p27 (Kip1 p27)

Contents: p27 (C18) Blocking Peptide
Catalog Number: 66-P716
Formulation: Each vial contains 100 μg of peptide in 0.5 ml PBS with 0.1% NaN₃ and 100 μg BSA.
Storage Conditions: Store at 4°C.
DO NOT FREEZE.

Prices for This Product*
Cat. No.	Size	Price	Qty	Action
66-P716-81	50 ug	$25

*International customers: Please contact your distributor for region specific pricing.

Available Formats of This Product
Cat. No.	Format	Excite (nm)	Emit (nm)	Reported Applications
66-P716	Blocking Peptides for anti-mouse/human/rat p27 (Kip1 p27) polyclonal	N/A	N/A	WB

Questions? Please consult our answers to frequently asked questions at http://www.ebioscience.com/faq.

Description

This is a peptide mapping to the carboxy terminus of human p27. The progression through the cell cycle is regulated by cyclins and their cognate Cdks by promoting cell cycle transitions (1,2,3). This orderly progression can be inhibited by a family of proteins known as CDK inhibitors (CDIs) that bind to cyclin/Cdk complexes and halt cell division (3). p21 (also designated WAF1/Cip1) is one has been shown to inhibit the activity of each member of the cyclin/Cdk family and over expression of this protein inhibits the proliferation of mammalian cells (5). The expression of p21 is inducible by a wide range of stress stimuli and its transcription can be enhanced by p53 (6). Another member of the CDIs is p27 (also known as Kip1), which also sees up regulation in response to antimitogenic stimuli (7). The increased protein expression of p27 results in cellular arrest by binding to cyclin/Cdk complexes, like cyclin D1/Cdk4 (4,8). An additional CDI has been found to bind Cdk4 and Cdk6, p16 (INK4A), and when such complexes are formed, the progression of the cell cycle is halted (9). It has become increasingly clear that p16 is a very important tumor suppressor gene whose frequent loss occurs early in many human cancers. p16 is a major target in carcinogenesis that is rivaled in frequency only by p53 (10).

Applications Reported

For research use only, not for diagnostic or therapeutic use. This blocking peptide has been reported for use in competition studies.

References

1. Harper JW, Adami GR, Wei N, Keyomarsi K, Elledge SJ. 1993. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell 75(4):805-816.
2. Gartel AL, Serfas MS, Tyner AL. 1996. p21 - -negative regulator of the cell cycle. Proc Soc Exp Biol Med 213(2):138-149.
3. Moller MB. 2000. p27 in cell cycle control and cancer. Leuk Lymphoma 39(1-2):19-27.
4. Sgambato A, Cittadini A, Faraglia B, Weinstein IB. 2000. Multiple functions of p27(Kip1) and its alterations in tumor cells: a review. J Cell Physiol 183(1):18-27.
5. Xiong Y, Hannon GJ, Zhang H, Casso D, Kobayashi R, Beach D. 1993. p21 is a universal inhibitor of cyclin kinases. Nature 366(6456):634.
6. Gorospe M, Wang X, Holbrook NJ. 1999. Functional role of p21 during the cellular response to stress. Gene Expr 7(4-6):377-385.
7. Slingerland J, Pagano M. 2000. Regulation of the cdk inhibitor p27 and its deregulation in cancer. J Cell Physiol 183(1):10-17.
8. Toyoshima H, Hunter T. 1994. p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21. Cell 78(1):67-74.
9. Shapiro GI, Edwards CD, Rollins BJ. 2000. The physiology of p16(INK4A)-mediated G1 proliferative arrest. Cell Biochem Biophys 33(2):189-197.
10. Liggett WH Jr, Sidransky D. 1998. Role of the p16 tumor suppressor gene in cancer. J Clin Oncol 16(3):1197-1206.

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