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Human Monoclonal UMPS Primary Antibody for IF, ELISA - ABIN521260
Griffith, Mwenifumbo, Cheung, Paul, Pugh, Tang, Chittaranjan, Morin, Asano, Ally, Miao, Lee, Chan, Taylor, Severson, Hou, Griffith, Cheng, Novik, Moore, Luk, Owen, Brown, Morin, Gill, Tai, Marra: Novel mRNA isoforms and mutations of uridine monophosphate synthetase and 5-fluorouracil resistance in colorectal cancer. in The pharmacogenomics journal 2013
Human Monoclonal UMPS Primary Antibody for IF, ELISA - ABIN521259
Koopman, Venderbosch, van Tinteren, Ligtenberg, Nagtegaal, Van Krieken, Punt: Predictive and prognostic markers for the outcome of chemotherapy in advanced colorectal cancer, a retrospective analysis of the phase III randomised CAIRO study. in European journal of cancer (Oxford, England : 1990) 2009
Cow (Bovine) Polyclonal UMPS Primary Antibody for IHC, WB - ABIN2783243
Ishikawa, Kondo, Yamaguchi, Sakamoto, Fujisawa: Effect of varicocelectomy on patients with unobstructive azoospermia and severe oligospermia. in BJU international 2008
Show all 2 Pubmed References
the conserved uridine monophosphate phosphoribosyltransferase (UMPS), which acts in pyrimidine biosynthesis, is required for NAD(+) biosynthesis in place of the missing QPRTase
Partial UMPS-deficiency should be included in the differential diagnosis of mild orotic aciduria.
The UMPS 638 CC genotype might be a candidate biomarker predicting toxicity in patients receiving tegafur-uracil/leucovorin-based preoperative chemoradiation for locally advanced rectal cancer
OPRT transition state analogues identify crucial components of potent inhibitors targeting OPRT enzymes.
The observed mutations, aberrant splicing and downregulation of UMPS represent novel mechanisms for acquired 5-FU resistance in colorectal cancer
[review] It is confirmed that the type I defect in hereditary orotic aciduria is caused by loss of uridine monophosphate (UMP)synthase activity
OPRT expression in colorectal carcinoma tissues is not correlated with the toxicity of 5-FU, but OPRT expression in the normal tissues can help predict the toxicity associated with 5-FU.
High expression levels of orotate phosphoribosyl transferase and thymidylate synthase in colorectal cancer appear to be significantly involved in metastasis after curative surgery
Although no association was detected between UMPS variants and gastrointestinal cancer risk in Caucasians, polymerase chain reaction-RFLP with BsrI digestion and DHPLC set up at 59 degrees C are reliable and cost-effective methods to genotype UMPS.
novel phosphoribosyltransferase transition states
orotate phosphoribosyl transferase/DPD ratio has a relation to cancer staging and survival rate.
Increased orotate phosphoribosyltransferase expression is associated with bladder cancers.
expression of OPRT gene and the OPRT/dihydropyrimidine dehydrogenase ratio might be useful as predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy for metastatic colorectal cancer
thymidylate synthase and orotate phosphoribosyl transferase, but not dihydropyrimidine dehydrogenase, are more highly expressed in prostate cancer than in benign prostatic hyperplasia
orotate phosphoribosyl transferase has a role in lymph node metastasis of gastric cancer
The investigated SNPs of OPRT may have no major influence on 5-FU sensitivity.
The OPRT Gly213Ala polymorphism seems to be a useful marker for predicting toxicity to bolus 5-FU chemotherapy.
Overexpression of the OPRT gene plays an important role in the antiproliferative effect of 5-FU.
High expression of OPRT is associated with the response to adjuvant chemotherapy in human pancreatic cancer
data suggest that OPRT is involved in early events of pancreatic and gallbladder carcinogenesis and invasion of hepatocellular carcinomas
decreased the sensitivities of the cultured tumor cells to 5-FU. These results suggest that the OPRT expression level in tumors is an additional determinant of the efficacy of 5-FU.
This gene encodes a uridine 5'-monophosphate synthase. The encoded protein is a bifunctional enzyme that catalyzes the final two steps of the de novo pyrimidine biosynthetic pathway. The first reaction is carried out by the N-terminal enzyme orotate phosphoribosyltransferase which converts orotic acid to orotidine-5'-monophosphate. The terminal reaction is carried out by the C-terminal enzyme OMP decarboxylase which converts orotidine-5'-monophosphate to uridine monophosphate. Defects in this gene are the cause of hereditary orotic aciduria. Alternate splicing results in multiple transcript variants.
Uridine MonoPhosphate Synthetase family member (umps-1)
, uridine 5'-monophosphate synthase
, uridine monophosphate synthetase
, uridine monophosphate synthase
, uridine monophosphate synthetase (orotate phosphoribosyl transferase and orotidine-5'-decarboxylase)
, UMP synthase
, orotate phosphoribosyltransferase
, orotidine 5'-phosphate decarboxylase
, orotate phosphoribosyl transferase and orotidine-5'-decarboxylase