electron-transferring-flavoprotein dehydrogenase (ETF dehydrogenase)

system formed of electron-transferring flavoproteins plus EC or EC (butyryl-CoA dehydrogenase or acyl-CoA dehydrogenase) which reduces ubiquinone & other acceptors, defects in ETFDH are the cause of glutaric aciduria type IIc
Also Known As:
ETF dehydrogenase; ETFDH protein, human; electron transfer flavoprotein-Q oxidoreductases; electron transfer flavoprotein-ubiquinone oxidoreductase; electron-transferring flavoprotein dehydrogenase; electron-transferring-flavoprotein dehydrogenase, human
Networked: 18 relevant articles (0 outcomes, 1 trials/studies)

Bio-Agent Context: Research Results


1. Angelini, Corrado: 2 articles (04/2015 - 09/2013)
2. DiMauro, Salvatore: 2 articles (10/2011 - 08/2007)
3. Yamaguchi, Seiji: 2 articles (10/2010 - 06/2010)
4. Leaver, Christopher J: 2 articles (05/2010 - 09/2005)
5. Graham, Ian A: 2 articles (05/2010 - 09/2005)
6. Ishizaki, Kimitsune: 2 articles (05/2010 - 09/2005)
7. Schauer, Nicolas: 2 articles (05/2010 - 09/2005)
8. Larson, Tony R: 2 articles (05/2010 - 09/2005)
9. Fernie, Alisdair R: 2 articles (05/2010 - 09/2005)
10. Semplicini, Claudio: 1 article (09/2013)

Related Diseases

1. Multiple Acyl Coenzyme A Dehydrogenase Deficiency
2. Muscular Diseases (Myopathy)
10/01/2011 - "Most patients with myopathy were found to harbor other genetic defects (mutations in electron-transferring-flavoprotein dehydrogenase or mitochondrial DNA). "
06/01/2013 - "Our previous data showed that in a group of Chinese patients, a mild type of MADD characterized by myopathy with clinically no other systemic involvement was caused by mutations in electron transfer flavoprotein dehydrogenase (ETFDH) gene, which encodes electron transfer flavoprotein: ubiquinone oxidoreductase (ETF:QO). "
04/01/2015 - "This review is focused on recent advances about GSDII and its treatment, and the most recent notions about the management and treatment of other metabolic myopathies will be briefly reviewed, including glycogenosis type V (McArdle disease), glycogenosis type III (debrancher enzyme deficiency or Cori disease), CPT-II deficiency, and ETF-dehydrogenase deficiency (also known as riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency or RR-MADD). "
09/01/2013 - "Pharmacological, immunotherapy, nutritional, and physical/rehabilitative treatments for late-onset Pompe disease and other metabolic myopathies are covered, including treatments for defects in glycogen metabolism, such as glycogenosis type V (McArdle disease), and glycogenosis type III (debrancher enzyme deficiency), and defects in lipid metabolism, such as carnitine palmitoyltransferase II deficiency and electron transferring flavoprotein dehydrogenase deficiency, or riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency. "
3. Starvation
4. Glycogen Storage Disease Type V (McArdle's Disease)
5. Glycogen Storage Disease (Glycogenosis)

Related Drugs and Biologics

1. Electron-Transferring Flavoproteins (Electron Transfer Flavoprotein)
2. Oxidoreductases
3. Acyl-CoA Dehydrogenases
4. Riboflavin (Vitamin B2)
5. Flavoproteins
6. Carnitine O-Palmitoyltransferase (Carnitine Palmitoyltransferase II)
7. Glycogen
8. Mitochondrial DNA (mtDNA)
9. Carbon
10. Acyl Coenzyme A (Acyl CoA)

Related Therapies and Procedures

1. Immunotherapy