Literature summary for 2.3.1.194 extracted from

Wu, D.M.; He, Z.; Chen, T.; Liu, Y.; Ma, L.P.; Ping, J.
DNA hypermethylation of acetoacetyl-CoA synthetase contributes to inhibited cholesterol supply and steroidogenesis in fetal rat adrenals under prenatal nicotine exposure (2016), Toxicology, 340, 43-52.

Search for more literature for 2.3.1.194

Application

Application	Comment	Organism
medicine	histological changes, decreased steroid hormone concentrations and decreased cholesterol supply are observed in nicotine-treated fetal adrenals. The expression of genes regulating ketone metabolic process decreases in nicotine-treated fetal adrenals. Acetoacetyl-CoA synthetase (AACS), the enzyme utilizing ketones for cholesterol supply, displays decreased expression and increased DNA methylation in the proximal promoter of AACS	Rattus norvegicus

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	Q9JMI1	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
fetus	prenatal nicotine exposure leads to decreased expression and increased DNA methylation in the proximal promoter of acetoacetyl-CoA synthetase	Rattus norvegicus	-

Synonyms

Synonyms	Comment	Organism
AACS	-	Rattus norvegicus

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)