Ask about this productRelated genes to: MBOAT1 antibody
- Gene:
- MBOAT1 NIH gene
- Name:
- membrane bound O-acyltransferase domain containing 1
- Previous symbol:
- OACT1
- Synonyms:
- MGC44669, dJ434O11.1, LPEAT1
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-26
- Date modifiied:
- 2014-11-18
Related products to: MBOAT1 antibody
Related articles to: MBOAT1 antibody
- Allergic asthma (AA) is a heterogeneous chronic inflammatory airway disorder. In this study, we performed a retrospective bioinformatics analysis based on public transcriptome datasets to identify critical genes associated with immune cell infiltration in AA and to establish a novel predictive model. - Source: PubMed
Liu WeihuaXu ShuanglanHe Quan - Inflammatory bowel disease (IBD) is a chronic intestinal disorder characterized by excessive inflammation and intestinal damage. Known for its chronic and relapsing nature, IBD currently lacks curative pharmacological therapies. Herein, we investigated the therapeutic potential of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) in IBD and explored the underlying mechanisms. In vivo and in vitro experiments demonstrated that the administration of hucMSC-Ex significantly attenuated inflammatory levels and ameliorated associated disease symptoms in IBD models. Concurrently, hucMSC-Ex treatment effectively modulated bile acid dysregulation in the IBD condition, contributing to the restoration of intestinal metabolic homeostasis. Mechanistically, the protective effects of hucMSC-Ex were mediated through the upregulation of farnesoid X receptor (FXR) expression. FXR, a critical regulator of intestinal homeostasis, plays a pivotal role, particularly in bile acid metabolism. Elevated FXR expression further suppressed ferroptosis in macrophages, as evidenced by reduced lipid peroxidation, diminished oxidative stress, restored iron metabolism homeostasis, and normalized expression of ferroptosis-related markers (GPX4, ACSL4, MBOAT1). Collectively, our findings indicate that hucMSC-Ex alleviates IBD by activating FXR in macrophages, thereby inhibiting lipid peroxidation and reducing ferroptosis, ultimately mitigating inflammation and ameliorating intestinal damage. This offers the potential of a FXR-targeted therapeutic strategy based on exosomes for the treatment of IBD. - Source: PubMed
Publication date: 2026/04/30
Xia YuxuanSun TingZhou MengjiaoWang BoMao Fei - Melanoma accounts for over 85% of all skin cancer deaths. Current therapies including drugs targeting BRAF and MEK significantly improve the prognosis of metastatic melanoma patients, yet innate or acquired resistance challenges long-term responses. We have shown previously that fatty acid beta-oxidation (FAO) is up-regulated during the acquisition of BRAF-inhibitor (BRAFi) resistance and that the FDA approved drug ranolazine, by targeting FAO attenuates the development of acquired resistance. However, how ranolazine-induced metabolic rewiring increases cell death is unclear. Here we identify ranolazine as a ferroptosis inducer in BRAFi-resistant melanoma, in which FAO serves as a ferroptosis surveillance mechanism. Accordingly, in progressed tumours of BRAFi treated patients up-regulation of FAO regulators correlates with increased expression of ferroptosis markers. BRAFi resistant cells are heavily poised for execution of ferroptosis; they display reduced glutathione levels, higher levels of long-chain polyunsaturated fatty acid (PUFA) membrane-incorporation, and increased membrane-resident phospholipid oxidation, all of which is amplified by ranolazine. Counteracting ranolazine action is MBOAT1/2 mediated phospholipid remodelling, which initiates reduced PUFA membrane-incorporation as ferroptosis surveillance mechanism. We show that the androgen receptor (AR), which is a determinant of BRAFi resistance, controls MBOAT1/2 expression, thereby contributing to ferroptosis resistance. In BRAFi resistant tumours and cell lines, we confirm AR upregulation predominantly in the MITF/AXL undifferentiated/neural-crest like state, but it also occurs in the MITF/AXL differentiated melanocytic state. The AR antagonist enzalutamide sensitises AR expressing melanoma cells to RSL3 and erastin independent of phenotype state, but in FAO BRAFi relapsed tumours AR up-regulation correlates with the undifferentiated/neural-crest like (UD/NC) state, and enzalutamide synergises with ranolazine in ferroptosis-induction in UD/NC cells. Thus, therapeutically combining ranolazine with the AR inhibitor enzalutamide to induce ferroptosis can circumvent dedifferentiation related BRAFi resistance and could increase therapeutic activity and long-term efficacy. - Source: PubMed
Publication date: 2026/03/23
Redondo-Muñoz MartaCaballe-Mestres AdriaReisz Julie AValero-Leria AneOlias-Arjona AnaAldaz PaulaD Alessandro AngeloWellbrock ClaudiaArozarena Imanol - Emerging evidence indicates that ferroptosis characterized by lipid peroxidation is becoming a promising therapeutic strategy in glioma. However, the role of the MBOAT family, key regulators of membrane phospholipids remodeling in ferroptosis, remains unexplored in glioma. - Source: PubMed
Fan JunqiHuang QingqingBao LanxinChen XueranFang ZhiyouShu Haifeng - Heat shock factor (HSF) family proteins modulate ferroptosis in various tumors. We previously confirmed that HSF4 performs a carcinogenic role in colorectal cancer (CRC), but its function in ferroptosis remains unclear. Therefore, this study aims to reveal whether HSF4 regulates the ferroptosis process in CRC and its potential molecular mechanisms. This study found that HSF4 overexpression markedly attenuated Erastin-induced cell death and mitochondrial damage in HT29 and HCT116 cells. HSF4 effectively reduced lipid peroxidation and Fe levels in CRC cells and reversed Erastin-induced changes in ferroptosis marker, including GPX4, SLC7A11, and ACSL4. ChIP-seq combined with GEO dataset analysis identified 249 potential HSF4 target genes, among which the promoter region of the lipid metabolism-related gene MBOAT1/2 binds to HSF4 and is transcriptionally activated. In vitro experiments, MBOAT1/2 knockdown reversed the inhibitory effect of HSF4 overexpression on CRC cell death, mitochondrial damage, lipid peroxidation, Fe2 + accumulation, and changes in ferroptosis marker. In vivo experiments, MBOAT1/2 knockdown effectively reduced tumor volume and downregulated the number of Ki-67-positive cells, GPX4, and SLC7A11, while upregulating ACSL4. In conclusion, HSF4 alleviates ferroptosis in CRC cells and facilitates tumor progression by upregulating MBOAT1/2 transcription, thereby limiting lipid peroxidation and Fe accumulation. - Source: PubMed
Publication date: 2026/02/02
Yue KelinWu HaolinLi KexinYang ShuBai XuanZhang WenjingZhang Yu