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Key Documents

SAB4500071

Sigma-Aldrich

Anti-p57 KIP2 antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

CDKN1C, CDN1C, CDNC, Cyclin-dependent kinase inhibitor 1C, Cyclin-dependent kinase inhibitor p57

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 32 kDa

Espèces réactives

mouse, human

Concentration

~1 mg/mL

Technique(s)

ELISA: 1:1000
immunofluorescence: 1:100-1:500
western blot: 1:500-1:1000

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CDKN1C(1028)

Description générale

Cyclin-dependent kinase inhibitor p57 (CDKN1C) or p57 KIP2 (Kinase inhibitory protein) is a tumor suppressor gene mapped to telomeric end of human chromosome 11p15.5, a region associated with sporadic cancers and Beckwith-Wiedemann syndrome. Human p57KIP2 codes for a 316 amino acid protein characterized with conserved amino- and carboxy-terminal domains, and consisting of sequences with proline-alanine repeats. During mouse embryogenesis, p57 KIP2 transcript is expressed highly in skeletal muscle, brain, heart, lungs, and eye.

Immunogène

The antiserum was produced against synthesized peptide derived from human p57 Kip2.

Immunogen Range: 267-316

Application

Anti-p57 KIP2, C-Terminal antibody produced in rabbit has been used for Western blot analysis.

Actions biochimiques/physiologiques

Cyclin-dependent kinase inhibitor p57 (CDKN1C) or p57 KIP2, plays a vital role as a tight-binding inhibitor of several G1 cyclin/ cyclin-dependent kinase (CDK) complexes. The encoded protein acts as a negative regulator of cell proliferation. Mutation of this gene results in Beckwith-Wiedemann syndrome. p57Kip2 protein is involved in the glucocorticoid mediated inhibition of cell proliferation in HeLa cells. p57Kip2 also facilitates direct inhibition of DNA replication by binding to the proliferating cell nuclear antigen. p57Kip2 is a tumor suppressor protein, and helps in normal developmental process.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Forme physique

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

p57KIP2, a structurally distinct member of the p21CIP1 Cdk inhibitor family, is a candidate tumor suppressor gene.
Matsuoka S, et al.
Genes & Development, 9(6), 650-662 (1995)
An imprinted gene p57KIP2 is mutated in Beckwith-Wiedemann syndrome.
Hatada I, et al.
Nature Genetics, 14(2), 171-173 (1996)
p57Kip2, a glucocorticoid-induced inhibitor of cell cycle progression in HeLa cells.
Samuelsson MK, et al.
Molecular Endocrinology, 13(11), 1811-1822 (1999)
Matthew Van De Pette et al.
PLoS genetics, 12(3), e1005916-e1005916 (2016-03-11)
The accurate diagnosis and clinical management of the growth restriction disorder Silver Russell Syndrome (SRS) has confounded researchers and clinicians for many years due to the myriad of genetic and epigenetic alterations reported in these patients and the lack of

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