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P0357

Sigma-Aldrich

Anti-p57Kip2 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonyme(s) :

Anti-Kip2

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200 μG
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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

954,00 $


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Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 57 kDa

Espèces réactives

human, mouse (predicted), bovine

Technique(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

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

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

Description générale

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.

Immunogène

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

Application

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

Actions biochimiques/physiologiques

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.

Forme physique

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

Notes préparatoires

Purified using protein A

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

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

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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