Product Pathways - DNA Damage
DPYD (D35A8) Rabbit mAb #4654
|W||H (M) (R) (Mk) (Dg)||Endogenous||110||Rabbit IgG|
Reactivity Key: H=Human M=Mouse R=Rat Mk=Monkey Dg=Dog
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
DPYD (D35A8) Rabbit mAb detects endogenous levels of total DPYD protein. The antibody also detects a 50-60 kDa band of unknown origin by western blot.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human DPYD protein.
Dihydropyrimidine dehydrogenase (DPD, DPYD) catalyzes the initial and rate-limiting step in uracil and thymidine catabolism as well as catabolism of the chemotherapeutic drug 5-fluorouracil (5-FU) and its derivatives. DPYD deficiency, which results from mutations in the DPYD gene, causes errors in pyrimidine metabolism and potentially life-threatening side effects in cancer patients treated with 5-FU (reviewed in 1). As a result, ongoing work examines whether or how DPYD gene variation and protein expression can be used to predict 5-FU toxicity (1,2). Several genes that impart resistance to 5-FU were recently identified in human hepatocellular carcinoma (HCC). AEG-1, which is highly expressed in HCC, increases the expression of DPYD. DPYD is expressed more highly in HCC than in normal liver, and this is thought to be one mechanism of 5-FU resistance (3,4).
- Yen, J.L. and McLeod, H.L. (2007) Eur J Cancer 43, 1011-6.
- Ofverholm, A. et al. (2010) Clin Biochem 43, 331-4.
- Yoo, B.K. et al. (2009) Proc Natl Acad Sci U S A 106, 12938-43.
- Yoo, B.K. et al. (2009) J Clin Invest 119, 465-77.
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For Research Use Only. Not For Use In Diagnostic Procedures.