MGSSHHHHHH SSGLVPRGSH MKPPSSIQTS EFDSSDEEPI EDEQTPIHIS WLSLSRVNCS QFLGLCALPG CKFKDVRRNV QKDTEELKSC GIQDIFVFCT RGELSKYRVP NLLDLYQQCG IITHHHPIAD GGTPDIASCC EIMEELTTCL KNYRKTLIHC YGGLGRSCLV AACLLLYLSD TISPEQAIDS LRDLRGSGAI QTIKQYNYLH EFRDKLAAHL SSRDSQSRSV SR.
CDKN3 is primarily involved in the regulation of the cell cycle. It dephosphorylates CDK2 at the threonine-160 residue, which is essential for CDK2 activation . By doing so, CDKN3 prevents the activation of CDK2, thereby inhibiting cell cycle progression from the G1 to the S phase . This regulatory mechanism is vital for maintaining proper cell division and preventing uncontrolled cell proliferation.
CDKN3 has been implicated in various cancers, including hepatocellular carcinoma, breast cancer, and prostate cancer . The gene can be deleted, mutated, or overexpressed in these cancers, leading to dysregulation of the cell cycle and contributing to tumorigenesis . Additionally, CDKN3 has been shown to interact with other CDKs, such as CDK3 and CDC2, further highlighting its role in cell cycle control .
Recombinant human CDKN3 is used in research to study its function and role in cancer. By understanding how CDKN3 interacts with CDKs and regulates the cell cycle, researchers can develop targeted therapies for cancers where CDKN3 is dysregulated . Various antibodies and assays are available for detecting and studying CDKN3 in laboratory settings .