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.[1]
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
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
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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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