Reactive species
Human;Rat;Mouse;;Bovine
Applications
WB;IHC;IF;ELISA
Antibody type
Polyclonal Antibody
Protein name
Cyclin-dependent kinase inhibitor 1B
Immunogen
The antiserum was produced against synthesized peptide derived from human p27 Kip1. AA range:149-198
Specificity
p27 Polyclonal Antibody detects endogenous levels of p27 protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB 1:500-2000, ELISA 1:10000-20000 IHC 1:50-300. IF 1:50-200
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Other name
CDKN1B; KIP1; Cyclin-dependent kinase inhibitor 1B; Cyclin-dependent kinase inhibitor p27; p27Kip1
Background
This gene encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21. The encoded protein binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state. Mutations in this gene are associated with multiple endocrine neoplasia type IV (MEN4). [provided by RefSeq, Apr 2014],
Function
disease:Defects in CDKN1B are the cause of multiple endocrine neoplasia type 4 (MEN4) [MIM:610755]. Multiple endocrine neoplasia (MEN) syndromes are inherited cancer syndromes of the thyroid. MEN4 is a MEN-like syndrome with a phenotypic overlap of both MEN1 and MEN2.,domain:A peptide sequence containing only AA 28-79 retains substantial Kip1 cyclin A/CDK2 inhibitory activity.,function:Important regulator of cell cycle progrssion. Involved in G1 arrest. Potent inhibitor of cyclin E- and cyclin A-CDK2 complexes. Positive regulator of cyclin D-dependent kinases such as CDK4. Regulated by phosphorylation and degradation events.,induction:Maximal levels in quiescence cells and early G(1). Levels decrease after mitogen stimulation as cells progress toward S-phase.,miscellaneous:Decreased levels of p27Kip1, mainly due to proteosomal degradation, are found in various epithelial tumors originati
