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P0357

Sigma-Aldrich

Anti-p57Kip2 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-Kip2

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About This Item

MDL number:
MFCD01633561
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

200

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 57 kDa

species reactivity

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

UniProt accession no.

P49918

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

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.

Immunogen

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.

Biochem/physiol Actions

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.

Physical form

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

Preparation Note

Purified using protein A

Disclaimer

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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Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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)
p57Kip2, a glucocorticoid-induced inhibitor of cell cycle progression in HeLa cells.
Samuelsson MK, et al.
Molecular Endocrinology, 13(11), 1811-1822 (1999)
Yoel Toledano et al.
Endocrinology, 153(10), 5011-5022 (2012-08-02)
Because pregnancy and estrogens both induce pituitary lactotroph hyperplasia, we assessed the expression of pituitary cell cycle regulators in two models of murine pituitary hyperplasia. Female mice were assessed during nonpregnancy, pregnancy, day of delivery, and postpartum. We also implanted
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