Ask about this productRelated genes to: ETFA Blocking Peptide
- Gene:
- ETFA NIH gene
- Name:
- electron transfer flavoprotein subunit alpha
- Previous symbol:
- -
- Synonyms:
- GA2, EMA, MADD
- Chromosome:
- 15q24.2-q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-04-23
Related products to: ETFA Blocking Peptide
Related articles to: ETFA Blocking Peptide
- Chronic cadmium chloride (CC) exposure is associated with diverse toxicological outcomes, yet its potential role in the pathogenesis of ankylosing spondylitis (AS) remains unclear. This study employed a network toxicology framework to computationally elucidate the potential molecular mechanisms linking CC exposure to AS. AS-associated differentially expressed genes (DEGs) were identified from the GSE73754 dataset. Potential CC toxicity targets were retrieved from the Comparative Toxicogenomics Database (CTD). Overlapping genes were subjected to functional enrichment analysis, protein-protein interaction (PPI) network construction, and identification of core targets using multiple machine learning algorithms (LASSO, SVM, random forest, and XGBoost). A predictive nomogram was developed. Pathway activity dysregulation was assessed via Gene Set Variation Analysis (GSVA), and immune cell infiltration patterns were evaluated using the MCPcounter method. Additionally, two-sample Mendelian randomization (MR) analysis was performed to evaluate the causal relationship between the core target ETFA and AS, and in silico knockout of ETFA was conducted using single-cell RNA-seq data (GSE194315) to assess its regulatory impact. We identified 45 shared targets between putative CC toxicity and AS-associated DEGs. Enrichment analysis revealed their significant involvement in cytokine-mediated signaling, immune response, necroptosis, and the HIF-1 signaling pathway. PPI network analysis highlighted key hub proteins, including TNF, STAT3, and CXCL8. Machine learning models prioritized ZFC3H1, SCRN1, and ETFA as core toxicity-related targets, and the constructed nomogram demonstrated high predictive accuracy. In vitro validation in a HFLS chronic CC exposure model confirmed significant dysregulation of these core targets, with ZFC3H1 expression suppressed and SCRN1 and ETFA markedly upregulated. GSVA indicated a downregulation of several immune-related pathways in AS. Immune infiltration analysis showed altered abundances of cytotoxic lymphocytes, monocytes, and neutrophils. Correlation analysis linked the core targets to dysregulated pathways, particularly associating ZFC3H1 with humoral immune response and osteoclast differentiation. MR analysis indicated that ETFA is a potential risk factor for AS, with the inverse variance weighted method showing a nominally significant association. Virtual knockout of ETFA in AS single‑cell data led to substantial upregulation of immune-related genes, including S100A8, S100A9, S100A12, and multiple HLA class II genes, and enriched pathways such as antigen processing and presentation and phagosome. This study suggests that chronic CC exposure may exacerbate AS pathogenesis by perturbing immune-inflammatory pathways and altering immune cell infiltration. The core targets identified (ZFC3H1, SCRN1, ETFA) offer novel mechanistic insights into this link, with MR and knockout analyses further supporting ETFA as a causal risk factor involved in immune dysregulation, thereby highlighting the need for further experimental validation. - Source: PubMed
Publication date: 2026/05/11
Liu ZhuchenXue ZhiruiSong HanbingChen QipengZhang JingwenWang Geqiang - Multiple Acyl-CoA Dehydrogenase Deficiency (MADD) is an autosomal recessive inborn error of metabolism caused by biallelic pathogenic variants in one of three known genes: ETFA, ETFB, and ETFDH. It can cause multisystem dysfunction, including cardiomyopathy in severe cases. Ketone supplementation has been reported to be beneficial in a few case reports, but its long-term effectiveness remains unclear. We report an infant with a clinical and biochemical diagnosis of MADD who showed a favorable response to ketone supplementation, with marked improvement in severe cardiac dysfunction and sustained near-normal cardiac function and biochemical profiles over 3.5 years. Although genome sequencing did not identify causative variants, RNA