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These findings suggest that CDK11 is involved in the regulation of AR pathway and AR can be a potential novel prognostic marker and therapeutic target for osteosarcoma treatment.
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DNA methylation exists in the CDC2L1 gene promoter region in keloid tissue fibroblasts. DNA methylation of the CDC2L1 gene promoter region dramatically inhibits the expression of CDK11p58 protein in keloid tissues.
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CDK11 has a role in human cancers [review]
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we showed high expression of CDK11 in metastatic and recurrent ovarian cancer and demonstrated that CDK11 is essential for ovarian cancer cell growth and survival in vitro and in vivo.
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CDK11 was found associated with the TREX/THOC, which recruited this kinase to DNA. Once at the viral genome, CDK11 phosphorylated serines at position 2 in the CTD of RNAPII, which increased levels of cleavage and polyadenylation factors at the HIV 3' end. In its absence, cleavage of viral transcripts was greatly attenuated.
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Real-time PCR and dual-luciferase assay showed CDK11(p58) inhibited the mRNA levels of VEGF and the promoter activity of VEGF
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Hepsin suppressed CDK11p58 internal ribosome entry site activity in prostate cancer cells by modulating UNR expression and eIF-2alpha phosphorylation.
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CDK11 and CK2 expression are individually essential for breast cancer cell survival, including TNBC.
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CDK11(p58) kinase activity appears to be involved in early events in the establishment of the centromere protection machinery.
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Data indicate that CDK11p58 is an anti-metastatic gene in ERalpha-positive breast cancer and that the regulation of integrin beta3 by CDK11p58 via the repression of ERalpha signaling may constitute part of a signaling pathway underlying breast cancer invasion.
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silencing induces cell death in osteosarcoma
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CHK2 kinase constitutively phosphorylates CDK11(p110) in a DNA damage-independent manner.
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CDK11 is critical for the growth and proliferation of liposarcoma cells.
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CDK11 signaling is essential in osteosarcoma cell growth and survival, further elucidating the regulatory mechanisms controlling the expression of CDK11 and ultimately develop a CDK11 inhibitor that may provide therapeutic benefit against osteosarcoma.
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We have identified a correlation between two exon 7 mutations of the CDC2L1 gene and keloid disease.
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Since PITSLRE/CDK11 regulates autophagy in both Drosophila and human cells, this kinase represents a novel phylogenetically conserved component of the autophagy machinery.
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These data suggest that CDK11 may play a vital role in cell cycle re-entry in Alzheimer disease neurons in an APP-dependent manner.
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CDK11(p58), which accumulates only in the vicinity of mitotic centrosomes, directly interacts with the centriole-associated protein kinase Plk4 that regulates centriole number in cells.
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Taken together, these results provide evidence for the novel role of CDK11p46 in the regulation of translation and cell apoptosis.
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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.
