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SAB4500071

Sigma-Aldrich

Anti-p57 KIP2 antibody produced in rabbit

affinity isolated antibody

Sinónimos:

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

origen biológico

rabbit

conjugado

unconjugated

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

formulario

buffered aqueous solution

mol peso

antigen 32 kDa

reactividad de especies

mouse, human

concentración

~1 mg/mL

técnicas

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

Nº de acceso NCBI

P49918

Nº de acceso UniProt

P49918

Condiciones de envío

wet ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... CDKN1C(1028)

Descripción general

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.

Inmunógeno

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

Immunogen Range: 267-316

Aplicación

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

Acciones bioquímicas o 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 y beneficios

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.

Cláusula de descargo de responsabilidad

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 clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

nwg

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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p57Kip2, a glucocorticoid-induced inhibitor of cell cycle progression in HeLa cells.
Samuelsson MK, et al.
Molecular Endocrinology, 13(11), 1811-1822 (1999)
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)
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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