![Purified Mouse Anti-p27[Kip1]](/content/dam/bdb/products/global/reagents/microscopy-imaging-reagents/immunofluorescence-reagents/610xxx/6102xx/610241_base/K25020_610241_image1.png)
![Purified Mouse Anti-p27[Kip1]](/content/dam/bdb/products/global/reagents/microscopy-imaging-reagents/immunofluorescence-reagents/610xxx/6102xx/610241_base/K25020_610241_image2.png)
Preparation And Storage
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
- Source of all serum proteins is from USDA inspected abattoirs located in the United States.
- 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.
Kip1 is a cyclin-dependent kinase (cdk) inhibitor that was identified as a result of its role in TGFβ-induced G1 phase arrest and cell-cell contact. In vitro , p27 [Kip1] binds tightly to Cyclin D-Cdk4, Cyclin E-Cdk2, and Cyclin A-Cdk2 complexes and inhibits their activity. In normal cells, Kip1 is sequestered and its activity gradually decreases as cells reach S phase. The addition of TGF-β in early G1 blocks this decline in activity, by preventing the sequestration of Kip1. TGF-β also reduces the levels of Cdk4. Kip1 preferentially binds Cyclin D-Cdk4, but the lower levels of Cdk4 in TGF-β treated cells allow Kip1 to be available for binding to Cyclin E-Cdk2 and Cyclin A-Cdk2. Kip1 is structurally related to Cip1/WAF1, having a similar 60 amino acid sequence in the N-terminal region. A 52 amino acid Kip1 peptide (residues 28-79) from this region is sufficient to inhibit cdk activity in vitro.
This antibody is routinely tested by western blot analysis. Other applications were tested at BD Biosciences Pharmingen during antibody development only or reported in the literature.
Development References (5)
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Barnouin K, Dubuisson ML, Child ES. H2O2 induces a transient multi-phase cell cycle arrest in mouse fibroblasts through modulating cyclin D and p21Cip1 expression. J Biol Chem. 2002; 277(16):13761-13770. (Clone-specific: Depletion, Immunofluorescence, Western blot). View Reference
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Frey MR, Clark JA, Leontieva O, Uronis JM, Black AR, Black JD. Protein kinase C signaling mediates a program of cell cycle withdrawal in the intestinal epithelium. J Cell Biol. 2000; 151(4):763-778. (Clone-specific: Immunofluorescence, Western blot). View Reference
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Polyak K, Kato JY, Solomon MJ, et al. p27Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-beta and contact inhibition to cell cycle arrest. Genes Dev. 1994; 8(1):9-22. (Biology). View Reference
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Polyak K, Lee MH, Erdjument-Bromage H, et al. Cloning of p27Kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals. Cell. 1994; 78(1):59-66. (Biology). View Reference
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Williamson EA, Dadmanesh F, Koeffler HP. BRCA1 transactivates the cyclin-dependent kinase inhibitor p27(Kip1). Oncogene. 2002; 21(20):3199-9206. (Clone-specific: Immunohistochemistry, Western blot). View Reference
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For Research Use Only. Not for use in diagnostic or therapeutic procedures.