Literature summary for 3.5.4.10 extracted from

Riedinger, C.; Mendler, M.; Schlotterer, A.; Fleming, T.; Okun, J.; Hammes, H.P.; Herzig, S.; Nawroth, P.P.
High-glucose toxicity is mediated by AICAR-transformylase/IMP cyclohydrolase and mitigated by AMP-activated protein kinase in Caenorhabditis elegans (2018), J. Biol. Chem., 293, 4845-4859 .

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Organism

Organism	UniProt	Comment	Textmining
Caenorhabditis elegans	Q95QQ4	-	-

Synonyms

Synonyms	Comment	Organism
AICAR-transformylase/IMP cyclohydrolase	-	Caenorhabditis elegans
atic-1	-	Caenorhabditis elegans

Expression

Organism	Comment	Expression
Caenorhabditis elegans	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	up

General Information

General Information	Comment	Organism
metabolism	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	Caenorhabditis elegans

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Release 2023.1 (January 2023)