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Article

Tissue-specific knockouts of ACAT2 reveal that intestinal depletion is sufficient to prevent diet-induced cholesterol accumulation in the liver and blood.

Journal of lipid research - 1 Jun 2012

Zhang Jun, Kelley Kathryn L, Marshall Stephanie M, Davis Matthew A, Wilson Martha D, Sawyer Janet K, Farese Robert V, Brown J Mark, Rudel Lawrence L

Abstract excerpt

Acyl-CoA:cholesterol acyltransferase 2 (ACAT2) generates cholesterol esters (CE) for packaging into newly synthesized lipoproteins and thus is a major determinant of blood cholesterol levels. ACAT2 is expressed exclusively in the small intestine and liver, but the relative contributions of ACAT2 expression in these tissues to systemic cholesterol metabolism is unknown. We investigated whether CE derived from the...

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Share to Cholesterol Esters
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 22460046
DOI: 10.1194/jlr.M024356
PMCID: PMC3351821

Genes

ACAT2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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