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Last update 08 May 2025

SOAT2

Last update 08 May 2025

Basic Info

Synonyms

ACACT2, ACAT-2, ACAT2

+ [4]

Introduction

Catalyzes the formation of fatty acid-cholesterol esters, which are less soluble in membranes than cholesterol (PubMed:11294643, PubMed:16647063). Plays a role in lipoprotein assembly and dietary cholesterol absorption (PubMed:11294643). Utilizes oleoyl-CoA ((9Z)-octadecenoyl-CoA) and linolenoyl-CoA ((9Z,12Z,15Z)-octadecatrienoyl-CoA) as substrates (PubMed:11294643). May provide cholesteryl esters for lipoprotein secretion from hepatocytes and intestinal mucosa (PubMed:11294643). Has lower enzymatic activity compared to isoform 1. Has lower enzymatic activity compared to isoform 1.

Drugs associated with SOAT2

PRD-001

Target

PCSK9 x SOAT2

Mechanism

PCSK9 inhibitors [+1]

Active Org.

PRD Therapeutics, Inc.

Originator Org.

PRD Therapeutics, Inc.

Active Indication

Homozygous familial hypercholesterolemia [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

PRD-002

Target

PCSK9 x SOAT2

Mechanism

PCSK9 inhibitors [+1]

Active Org.

PRD Therapeutics, Inc.

Originator Org.

PRD Therapeutics, Inc.

Active Indication

Homozygous familial hypercholesterolemia [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

PRD-003

Target

SOAT2

Mechanism

SOAT2 inhibitors

Active Org.

PRD Therapeutics, Inc.

Originator Org.

PRD Therapeutics, Inc.

Active Indication

Hyper LDL cholesterolaemia

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SOAT2

100 Translational Medicine associated with SOAT2

0 Patents (Medical) associated with SOAT2

Literatures (Medical) associated with SOAT2

01 Feb 2025·Ecotoxicology and Environmental Safety

Elucidating the mechanism of phthalates induced osteoporosis through network toxicology and molecular docking

Article

Author: Niu, Tenyao ; Mao, Pengcheng ; Zhang, Xiao ; Li, Xusheng ; Gu, Wenbo ; Yuan, Haifeng ; Zhu, Xi

OBJECTIVEThis study investigated the effects of plasticizers (phthalates) on the pathogenesis of osteoporosis (OP) and the associated molecular mechanisms, especially the interaction of plasticizers with key pathways.METHODSWe performed differential expression analysis of different datasets by machine learning to identify target genes associated with OP. And, we also investigated the binding of plasticizers to target proteins using network toxicology and molecular docking techniques.RESULTSA total of 29 genes are potential targets associated with plasticizer-induced OP. Subsequently, machine learning analysis identified six core target genes as key genes for plasticizer-induced OP. Among them, the up-regulated genes were CKM and SOAT2, and the down-regulated genes were TACR3, SGK1, ERAP2, and MMP12 (P＜0.05). Molecular docking revealed the specific binding effect between plasticizers and target proteins.CONCLUSIONThis study demonstrates that plasticizers may influence the pathogenesis of OP by targeting specific genes and pathways. And the molecular docking simulations indicate a distinct binding specificity between plasticizers and target proteins. These results provide a foundation for further investigation into the mechanisms by which plasticizers affect bone health. Future research should focus on the dose-response relationship between plasticizer exposure and the risk of OP, and explore potential intervention measures to mitigate the adverse effects of plasticizers on bone health.

01 Jan 2025·The Kaohsiung Journal of Medical Sciences

ELAVL1‐dependent SOAT2 exacerbated the pancreatitis‐like cellular injury of AR42J cells induced by hyperstimulation with caerulein

Article

Author: Chen, Hua‐Ying ; Lai, Xiao‐Qin ; Sun, Yu‐Jing

AbstractPancreatitis is a severe inflammatory condition characterized by damage to the pancreas. Sterol o‐acyltransferase 2 (SOAT2) has been reported to aggravate acute pancreatitis, however, the underlying mechanism remains to be elucidated. Rat pancreatic exocrine cells (AR42J) were treated with caerulein to induce pancreatitis‐like cellular injury. Cell viability was determined using a cell counting kit‐8 (CCK‐8) assay, while cell proliferation was analyzed through a 5‐Ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was measured using flow cytometry, and enzyme‐linked immunosorbent assays were performed to detect levels of pro‐inflammatory cytokines IL‐6 and TNF‐α. Additionally, Fe2+ levels were analyzed using a colorimetric assay kit, reactive oxygen species (ROS) levels were assessed with a Cellular ROS Assay kit, and lipid peroxidation was measured using a malondialdehyde assay kit. Glutathione levels were analyzed with a detection assay. Protein and mRNA expression were evaluated through western blotting and quantitative real‐time polymerase chain reaction, respectively. Furthermore, an RNA immunoprecipitation assay was conducted to investigate the association between ELAV‐like RNA binding protein 1 (ELAVL1) and SOAT2. Actinomycin D assay was performed to explore the effect of ELAVL1 depletion on the transcript stability of SOAT2 mRNA. SOAT2 and ELAVL1 expression were upregulated in caerulein‐exposed AR42J cells. Caerulein treatment induced pancreatitis‐like cellular apoptosis, inflammatory response, ferroptosis, and cell proliferation inhibition. Silencing of SOAT2 protected against caerulein‐induced AR42J cell injury. Moreover, ELAVL1 stabilized SOAT2 mRNA expression in AR42J cells. SOAT2 overexpression attenuated the effects induced by ELAVL1 silencing in caerulein‐exposed AR42J cells. Additionally, ELAVL1 knockdown activated the NRF2/HO‐1 pathway by downregulating SOAT2 expression in caerulein‐exposed AR42J cells. SOAT2 silencing protected AR42J cells from caerulein‐induced injury by inactivating the NRF2 pathway. In conclusion, ELAVL1‐dependent SOAT2 exacerbated pancreatic exocrine cell injury by inactivating the NRF2/HO‐1 pathway in pancreatitis. These findings provide new insights into the molecular mechanisms underlying pancreatitis and offer potential therapeutic targets for the treatment of this condition.

01 Dec 2024·The Journal of Antibiotics

Drimane sesquiterpene esters produced by Aspergillus insuetus BF-1613 as inhibitors of sterol O-acyltransferase

Article

Author: Kobayashi, Keisuke ; Nur, Elyza Aiman Azizah ; Tejima, Rio ; Tomoda, Hiroshi ; Ohshiro, Taichi ; Katada, Yosuke

A new drimane sesquiterpene ester, designated insuetusolate (1), and four reported ones (2-5) were isolated from a culture broth of Aspergillus insuetus BF-1613. The chemical structure of 1 was elucidated by extensive spectroscopic analyses, including MS and NMR. Compound 1 has a drimane-type sesquiterpene core with a 2'E,4'E,6'E-octatrienoate side chain. All these drimane sesquiterpene esters inhibited both sterol O-acyl transferase 1 (SOAT1) and 2 (SOAT2), but exhibited slightly potent inhibition against SOAT1 than SOAT2 with selectivity index (SI) [log (IC₅₀ for SOAT1/ IC₅₀ for SOAT2)] values ranging from -0.24 to -0.94.

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SOAT2

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