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Key Documents

SAB4500071

Sigma-Aldrich

Anti-p57 KIP2 antibody produced in rabbit

affinity isolated antibody

Synonym(s):

CDKN1C, CDN1C, CDNC, Cyclin-dependent kinase inhibitor 1C, Cyclin-dependent kinase inhibitor p57

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 32 kDa

species reactivity

mouse, human

concentration

~1 mg/mL

technique(s)

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

NCBI accession no.

P49918

UniProt accession no.

P49918

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CDKN1C(1028)

General description

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.

Immunogen

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

Immunogen Range: 267-316

Application

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

Biochem/physiol Actions

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.

Features and Benefits

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.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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

WGK

nwg

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