
bio_10.1101_2025.09.27.678947
|
| 2026 |
CDK10 phosphorylates DNMT1 and RAP80, reducing accumulation of double-stranded RNA and R-loops, thereby suppressing activation of innate immune pathways mediated by MDA5 and cGAS in tumor cells; genetic and pharmacological CDK10 inhibition activates MDA5 and cGAS pathways and fosters an immunoactive tumor microenvironment. |
In vivo kinome CRISPR screen, phosphorylation assays, kinase inhibitor screens (NVP-AST487, ponatinib identified as CDK10 inhibitors), mouse tumor models |
Nature cancer |
High |
41507536
|