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
- 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 - Edwardsiellosis, caused by Edwardsiella tarda, is a highly pathogenic disease affecting both freshwater and marine fish, leading to mass mortality. This study encompassed the molecular detection, virulence and antibiogram profiling of E. tarda from Heteropneustes fossilis (stinging catfish). A total of 40 fish samples were collected from different fish farms in the Mymensingh district. Isolation of E. tarda was performed using selective media, followed by identification through morphological, cultural, and biochemical testing, and confirmed through polymerase chain reaction (PCR). Antibiogram was performed following the disc diffusion method, and virulence and antibiotic resistance genes were detected through PCR. 19 out of 40 fishes were positive for Edwardsiella infection and 32 E. tarda were isolated. PCR assays consistently amplified groEL (623 bp), gyrB (415 bp), etfA (415 bp), and etfD (445 bp) genes, respectively. The prevalence of virulence genes was: gadB (17%), mukF (35%), fimA (10%), and citC (12.5%). The antibiogram revealed that the highest resistance (90.63%) was found against cotrimoxazole and amoxicillin, whereas sensitive (100%) to gentamicin and meropenem. Among 32 isolates, 90.75% were found to be multi-drug resistant (MDR). Again, multiple antibiotic resistance (MAR) index analysis revealed the highest value of 0.61, and 93.75% of isolates have an MAR index above 0.2. Resistance gene distribution was observed as the highest (62.5%) isolates harbored the tetA gene and the lowest (21.88%) isolates harbored qnrB. It could be concluded that MDR and pathogenic potential E. tarda was present in stinging catfish, posing a potential threat to animals, humans, and the environment. - Source: PubMed
Publication date: 2026/01/30
Aktar Mst TachhlimaPrapti Bushra Benta RahmanRahman AminurSiddyqua Mst AyeshaHossain Muhammad TofazzalSiddique Mahbubul Pratik