EC Number   |
General Information |
Reference |
|---|
    2.1.2.3 | physiological function |
10-formyl-7,8-dihydrofolate, not 10-formyl-5,6,7,8-tetrahydrofolate, is the predominant in vivo substrate for mammalian aminoimidazolecarboxamide ribotide transformylase, an enzyme in purine nucleotide biosynthesis de novo, which introduces C2 into the purine ring |
719415 |
| 2.1.2.3 | more |
5-amino-1-(5-phospho-D-ribosyl)imidazole-4-carboxamide is a is a potent allosteric AMPK activator |
736802 |
| 2.1.2.3 | more |
5-amino-1-(5-phospho-D-ribosyl)imidazole-4-carboxamide is a is a potent allosteric AMPK activator. Insulin receptor autophosphorylation in isolated endosomes incubated in the presence of purified enzyme ATIC |
736802 |
| 2.1.2.3 | metabolism |
aminoimidazolecarboxamide ribotide transformylase is involved in the de novo purine nucleotide biosynthesis |
719415 |
| 2.1.2.3 | metabolism |
aminoimidazolecarboxamide ribotide transformylase is involved in the de novo purine nucleotide biosynthesis. No enzyme complex that generates 10-formyl-5,6,7,8-tetrahydrofolate and immediately channels or furnishes it to AICAR transformylase is needed because the first oxidation product of 10-formyl-5,6,7,8-tetrahydrofolate is 10-formyl-7,8-dihydrofolate that is utilized by this transformylase |
719415 |
| 2.1.2.3 | physiological function |
enzyme overexpression decreases the median lifespan from 23.6 to 20.6 days compared with control nematodes under standard conditions |
757213 |
| 2.1.2.3 | malfunction |
growth deficiency phenotypes (in un-supplemented M9 minimal medium containing thymidine) are direct consequences of the gene deletions |
-, 757625 |
| 2.1.2.3 | malfunction |
inhibition of the enzyme results in depletion of purine nucleotides |
736619 |
| 2.1.2.3 | malfunction |
insulin stimulation and enzyme ATIC knockdown readily increase the level of AMP-activated protein kinase-Thr172 phosphorylation in insulin receptor complexes. Enzyme ATIC, protein-tyrosine phosphatase-like A domain-containing protein 1, and AMP-activated protein kinase knockdown affects insulin receptor internalization in HEK-293 cells |
736802 |
| 2.1.2.3 | malfunction |
insulin stimulation and enzyme ATIC knockdown readily increase the level of AMPK-Thr172 phosphorylation in insulin receptor complexes |
736802 |
