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Western blot analysis of recombinant purified wild-type p27 and p27 (S10A) mutants after phosphorylation in vivo by either cyclin E-Cdk2 (lanes 1 and 2) or ERK2 (lanes 3 and 4) using Rb anti-phospho-p27 (Ser10) (Cat No. 34-6300) (top), Rb anti-phospho-p27 (Thr187) (Cat. no. 71-7700) (middle), and a monoclonal antibody to p27 (bottom). Image reproduced from Rodier G, et al. EMBO J 2001.
|Tested species reactivity||Human , Mouse , Rat|
|Published species reactivity||Human , Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide encompassing the phosphorylated Ser10 residue of p27/Kip1.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|Immunofluorescence (IF)||Assay Dependent|
|Immunoprecipitation (IP)||Assay Dependent|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Western Blot (WB)||See 4 publications below|
p27Kip1 is 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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Cdk5 and its substrates, Dcx and p27kip1, regulate cytoplasmic dilation formation and nuclear elongation in migrating neurons.
34-6300 was used in western blot to elucidate the molecular mechanisms of dilation formation and nuclear elongation
|Nishimura YV,Shikanai M,Hoshino M,Ohshima T,Nabeshima Y,Mizutani K,Nagata K,Nakajima K,Kawauchi T||Development (Cambridge, England) (141:3540)||2014|
Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice.
||Uchida T,Nakamura T,Hashimoto N,Matsuda T,Kotani K,Sakaue H,Kido Y,Hayashi Y,Nakayama KI,White MF,Kasuga M||Nature medicine (11:175)||2005|
The cyclin-dependent kinase inhibitor p27Kip1 is stabilized in G(0) by Mirk/dyrk1B kinase.
||Deng X,Mercer SE,Shah S,Ewton DZ,Friedman E||The Journal of biological chemistry (279:22498)||2004|
The role of cyclin-dependent kinase inhibitor p27Kip1 in anti-HER2 antibody-induced G1 cell cycle arrest and tumor growth inhibition.
||Le XF,Claret FX,Lammayot A,Tian L,Deshpande D,LaPushin R,Tari AM,Bast RC||The Journal of biological chemistry (278:23441)||2003|
p27, CDKN4, Cdki1b, Kip1, MEN4, KIP1, P27KIP1, AA408329, p27Kip1, MEN1B, AI843786
Cyclin-dependent kinase inhibitor 1B (p27 Kip1), Cyclin-dependent kinase inhibitor 1B (p27, Kip1), cyclin-dependent kinase inhibitor 1B, cyclin-dependent kinase inhibitor p27, cyclin-dependent kinase inhibitor p27/Kip1, CDKN1B, CDN1B, Cyclin-dependent kinase inhibitor 1B, KIP1