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Data show that knockdown of thymidylate synthase (TS) significantly impairs TH17 and TH1 (show HAND1 Proteins) cell differentiation.
Possible interaction routes between hydrophobic residues of the mouse thymidylate synthase protein N-terminal segment and the active site are also discussed
SHMT1 (show SHMT1 Proteins) and TYMS localization to the nucleus is essential to prevent uracil accumulation in DNA
Synergistic activation of the TATA-less thymidylate synthase promoter by the Ets transcription factor (show ELF2 Proteins) GABP and Sp1 (show SP1 Proteins).
downregulation of expression results in block of cell cycle expression when influenced by Fe65 (show APBB1 Proteins)
posttranslationally-modified thymidylate synthase is associated with cell resistance to 5-fluoro-dUrd
This study finds that measurement of tumor levels of thymidylate synthase is not helpful in assigning specific adjuvant treatment for colorectal cancer. It also highlights the importance of using prospective analyses within treatment clinical trials as the optimal method of determining biomarker utility.
Study shows that the TYMS TSER 3R allele increases the risk of thymic lymphoid hyperplasia in AChR+ Myasthenia Gravis (MG) patients and that the 3R allele in the promoter enhancer region results in increased protein production required for the synthesis of DNA precursors.
polymorphisms of TS 5'-UTR 2R (double repeats)/3R (triple repeats) of a 28-bp sequence (11 articles) and 3'-UTR del6/ins6 (seven articles) were not significantly associated with increased risk of gastric cancer.
There was significantly higher thymidylate synthase (TS) expression in non-small cell lung cancer (NSCLC) tumor tissue comparing to normal lung tissue.
Crystal structure of the active form of native human thymidylate synthase in the absence of bound substrates has been reported.
The Thymidylate synthase (TS)-ZEB1 association was confirmed in clinical specimens from lung tumours and in a genetic mouse model of pancreatic cancer with ZEB1 deletion. Interestingly, TS itself appeared to have a regulatory role in epithelial-to-mesenchymal in cancer cells, as TS knockdown could directly reduce the EMT (show ITK Proteins) phenotype, the migratory ability of cells, the expression of stem-like markers, and chemoresistance.
Study of genetic risk of prevalent hrHPV infections in Nigerian women found significant associations with SNPs on ribosomal protein gene S19 (RPS19 (show RPS19 Proteins)) and Thymidylate Synthase gene (TYMS), in an allelic model. This risk remained significant, after adjusting for age, body mass index, smoking, age at menarche, age at sexual debut, lifetime total number of sexual partners and the total number of pregnancies.
High thymidylate synthetase expression is associated with chemoresistance in glioblastoma multiforme.
A PCR technique was used for genotyping TYMS-TSER.
Data suggest that TYMS exhibits a ligand-binding site in dimer interface, suggesting that cavity in dimer interface serves as an allosteric site to regulate conformational switching between active and inactive states of the enzyme.
Thymidylate synthase catalyzes the methylation of deoxyuridylate to deoxythymidylate using 5,10-methylenetetrahydrofolate (methylene-THF) as a cofactor. This function maintains the dTMP (thymidine-5-prime monophosphate) pool critical for DNA replication and repair. The enzyme has been of interest as a target for cancer chemotherapeutic agents. It is considered to be the primary site of action for 5-fluorouracil, 5-fluoro-2-prime-deoxyuridine, and some folate analogs. Expression of this gene and that of a naturally occuring antisense transcript rTSalpha (GeneID:55556) vary inversely when cell-growth progresses from late-log to plateau phase.
, thymidylate synthase
, thymidylate synthetase
, thymidylate synthase-like