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Merck
CN

P0357

Anti-p57Kip2 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

别名:

Anti-Kip2

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UNSPSC Code:
12352203
NACRES:
NA.41
MDL number:
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产品名称

Anti-p57Kip2 antibody produced in rabbit, IgG fraction of antiserum, buffered aqueous solution

biological source

rabbit

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.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

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

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.

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.

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.

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

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存储类别

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

常规特殊物品
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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
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
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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