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SAB4500071

Sigma-Aldrich

Anti-p57 KIP2 antibody produced in rabbit

affinity isolated antibody

Sinônimo(s):

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

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41
conjugado:
unconjugated
application:
ELISA
IF
WB
clone:
polyclonal
reatividade de espécies:
mouse, human
citations:
4
técnica(s):
ELISA: 1:1000
immunofluorescence: 1:100-1:500
western blot: 1:500-1:1000

fonte biológica

rabbit

Nível de qualidade

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

Formulário

buffered aqueous solution

peso molecular

antigen 32 kDa

reatividade de espécies

mouse, human

concentração

~1 mg/mL

técnica(s)

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

nº de adesão NCBI

nº de adesão UniProt

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... CDKN1C(1028)

Descrição geral

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.

Imunogênio

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

Immunogen Range: 267-316

Aplicação

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

Ações bioquímicas/fisiológicas

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.

Características e benefícios

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.

forma física

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

nwg

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Visite a Biblioteca de Documentos

p57Kip2, a glucocorticoid-induced inhibitor of cell cycle progression in HeLa cells.
Samuelsson MK, et al.
Molecular Endocrinology, 13(11), 1811-1822 (1999)
An imprinted gene p57KIP2 is mutated in Beckwith-Wiedemann syndrome.
Hatada I, et al.
Nature Genetics, 14(2), 171-173 (1996)
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)
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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