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Results 1 - 7 of 7
EC Number General Information Commentary Reference
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10malfunction growth deficiency phenotypes (in un-supplemented M9 minimal medium containing thymidine) are direct consequences of the gene deletions -, 757625
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10malfunction impact of the ITGA2 gene polymorphism C807T on gastric cancer risk, overview. Increased risk of gastric cancer associated with the polymorphism is pronounced in rural subjects, but not in urban subjects 719305
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10metabolism last enzyme of the de novo purine synthesis pathway. The enzyme plays a central role in insulin signaling and the Golgi/endosomes protein network 757662
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10metabolism the 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) transformylase/inosine monophosphate (IMP) cyclohydrolase (ATIC) catalyzes final two steps of purine nucleotide de novo biosynthetic pathway. The cell proliferation activity of the enzyme is observed where it promotes proliferation and viability of NIH 3T3 and RIN-5F cells, exhibits in vitro wound healing in NIH 3T3 fibroblast cells, and rescues RIN-5F cells from the cytotoxic effects of palmitic acid and high glucose 756701
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10metabolism the enzyme AICAR-transformylase/IMP cyclohydrolase (ATIC) catalyzes the last two steps of purine de novo synthesis. High glucose up-regulates the expression and activity of the enzyme and increases the levels of reactive oxygen species and methylglyoxal-derived advanced glycation end products. Overexpression of the enzyme (atic-1) decreases the lifespan and head motility and increases neuronal damage under both standard and high glucose conditions. Inhibition of atic-1 expression, by RNAi, under high glucose is associated with increased lifespan and head motility and reduced neuronal damage, reactive oxygen species, and methylglyoxal-derived advanced glycation end product accumulation. The enzyme (atic-1) is involved in glucotoxic effects under high glucose conditions, either by blocked atic-1 expression or viainduction of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and AMP-activated kinase (AMPK) induction 757213
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10metabolism the enzyme catalyze the final step of de novo purine biosynthesis -, 758185
Show all pathways known for 3.5.4.10Display the word mapDisplay the reaction diagram Show all sequences 3.5.4.10metabolism the enzyme is involved in the folate recycling pathway -, 757625
Results 1 - 7 of 7