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KIAA1524
Protein CIP2A also known as cancerous inhibitor of PP2A (CIP2A) is a protein that in humans is encoded by the ''KIAA1524'' gene.〔(【引用サイトリンク】 url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57650 )〕
== Function ==
Protein phosphatase 2A (PP2A) is a trimeric serine-threonine phosphatase consisting of a catalytic C-subunit (PP2Ac), a scaffolding A-subunit and various regulatory B-subunits. Importantly, it has been estimated that collectively PP2A complexes can dephosphorylate a vast majority of all cellular serine/threonine phosphorylated proteins including large number of phosphoproteins involved in cancer maintenance and progression. The functional role of PP2A as a human tumor suppressor was validated by studies initiated by the Weinberg laboratory, which demonstrated that normal human cells immortalized by overexpression of TERT and inhibition of p53 and Rb, could not be transformed by oncogenic forms of H-Ras without simultaneous inhibition of PP2A activity. These studies established the paradigm that increased activity of oncogenic kinases is not sufficient to drive human cell transformation if PP2A activity is not simultaneously inhibited. In striking contrast to the tumor suppressor p53, which in human tumors is mainly inactivated by mutations, PP2A complex proteins are mutated at low frequency (http://www.cbioportal.org) and rather seem to be inhibited by overexpression of PP2A inhibitor proteins such as CIP2A, PME-1 and SET.
CIP2A inhibits PP2A tumor suppressor activity in human malignancies. More specifically, CIP2A was demonstrated to inhibit PP2A activity towards oncogenic transcription factor c-Myc, and thereby prevent c-Myc proteolytic degradation. Moreover, CIP2A is required for the malignant cellular growth and for in vivo tumor formation. In accordance with the oncogenic role of CIP2A, overexpression of CIP2A promotes Ras-elicited cell growth and transforms immortalized human cells (HEK-TERVs). More recently CIP2A has been shown to regulate phosphorylation and activity of many other oncoproteins and to drive malignant cell growth and tumorigenesis in various human cancer types. Importantly, CIP2A deficient mice are viable, suggesting that targeting of oncogenic function of CIP2A would not results in serious side-effects.
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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