ArticleThe Journal of biological chemistry2011
Thr-370 is responsible for CDK11(p58) autophosphorylation, dimerization, and kinase activity.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- CDK7-CDK11 axis in spliceosome regulation and pre-mRNA splicing.Nucleic acids research · 2025Article
- CDK11 Promotes Cytokine-Induced Apoptosis in Pancreatic Beta Cells Independently of Glucose Concentration and Is Regulated by Inflammation in the NOD Mouse Model.Frontiers in immunology · 2021Article
- A cyclin-dependent kinase, CDK11/p58, represses cap-dependent translation during mitosis.Cellular and molecular life sciences : CMLS · 2020Article
- CDK11 Loss Induces Cell Cycle Dysfunction and Death of BRAF and NRAS Melanoma Cells.Pharmaceuticals (Basel, Switzerland) · 2019Article
- CAPG enhances breast cancer metastasis by competing with PRMT5 to modulate STC-1 transcription.Theranostics · 2018Article
- Identification and characterization of the BmCyclin L1-BmCDK11A/B complex in relation to cell cycle regulation.Cell cycle (Georgetown, Tex.) · 2017Article
- Androgen receptor is a potential novel prognostic marker and oncogenic target in osteosarcoma with dependence on CDK11.Scientific reports · 2017Article
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- CDK11p58 inhibits ERα-positive breast cancer invasion by targeting integrin β3 via the repression of ERα signaling.BMC cancer · 2014Article
- Androgen receptor phosphorylation: biological context and functional consequences.Endocrine-related cancer · 2014Review
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- Orphan kinases turn eccentric: a new class of cyclin Y-activated, membrane-targeted CDKs.Cell cycle (Georgetown, Tex.) · 2012Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDK11(p58), a member of the p34(cdc2)-related kinase family, is associated with cell cycle progression, tumorigenesis, and proapoptotic signaling. It is also required for the maintenance of chromosome cohesion, the maturation of centrosome, the formation of bipolar spindle, and the completion of mitosis. Here we identified that CDK11(p58) interacted with itself to form homodimers in cells, whereas D224N, the kinase-dead mutant, failed to form homodimers. CDK11(p58) was autophosphorylated, and the main functions of CDK11(p58), such as kinase activity, transactivation of nuclear receptors, and proapoptotic signal transduction, were dependent on its autophosphorylation. Furthermore, the in vitro kinase assay indicated that CDK11(p58) was autophosphorylated at Thr-370. By mutagenesis, we created CDK11(p58) T370A and CDK11(p58) T370D, which mimic the dephosphorylated and phosphorylated forms of CDK11(p58), respectively. The T370A mutant could not form dimers and be phosphorylated by the wild type CDK11(p58) and finally lost the kinase activity. Further functional research revealed that T370A failed to repress the transactivation of androgen receptor and enhance the cell apoptosis. Overall, our data indicated that Thr-370 is responsible for the autophosphorylation, dimerization, and kinase activity of CDK11(p58). Moreover, Thr-370 mutants might affect CDK11(p58)-mediated signaling pathways.
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