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P0357

Sigma-Aldrich

Anti-p57Kip2 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinônimo(s):

Anti-Kip2

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200 μG
R$ 6.714,00

R$ 6.714,00


Previsão de entrega em24 de abril de 2025



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200 μG
R$ 6.714,00

About This Item

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

R$ 6.714,00


Previsão de entrega em24 de abril de 2025


fonte biológica

rabbit

Nível de qualidade

conjugado

unconjugated

forma do anticorpo

IgG fraction of antiserum

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

Formulário

buffered aqueous solution

peso molecular

antigen 57 kDa

reatividade de espécies

human, mouse (predicted), bovine

técnica(s)

immunoprecipitation (IP): 5 μg using 0.5-1 mg of HeLa nuclear extract and a bovine brain nuclear extract
western blot: 2 μg/mL using HeLa nuclear extract and bovine brain nuclear extract

nº de adesão UniProt

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... CDKN1C(1028)
mouse ... Cdkn1c(12577)

Descrição geral

Cyclin-dependent kinase inhibitor p57 (CDKN1C) or p57KIP2 (kinase inhibitory protein) is a tumor suppressor gene. It is a 316 amino acid protein with conserved amino- and carboxy-terminal domains and sequences with proline-alanine repeats. During mouse embryogenesis, p57KIP2 transcript is highly expressed in skeletal muscles, brain, heart, lungs and eye. The gene encoding this protein is localized on human chromosome 11p15.4.

Imunogênio

synthetic peptide corresponding to amino acids 303-316 of human Kip2, conjugated to KLH.

Aplicação

Anti-p57Kip2 antibody produced in rabbit has been used in Western blotting.

Ações bioquímicas/fisiológicas

Cyclin-dependent kinase inhibitor p57 (CDKN1C) or p57KIP2 (kinase inhibitory protein) plays a vital role as a tight-binding inhibitor of several G1 cyclin/cyclin-dependent kinase (CDK) complexes. It is a negative regulator of cell proliferation. Mutation in this gene has been associated with Beckwith-Wiedemann syndrome. p57Kip2 facilitates direct inhibition of DNA replication by binding to the proliferating cell nuclear antigen.

forma física

Solution in 0.1 M Tris-glycine, pH 7.4, containing 0.15 M NaCl, and 0.05% sodium azide.

Nota de preparo

Purified using protein A

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

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Antonio Cerqueira et al.
Molecular and cellular biology, 34(8), 1452-1459 (2014-02-12)
The Cip/Kip family, namely, p21(Cip1), p27(Kip1), and p57(Kip2), are stoichiometric cyclin-dependent kinase inhibitors (CKIs). Paradoxically, they have been proposed to also act as positive regulators of Cdk4/6-cyclin D by stabilizing these heterodimers. Loss of p21(Cip1) and p27(Kip1) reduces Cdk4/6-cyclin D
Sabrina Pfurr et al.
Development (Cambridge, England), 144(21), 3917-3931 (2017-09-25)
During corticogenesis, distinct classes of neurons are born from progenitor cells located in the ventricular and subventricular zones, from where they migrate towards the pial surface to assemble into highly organized layer-specific circuits. However, the precise and coordinated transcriptional network
Sesamin, a lignan of sesame, down-regulates cyclin D1 protein expression in human tumor cells
Tomoya Yakota
Cancer Science, 98(9), 1447?1453-1447?1453 (2007)
Yuhei Yamauchi et al.
Genes to cells : devoted to molecular & cellular mechanisms, 25(6), 427-438 (2020-04-09)
All trophoblast subtypes of the placenta are derived from trophoblast stem cells (TSCs). TSCs have the capacity to self-renew, but how the proliferation of these cells is regulated in the undifferentiated state has been largely unclear. We now show that
Fetal growth patterns in Beckwith-Wiedemann syndrome.
Mussa A
Clinical Genetics, 90(1), 21-27 (2016)

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