Soat2 sterol O-acyltransferase 2 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Soat2provided by MGI
Official Full Name: sterol O-acyltransferase 2provided by MGI
Primary source: MGI:MGI:1332226
See related: Ensembl:ENSMUSG00000023045 AllianceGenome:MGI:1332226
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: ACAT2; D15Wsu97e
Summary: Enables sterol O-acyltransferase activity. Acts upstream of or within cholesterol metabolic process and cholesterol storage. Located in membrane. Human ortholog(s) of this gene implicated in coronary artery disease and hepatocellular carcinoma. Orthologous to human SOAT2 (sterol O-acyltransferase 2). [provided by Alliance of Genome Resources, Nov 2024]
Expression: Biased expression in duodenum adult (RPKM 116.4), small intestine adult (RPKM 111.2) and 6 other tissues See more
Orthologs: human all
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Genomic context

Location:: 15 F2; 15 57.33 cM

Exon count:: 15

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	15	NC_000081.7 (102058853..102071871)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	15	NC_000081.6 (102150415..102163469)

Chromosome 15 - NC_000081.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Soat2 ties cholesterol metabolism to beta-oxidation and glucose tolerance in male mice.
Title: Soat2 ties cholesterol metabolism to β-oxidation and glucose tolerance in male mice.
Delineation of metabolic responses of Npc1(-/-nih) mice lacking the cholesterol-esterifying enzyme SOAT2 to acute treatment with 2-hydroxypropyl-beta-cyclodextrin.
Title: Delineation of metabolic responses of Npc1(-/-nih) mice lacking the cholesterol-esterifying enzyme SOAT2 to acute treatment with 2-hydroxypropyl-β-cyclodextrin.
The study found that Soat2-/- mice fed high-fat, low-cholesterol diet to have less hepatic steatosis, decreased expression of genes involved in de novo lipogenesis and lower hepatic GLUT2.
Title: Genetic depletion of Soat2 diminishes hepatic steatosis via genes regulating de novo lipogenesis and by GLUT2 protein in female mice.
SOAT2 knockout in NPC1-deficient mice decreases hepatic cholesterol accumulation and improves liver function.
Title: Niemann-Pick C1-deficient mice lacking sterol O-acyltransferase 2 have less hepatic cholesterol entrapment and improved liver function.
ACAT2 provides core CE of newly secreted VLDL, whereas LCAT adds CE during LDL particle formation
Title: ACAT2 contributes cholesteryl esters to newly secreted VLDL, whereas LCAT adds cholesteryl ester to LDL in mice.
ABCA1, especially in the absence of ACAT2, can have a significant effect on cholesterol absorption, although ACAT2 has a more substantial role in this process than ABCA1
Title: Intestinal cholesterol absorption is substantially reduced in mice deficient in both ABCA1 and ACAT2.
depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss
Title: Targeted depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss.
Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization.
Title: Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 (ACAT2) prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization.
Pyripyropene ACAT2-selective inhibition in the intestine and the liver can be effective against atherosclerosis.
Title: Pyripyropene A, an acyl-coenzyme A:cholesterol acyltransferase 2-selective inhibitor, attenuates hypercholesterolemia and atherosclerosis in murine models of hyperlipidemia.
inhibition of intestinal or hepatic ACAT2 improves atherogenic hyperlipidemia and limits hepatic cholesteryl ester accumulation
Title: Tissue-specific knockouts of ACAT2 reveal that intestinal depletion is sufficient to prevent diet-induced cholesterol accumulation in the liver and blood.

Submit: New GeneRIF Correction See all GeneRIFs (24)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Endonuclease-mediated (4)
Gene trapped (1)
Targeted (7) 1 citation

General gene information

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Markers

RH131180 (e-PCR)
- UniSTS:214463

RH125926 (e-PCR)
- UniSTS:142033

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables cholesterol O-acyltransferase activity	IBA Inferred from Biological aspect of Ancestor more info
enables cholesterol O-acyltransferase activity	IEA Inferred from Electronic Annotation more info
enables cholesterol O-acyltransferase activity	ISO Inferred from Sequence Orthology more info
enables cholesterol binding	IBA Inferred from Biological aspect of Ancestor more info
enables cholesterol binding	IEA Inferred from Electronic Annotation more info
enables cholesterol binding	ISO Inferred from Sequence Orthology more info
enables fatty-acyl-CoA binding	IBA Inferred from Biological aspect of Ancestor more info
enables fatty-acyl-CoA binding	IEA Inferred from Electronic Annotation more info
enables fatty-acyl-CoA binding	ISO Inferred from Sequence Orthology more info
enables sterol O-acyltransferase activity	IDA Inferred from Direct Assay more info	PubMed
enables sterol O-acyltransferase activity	ISO Inferred from Sequence Orthology more info

Process	Evidence Code	Pubs
involved_in cholesterol efflux	IBA Inferred from Biological aspect of Ancestor more info
involved_in cholesterol efflux	IEA Inferred from Electronic Annotation more info
involved_in cholesterol efflux	ISO Inferred from Sequence Orthology more info
involved_in cholesterol homeostasis	IEA Inferred from Electronic Annotation more info
involved_in cholesterol metabolic process	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within cholesterol metabolic process	IDA Inferred from Direct Assay more info	PubMed
involved_in cholesterol metabolic process	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within cholesterol storage	IGI Inferred from Genetic Interaction more info	PubMed
involved_in very-low-density lipoprotein particle assembly	IEA Inferred from Electronic Annotation more info
involved_in very-low-density lipoprotein particle assembly	ISO Inferred from Sequence Orthology more info

Component	Evidence Code	Pubs
located_in brush border	IEA Inferred from Electronic Annotation more info
located_in brush border	ISO Inferred from Sequence Orthology more info
located_in endoplasmic reticulum	ISO Inferred from Sequence Orthology more info
is_active_in endoplasmic reticulum membrane	IBA Inferred from Biological aspect of Ancestor more info
located_in endoplasmic reticulum membrane	IEA Inferred from Electronic Annotation more info
located_in endoplasmic reticulum membrane	ISO Inferred from Sequence Orthology more info
located_in membrane	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: sterol O-acyltransferase 2

Names: ACAT-2; acyl-CoA:cholesterol acyltransferase; acyl-coenzyme A:cholesterol acyltransferase 2; cholesterol acyltransferase 2

NP_666176.1

EC 2.3.1.26

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.