Literature summary for 2.3.1.26 extracted from

Toledo, J.D.; Garda, H.A.; Cabaleiro, L.V.; Cuellar, A.; Pellon-Maison, M.; Gonzalez-Baro, M.R.; Gonzalez, M.C.
Apolipoprotein A-I Helsinki promotes intracellular acyl-CoA cholesterol acyltransferase (ACAT) protein accumulation (2013), Mol. Cell. Biochem., 377, 197-205.

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Cloned(Commentary)

Cloned (Comment)	Organism
gene Soat1, quantitative real-time PCR expression analysis	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q61263	gene Soat1	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
macrophage	-	Mus musculus	-
RAW 264.7 cell	-	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
ACAT	-	Mus musculus
acyl-CoA cholesterol acyltransferase	-	Mus musculus

General Information

General Information	Comment	Organism
additional information	no significant change in the amount of ACAT1 mRNA when the cells are treated with apolipoprotein AI and its lysine deletion variants with respect to control. The treatment of murine macrophages with apolipoprotein A-I mutant DELTAK107, i.e. apoA-I Helsinki, produces an increment of more than ten folds in the ACAT1 cellular level detected by western-blotting with a specific antibody. This effect is specific for the variant with the lysine deletion at the central region, since it is not produced by the lysine deletion at the C-terminus (DELTAK226) or the wild-type apoA-I. ACAT1 protein accumulation evoked by DELTAK107 in RAW cells is independent of cholesterol-loading conditions. ACAT1 protein accumulation is not accompanied by an enhanced mRNA level, but it is due to an increased translation rate or to a decreased protein degradation rate	Mus musculus
physiological function	a key event for the transformation of macrophages in foam cells is the activation of ACAT1 leading to an increased uptake of modified low-density lipoprotein, accumulation of cholesteryl esters, and decreased cholesterol efflux to high-density lipoprotein	Mus musculus

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Release 2023.1 (January 2023)