|Application ||WB, E|
|Description||p27 KIP 1 is a cell cycle regulatory mitotic inhibitor of cdk activity. p27 KIP 1 is a candidate tumor suppressor gene, and has been proposed to function as a possible mediator of TGF beta induced G1 arrest. p27 KIP 1 is up regulated in response to antimitogenic stimuli. The increased protein expression of p27 results in cellular arrest by binding to cyclin/Cdk complexes such as cyclin D1/Cdk4. Decreased levels of p27Kip1, mainly due to proteosomal degradation, are found in various epithelial tumors originating from lung, breast, colon, ovary, esophagus, thyroid and prostate.Tissue specificity: Expressed in all tissues tested. Highest levels in skeletal muscle, lowest in liver and kidney.|
|Immunogen||Purified recombinant fragment of human CDKN1B expressed in E. Coli.|
|Formulation||Ascitic fluid containing 0.03% sodium azide.|
|Other Names||Cyclin-dependent kinase inhibitor 1B, Cyclin-dependent kinase inhibitor p27, p27Kip1, CDKN1B, KIP1|
|Dilution||WB~~1/500 - 1/2000|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||CDKN1B Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Important regulator of cell cycle progression. Inhibits the kinase activity of CDK2 bound to cyclin A, but has little inhibitory activity on CDK2 bound to SPDYA (PubMed:28666995). Involved in G1 arrest. Potent inhibitor of cyclin E- and cyclin A- CDK2 complexes. Forms a complex with cyclin type D-CDK4 complexes and is involved in the assembly, stability, and modulation of CCND1-CDK4 complex activation. Acts either as an inhibitor or an activator of cyclin type D-CDK4 complexes depending on its phosphorylation state and/or stoichometry.|
|Cellular Location||Nucleus. Cytoplasm. Endosome. Note=Nuclear and cytoplasmic in quiescent cells. AKT- or RSK- mediated phosphorylation on Thr-198, binds 14-3-3, translocates to the cytoplasm and promotes cell cycle progression. Mitogen- activated UHMK1 phosphorylation on Ser-10 also results in translocation to the cytoplasm and cell cycle progression Phosphorylation on Ser-10 facilitates nuclear export. Translocates to the nucleus on phosphorylation of Tyr-88 and Tyr-89 Colocalizes at the endosome with SNX6; this leads to lysosomal degradation (By similarity).|
|Tissue Location||Expressed in all tissues tested. Highest levels in skeletal muscle, lowest in liver and kidney|
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Provided below are standard protocols that you may find useful for product applications.
1. Exp Mol Med. 2009 Nov 30;41(11):765-71. 2. Int J Gynecol Pathol. 2010 Jan;29(1):8-18.
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