catalog number :
MBS440016
products full name :
p21 (C19) Antibody
products short name :
p21
other names :
p21; Cyclin-dependent kinase inhibitor 1; cyclin-dependent kinase inhibitor 1; CDK-interacting protein 1; CDK-interaction protein 1; DNA synthesis inhibitor; melanoma differentiation associated protein 6; wild-type p53-activated fragment 1; cyclin-dependent kinase inhibitor 1A (p21, Cip1); CDK-interacting protein 1; Melanoma differentiation-associated protein 6; MDA-6; p21
other gene names :
CDKN1A; CDKN1A; P21; CIP1; SDI1; WAF1; CAP20; CDKN1; MDA-6; p21CIP1; CAP20; CDKN1; CIP1; MDA6; PIC1; SDI1; WAF1; MDA-6
uniprot entry name :
CDN1A_HUMAN
reactivity :
Mouse, rat, human
specificity :
Mouse, rat, and human p21 (also designated WAF1/Cip1)
form :
200 ug/ml rabbit polyclonal IgG in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin.
concentration :
0.200 mg/ml
storage stability :
Store this product at 4 degree C, do not freeze. The product is stable for one year from the date of shipment.
tested application :
Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC)
app notes :
Western blotting starting dilution: 1:200.
other info1 :
Origin: p21 (C19) is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the carboxy terminus of human p21.
other info2 :
Immunogen: Synthetic peptide mapping to the carboxy terminus of human p21.
products description :
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).
products references :
1.)Blank M, Lerenthal Y, Mittelman L, Shiloh Y. 2006. Condensin I recruitment and uneven chromatin condensation precede mitotic cell death in response to DNA damage. J Cell Biol. Jul 17;174(2):195-206.2.) Kwak YE, Jeon NK, Kim J, and Lee EJ. 2006. The mechanism of Cell Growth Inhibition and Apoptosis by Cyclooxygenase-2 Inhibitor in Oral Squamous Carcinoma Cells. Cancer Prev Res Vol.11, No.2, 89-98.3.) Kim TH, Oh S, Kim SS. 2005. Recombinant human prothrombin kringle-2 induces bovine capillary endothelial cell cycle arrest at G0-G1 phase through inhibition of cyclin D1/CDK4 complex: modulation of reactive oxygen species generation and up-regulation of cyclin-dependent kinase inhibitors. Angiogenesis. 8(4):307-14. 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.
ncbi acc num :
AAB29246.1
ncbi mol weight :
18,119 Da
ncbi pathways :
AKT Phosphorylates Targets In The Cytosol Pathway 106475!!AMPK Signaling Pathway 198868!!Adaptive Immune System Pathway 366160!!Adipogenesis Pathway 198832!!AhR Pathway 755436!!Alpha6-Beta4 Integrin Signaling Pathway 198807!!Androgen Receptor Signaling Pathway 198806!!Angiopoietin Receptor Tie2-mediated Signaling Pathway 137917!!Bladder Cancer Pathway 83115!!Bladder Cancer Pathway 527
ncbi summary :
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Multiple alternatively spliced variants have been found for this gene. [provided by RefSeq, Nov 2010]