This MAb recognizes a 21kDa protein, identified as the p21WAF1 tumor suppressor protein. This MAb is highly specific to p21 and shows no cross-reaction with other closely related mitotic inhibitors. p21WAF1 is a specific inhibitor of cdk s and a tumor suppressor involved in the pathogenesis of a variety of malignancies. The expression of this gene acts as an inhibitor of the cell cycle during G1 phase and is tightly controlled by the tumor suppressor protein p53. Its expression is induced by the wild type, but not mutant, p53 suppressor protein. Normal cells generally display a rather intense nuclear p21 expression. Loss of p21 expression has been reported in many carcinomas (gastric carcinoma, non-small cell lung carcinoma, thyroid carcinoma). In ELISA, MAb WA-1 is useful either as a solid phase or for detection of p21 protein.
Protein A or G purified
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Immunohistochemistry (Formalin-fixed): 1-2ug/ml for 30 minutes at RT. Staining of formalin-fixed tissues requires heating tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 45 min at 95C followed by cooling at RT for 20 minutes. Optimal dilution for a specific application should be determined. Use in Western blot reported in scientific literature (PMID 28137862).
21 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Alternate Names for p21/CIP1/CDKN1A Antibody (WA-1)
CAP20cyclin-dependent kinase inhibitor 1
CDK-interacting protein 1
CDKN1melanoma differentiation associated protein 6
CIP1WAF1CDK-interaction protein 1
cyclin-dependent kinase inhibitor 1A (p21, Cip1)
Melanoma differentiation-associated protein 6
SDI1DNA synthesis inhibitor
wild-type p53-activated fragment 1
p21 (WAF1), a member of the cycle dependent kinase (CDK) inhibitor family, was first identified as a tumor suppressor or anti-oncogenic protein and negative regulator of the cell cycle. Over the years it became apparent that p21 has broad functions in regulating fundamental cellular programs including proliferation, differentiation, migration, senescence, and has both anti-oncogenic and oncogenic properties (reviewed in Romanov, 2012). Many antibody and other studies have demonstrated that p21 levels are frequently elevated in situations associated with reduced proliferation, including differentiation and senescence, and decreased in proliferative states. Subcellular localization may significant and nuclear antibody staining may be indicative of p21 functioning as a cell cycle inhibitor, tumor suppressor, or in a senescence program. In contrast, cytoplasmic antibody staining may indicate p21 is acting an oncogene through regulatation of migration, proliferation, or apoptosis.
It is interesting to note that p21 expression is induced by wild type, but not mutant p53. The HJ21/WA-1 antibody clone has been used to demonstrate this phenomenon by western blot (Blaydes, 2001). The inability of mutant p53 to induce p21 essentially means that normal functions of p21 are compromised when p53 gene mutations are present. Since p53 gene mutations are present in up to 50% of human cancers, the loss of p21 function in cancer is significant.
In its normal functioning state, p21 binds to cyclin/CDK complexes. When it binds to these complexes, it inhibits their kinase activity which, in turn, stops cell cycle progression and hence p21 gains its reputation as a mitotic cell cycle inhibitor. In this regard, the antibody showed that decreased Cdk2-cyclin E1 activity corresponded with a decrease in cyclin E1 and increase in p21 protein levels (White, 2005).
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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