P0357
Anti-p57Kip2 antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
동의어(들):
Anti-Kip2
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크기 선택
제품정보 (DICE 배송 시 비용 별도)
Conjugate:
unconjugated
Clone:
polyclonal
Application:
IP, WB
Citations:
18
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)
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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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저장 등급
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
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Tomoya Yakota
Cancer Science, 98(9), 1447?1453-1447?1453 (2007)
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
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
Peter Göttle et al.
Glia, 67(1), 160-170 (2018-11-16)
Remyelination in the adult CNS depends on activation, differentiation, and functional integration of resident oligodendroglial precursor cells (OPCs) and constitutes the only spontaneous neuroregenerative process able to compensate for functional deficits upon loss of oligodendrocytes and myelin sheaths as it
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