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p57/KIP2 Antibody

Rabbit Monoclonal Antibody

  • WB - p57/KIP2 Antibody AJ1574a
    A. Western blot analysis on HeLa (A) untreated (B) treated with dexamethasone using anti-p57/KIP2 RabMAb (Cat. #AJ1574a)
Product Information
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
Primary Accession P49918
Reactivity Human
Host Rabbit
Clonality Monoclonal
Clone Names EP2516
Calculated MW 32177 Da
Gene ID 1028
Other Names Cyclin-dependent kinase inhibitor 1C, Cyclin-dependent kinase inhibitor p57, p57Kip2, CDKN1C, KIP2
Target/Specificity A synthetic peptide corresponding to residue within the internal region of human p57/KIP2 was used as an immunogen.
Dilution WB~~1:1000~10000
Format 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
StorageMaintain 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.
Precautionsp57/KIP2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Synonyms KIP2
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.
Cellular Location Nucleus.
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.
Research Areas
Citations (0)

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p57/KIP2 is a potent, tight-binding inhibitor of several G1 cyclin/Cdk complexes, and its binding is cyclin dependent. Its over-expression leads to arrest of the cell in G1 phase. Human p57/KIP2 appears to have conserved the amino- and carboxy-terminal domains but has replaced the internal regions with sequences containing proline-alanine repeats. Expression patterns suggest a complex role for p57/KIP2 cell cycle control and development (1). The gene encoding p57/KIP2 is located at a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome (BWS). Nonsense mutation found in the Cdk inhibitory domain in a BWS patient rendered p57/KIP2 inactive with consequent complete loss of its role as a cell cycle inhibitor and of its nuclear localization. Additionally, the mutation in the QT domain, although completely retaining its cell cycle regulatory activity, lacked nuclear localization and was thus prevented from performing its role as an active cell cycle inhibitor. (2). Mice lacking the imprinted Cdk inhibitor p57/KIP2 have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes (3).


1. Matsuoka S, et al. Genes Dev 9(6):650-62, 1995 2. Bhuiyan ZA, et al. Hum Genet 104(3):205-10, 1999 3. Zhang P et al. Nature 387(6629):151-8, 1997

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Cat# AJ1574a
(40 western blots)
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