anti-p27Kip1 (human), Rabbit Monoclonal (RM302)

RevMAb Biosciences

anti-p27Kip1 (human), Rabbit Monoclonal (RM302)

10

Western Blot, ImmunoHistoChemistry

Research Use Only

Monoclonal

RM302

CDKN1B

cyclin dependent kinase inhibitor 1B

CDKN4; cyclin-dependent kinase inhibitor 1B; cyclin-dependent kinase inhibitor 1B (p27, Kip1); KIP1; MEN1B; MEN4; P27KIP1

Rabbit

IgG

Cyclin-dependent kinase inhibitor 1B

p27Kip1 (p27) is a member of the universal cyclin-dependent kinase inhibitor (CDKI) family. p27Kip1 binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. Degradation of p27Kip1 is triggered by CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes that are required for the cellular transition from quiescence to the proliferative state. p27Kip1 expression is regulated by cell contact inhibition and by specific growth factors, such as transforming growth factor (TGF)-beta. In addition to its role as a CDKI, p27Kip1 is a putative tumor suppressor gene, regulator of drug resistance in solid tumors, and promoter of apoptosis; acts as a safeguard against inflammatory injury; and has a role in cell differentiation. The level of p27Kip1 protein expression decreases during tumor development and progression in some epithelial, lymphoid, and endocrine tissues. This decrease occurs mainly at the post-translational level with protein degradation by the ubiquitin-proteasome pathway. A large number of studies have characterized p27Kip1 as an independent prognostic factor in various human cancers, including breast, colon and prostate adenocarcinomas. - Recombinant Antibody. This antibody reacts to human p27Kip1 (Cyclin-dependent kinase inhibitor 1B). It may also react to mouse p27Kip1, as predicted by immunogen homology. Applications: WB, IHC. Source: Rabbit. Liquid. 50% Glycerol/PBS with 1% BSA and 0.09% sodium azide. p27Kip1 (p27) is a member of the universal cyclin-dependent kinase inhibitor (CDKI) family. p27Kip1 binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. Degradation of p27Kip1 is triggered by CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes that are required for the cellular transition from quiescence to the proliferative state. p27Kip1 expression is regulated by cell contact inhibition and by specific growth factors, such as transforming growth factor (TGF)-beta. In addition to its role as a CDKI, p27Kip1 is a putative tumor suppressor gene, regulator of drug resistance in solid tumors, and promoter of apoptosis; acts as a safeguard against inflammatory injury; and has a role in cell differentiation. The level of p27Kip1 protein expression decreases during tumor development and progression in some epithelial, lymphoid, and endocrine tissues. This decrease occurs mainly at the post-translational level with protein degradation by the ubiquitin-proteasome pathway. A large number of studies have characterized p27Kip1 as an independent prognostic factor in various human cancers, including breast, colon and prostate adenocarcinomas.

-20°C

12352203