sequencing revealed reduced ETFB transcript levels, and western blot analysis showed decreased ETFB protein levels. This case report illustrates MADD without an identified molecular diagnosis and provides evidence that near-absent ETFB expression is likely responsible for his presentation. These observations can guide further studies investigating the transcriptional regulation of ETFB, thereby elucidating an underappreciated molecular mechanism underlying MADD. Initiating metabolic therapy in patients with clinically suspected MADD, even in the absence of a confirmed molecular diagnosis, can be beneficial as suggested by the clinical and biochemical responses to our therapeutic trial. - Source: PubMed
Publication date: 2026/04/27
Furuta YutakaBloom Kaitlyn NVockley JerryGrochowsky Angela RAgrawal Neena SStrickler Ellen WOwen Natalie NGray Erica TPerera B Lakshitha AGamazon Eric RRives Lynette CChen Hua-ChangLiu QiHamid RizwanCogan Joy DPhillips John ACassini Thomas ASchuler Bryce A - To identify and functionally characterize the pig septin12 gene, including its expression pattern, subcellular localization, and interacting proteins, to explore its potential roles in male reproduction. - Source: PubMed
Publication date: 2026/04/02
Wang PeiWang XiaHuo HailongLi LuogangWen FeidiWang ShuyanZhang YongYunTurgong RenaguliHuo Jinlong - Integrating high-nickel cathodes with lithium metal anodes enables ultrahigh-energy-density batteries but remains challenged by electrolyte instability under extreme temperatures. Here, we design an anion-dominated loose solvation structure, where fluorine-rich weak solvents occupy coordination sites. γ-Valerolactone (GVL) serves as the primary solvent, assisted by two weakly coordinating co-solvents: difluoroethylene carbonate (DFEC) to modulate solvation and ethyl trifluoroacetate (ETFA) to reduce viscosity and freezing point. This balanced solvation environment enhances ionic transport, interfacial stability, and desolvation kinetics. Consequently, Li||NCM811 cells deliver stable cycling at 100°C, exceeding 90 cycles, negligible capacity loss at -40°C, and 90.4 mAh g at -60°C. Full cells (N/P ≈ 1.8) retain 90.3% capacity after 130 cycles. This work offers a viable solvation design for high-voltage lithium metal batteries operating across extreme temperatures. - Source: PubMed
Publication date: 2026/02/06
Zhang LeiZheng TianleMing QingZheng KeyuZhu JinXiao YiyaoAmzil SaidWu MengqiLuo ShengyaoPeng MeilanLi YinghuiZuo XiuxiaMüller-Buschbaum PeterCheng Ya-JunXia Yonggao - Pathological cardiac hypertrophy is a major contributor to heart failure and is often accompanied by ferroptosis and mitochondrial dysfunction. However, the upstream transcriptional mechanisms governing these processes remain poorly defined. We performed integrative bioinformatics analysis using transverse aortic constriction (TAC)-induced hypertrophic heart datasets to identify mitochondria-related differentially expressed genes (MitoDEGs), followed by transcription factor prediction and experimental validation in both in vivo and in vitro models. Adeno-associated virus-mediated overexpression and knockdown strategies were used to assess the regulatory effects of Irx3 and its downstream target Etfa. We identified Etfa as a hub MitoDEG directly regulated by the transcription factor Irx3, which was significantly upregulated in hypertrophic hearts. Mechanistically, Irx3 directly bound to the Etfa promoter and restored Etfa expression in hypertrophic cardiomyocytes. Through integrated transcriptomic analysis, an angiotensin II-induced cardiomyocyte hypertrophy model, and a TAC mouse model, we demonstrate that the Irx3-Etfa axis attenuates hypertrophic remodeling by suppressing ferroptosis. In vitro, overexpression of Irx3 or Etfa alleviates cardiomyocyte hypertrophy and ferroptotic injury, whereas Etfa knockdown abolishes the protective effects of Irx3. In vivo, Irx3 overexpression improves cardiac function, reduces ferroptosis, and limits structural remodeling in TAC mice. These findings reveal a novel transcriptional pathway connecting mitochondrial metabolism to ferroptosis regulation and suggest the Irx3-Etfa axis as a promising therapeutic target for pathological cardiac hypertrophy. - Source: PubMed
Li BingZhang YaotingFu YuZheng YangDou KefeiSun Wanqing