|Application ||IHC, IF, FC|
|Other Accession||1028, 106070|
|Isotype||Mouse / IgG2b, kappa|
|Other Names||Cyclin-dependent kinase inhibitor 1C, Cyclin-dependent kinase inhibitor p57, p57Kip2, CDKN1C, KIP2|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||p57Kip2 (Mitotic Inhibitor/Suppressor Protein) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Potent tight-binding inhibitor of several G1 cyclin/CDK complexes (cyclin E-CDK2, cyclin D2-CDK4, and cyclin A-CDK2) and, to lesser extent, of the mitotic cyclin B-CDC2. Negative regulator of cell proliferation. May play a role in maintenance of the non- proliferative state throughout life.|
|Tissue Location||Expressed in the heart, brain, lung, skeletal muscle, kidney, pancreas and testis. Expressed in the eye. High levels are seen in the placenta while low levels are seen in the liver.|
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Recognizes a protein of 57kDa, identified as p57Kip2. It shows no cross-reaction with p27Kip1. p57Kip2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. Anti-p57 has been used as an aide in identification of complete hydatidiform mole (CHM) (no nuclear labeling of cytotrophoblasts and stromal cells) from partial hydatidiform mole (PHM) in which both cytotrophoblasts and stromal cells stain. The histological differentiation of complete mole, partial mole, and hydropic spontaneous abortion is problematic. Most complete hydatidiform moles are diploid, whereas most partial moles are triploid. Ploidy studies will identify partial moles, but will not differentiate complete moles from non-molar gestations. Complete moles carry a high risk of persistent disease and choriocarcinoma, while partial moles have a very low risk. In normal placenta, many cytotrophoblast nuclei and stromal cells are labeled with this antibody. Similar findings apply to PHM and hydropic abortus tissues. Intervillous trophoblastic islands (IVTIs) demonstrate nuclear labeling in all three entities and serve as an internal control.
Lee, M.-H., et al. 1995. Cloning of p57, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev. 9: 639-649. |
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