Cyclin-dependent kinase 4 inhibitor C is an enzyme that in humans is encoded by the CDKN2Cgene.[5][6][7]
Function
The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. This protein has been shown to interact with CDK4 or CDK6, and prevent the activation of the CDK kinases, thus function as a cell growth regulator that controls cell cycle G1 progression. Ectopic expression of this gene was shown to suppress the growth of human cells in a manner that appears to correlate with the presence of a wild-type RB1 function. Studies in the knockout mice suggested the roles of this gene in regulating spermatogenesis, as well as in suppressing tumorigenesis. Two alternatively spliced transcript variants of this gene, which encode an identical protein, have been reported.[7]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
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Li J, Byeon IJ, Ericson K, Poi MJ, O'Maille P, Selby T, Tsai MD (1999). "Tumor suppressor INK4: determination of the solution structure of p18INK4C and demonstration of the functional significance of loops in p18INK4C and p16INK4A". Biochemistry. 38 (10): 2930–40. CiteSeerX10.1.1.386.342. doi:10.1021/bi982286e. PMID10074345.
Schreiber M, Muller WJ, Singh G, Graham FL (1999). "Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity". Oncogene. 18 (9): 1663–76. doi:10.1038/sj.onc.1202466. PMID10208428.
Korshunov A, Golanov A (2002). "Immunohistochemical analysis of p18INK4C and p14ARF protein expression in 117 oligodendrogliomas: correlation with tumor grade and clinical outcome". Arch. Pathol. Lab. Med. 126 (1): 42–8. doi:10.1043/0003-9985(2002)126<0042:IAOPAP>2.0.CO;2 (inactive 2020-06-05). PMID11800646.{{cite journal}}: CS1 maint: DOI inactive as of June 2020 (link)
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