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P0357

Sigma-Aldrich

Anti-p57Kip2 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinonimo/i:

Anti-Kip2

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200 μG
CHF 685.00

CHF 685.00


Spedizione prevista il24 aprile 2025



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Cambia visualizzazione
200 μG
CHF 685.00

About This Item

Numero MDL:
Codice UNSPSC:
12352203
NACRES:
NA.41

CHF 685.00


Spedizione prevista il24 aprile 2025


Origine biologica

rabbit

Livello qualitativo

Coniugato

unconjugated

Forma dell’anticorpo

IgG fraction of antiserum

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Stato

buffered aqueous solution

PM

antigen 57 kDa

Reattività contro le specie

human, mouse (predicted), bovine

tecniche

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

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

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

Descrizione generale

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.

Immunogeno

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

Applicazioni

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

Azioni biochim/fisiol

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.

Stato fisico

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

Nota sulla preparazione

Purified using protein A

Esclusione di responsabilità

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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Codice della classe di stoccaggio

10 - Combustible liquids

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°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
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)
Fetal growth patterns in Beckwith-Wiedemann syndrome.
Mussa A
Clinical Genetics, 90(1), 21-27 (2016)
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
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

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