Cyclin-Dependent Kinase Inhibitor 1C (p57, Kip2) (CDKN1C) antibody

Details for Product No. ABIN967507
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Antigen
Synonyms DFNB48, KIP2, USH1J, Kip2, p57, p57KIP2, cb961, p27Xic1-a, zgc:86618, BWCR, BWS, WBS, p57Kip2, AL024410, CDKI, p57(kip2)
Reactivity
Human
(136), (49), (31), (13), (4), (1)
Host
Mouse
(104), (40)
Clonality (Clone)
Monoclonal ()
Conjugate
Un-conjugated
(6), (3), (3), (2), (2), (2), (2), (2), (2), (2), (2), (1), (1), (1)
Application
Western Blotting (WB)
(76), (47), (43), (30), (25), (20), (16), (6), (2), (2), (1), (1)
Pubmed 3 references available
Quantity 0.1 mg
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Catalog No. ABIN967507
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Immunogen p57[Kip2] Recombinant Human
Clone A120-1
Isotype IgG1
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Alternative Name p57 Kip2
Background Cyclin dependent kinase inhibitors (CdkIs) inhibit progression through the cell cycle by binding to cyclins, Cdks, or cyclin-Cdk complexes. CdkIs are classified into two groups based on protein structure. p57[Kip2] belongs to a group that also includes p27[Kip1] and p21 (also known as Sdi1, Cip1, Waf1 and Pic1). Members of this group have a homologous amino-terminal Cdk inhibitory domain. Members of the second group [p16 (INK4A), p15 (INK4B), p18 (INK4C), and p19 (INK4D)] contain ankyrin repeat motifs. p57[Kip2] is a potent, tight-binding inhibitor of several G1 and S phase cyclin-Cdk complexes including cyclin E-Cdk2, cyclin D2-Cdk4, and cyclin A-Cdk2. It inhibits the mitotic cyclin B1-Cdk1 complex to a lesser extent. mRNA studies suggest that p57[Kip2] expression is tissue-specific, the highest levels have been found in embryonic and adult skeletal muscle, heart, kidney, lung, eye and brain. This is in contrast to the widespread tissue expression of p27[Kip1] and p21 mRNA. The expression of p57[Kip2] to primarily terminally differentiated cells suggests that p57[Kip2] may play a specialized role in cell cycle control. Clone A120-1 reacts with human p57[Kip2]. Recombinant human p57[Kip2] was used as immunogen.
Molecular Weight 57 kDa
Research Area Cancer, Cell Cycle
Application Notes Applications for clone A120-1 include western blot analysis (1-2 µg/ml). SJCRH30 human rhabdomyosarcoma cells are suggested as a positive control (ATCC CRL-2061).
Comment

Related Products: ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 0.5 mg/ml
Buffer Aqueous buffered solution.
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage 4 °C
Supplier Images
anti-Cyclin-Dependent Kinase Inhibitor 1C (p57, Kip2) (CDKN1C) antibody Western blot analysis of p57[Kip2]. Lane 1, SJCRH30 human rhabdomyosarcoma cell lysate was probed with anti-p57[Kip2]. In lane 2, mouse IgG1 isotype (negative) control. p57[Kip2] is identified as an ~57 kDa doublet.
anti-Cyclin-Dependent Kinase Inhibitor 1C (p57, Kip2) (CDKN1C) antibody (2) anti-Cyclin-Dependent Kinase Inhibitor 1C (p57, Kip2) (CDKN1C) antibody (Image 2)
Product cited in: Graña, Reddy: "Cell cycle control in mammalian cells: role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs)." in: Oncogene, Vol. 11, Issue 2, pp. 211-9, 1995 (PubMed).

Lee, Reynisdóttir, Massagué: "Cloning of p57KIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution." in: Genes & development, Vol. 9, Issue 6, pp. 639-49, 1995 (PubMed).

Matsuoka, Edwards, Bai et al.: "p57KIP2, a structurally distinct member of the p21CIP1 Cdk inhibitor family, is a candidate tumor suppressor gene." in: Genes & development, Vol. 9, Issue 6, pp. 650-62, 1995 (PubMed).

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