Cyclin-Dependent Kinase Inhibitor 1C (p57, Kip2) (CDKN1C) antibody

Details for Product No. ABIN650194
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Antigen
Synonyms BWCR, BWS, KIP2, WBS, p57, p57Kip2, AL024410, CDKI, Kip2, p57(kip2), p57KIP2, cb961, p27Xic1-a, zgc:86618
Reactivity
Human
(119), (47), (32), (13), (3), (1)
Host
Rabbit
(83), (43)
Clonality
Monoclonal
Conjugate
Un-conjugated
(5), (2), (2), (2), (2), (2), (2), (2), (2), (2), (2)
Application
Western Blotting (WB)
(60), (40), (39), (25), (22), (20), (12), (3), (3), (1), (1)
Pubmed 3 references available
Catalog no. ABIN650194
Quantity 100 µL
Price
392.86 $   Plus shipping costs $45.00
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  • +1 404 474 4654
  • +1 888 205 9894 (TF)
Immunogen A synthetic peptide corresponding to residue within the internal region of human p57/KIP2 was used as an immunogen.
Specificity A synthetic peptide corresponding to residue within the internal region of human p57/KIP2 was used as an immunogen.
Alternative Name p57/KIP2
Background 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).
Molecular Weight 57 kDA
Gene ID 9636
UniProt P49918
Research Area Phospho-specific antibodies, Protein Modifications, Cancer, Cell Structure
Application Notes The suggested dilution is: WB: = 1:1000-10000
Comment

Background: 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).

Restrictions For Research Use only
Format Liquid
Buffer 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage -20 °C
Storage Comment p57/KIP2 Antibody can be stored at -20°C for up to 12 months from time of receipt.
Expiry Date 12 months
Background publications Matsuoka, Edwards, Bai et al.: "p57KIP2, a structurally distinct member of the p21CIP1 Cdk inhibitor family, is a candidate tumor suppressor gene." in: Genes & development, Vol. 9, Issue 6, pp. 650-62, 1995 (PubMed).

Zhang, Liégeois, Wong et al.: "Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith-Wiedemann syndrome." in: Nature, Vol. 387, Issue 6629, pp. 151-8, 1997 (PubMed).

Bhuiyan, Yatsuki, Sasaguri et al.: "Functional analysis of the p57KIP2 gene mutation in Beckwith-Wiedemann syndrome." in: Human genetics, Vol. 104, Issue 3, pp. 205-10, 1999 (PubMed).

Hosts (83), (43)
Reactivities (119), (47), (32), (13), (3), (1)
Applications (60), (40), (39), (25), (22), (20), (12), (3), (3), (1), (1)
Conjugates (5), (2), (2), (2), (2), (2), (2), (2), (2), (2), (2)
Epitopes (19), (17), (7), (2), (1), (1), (1), (1), (1)
Request Want additional data for this product?

The Independent Validation Initiative strives to provide you with high quality data. Find out more

Order hotline:

  • +1 404 474 4654
  • +1 888 205 9894 (TF)
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