Long-chain 3-hydroxyacyl–coenzyme A dehydrogenase deficiency with the G1528C mutation: Clinical presentation of thirteen patients-Reference-Cited by-同舟云学术

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Long-chain 3-hydroxyacyl–coenzyme A dehydrogenase deficiency with the G1528C mutation: Clinical presentation of thirteen patients

Published:1997-01 Issue:1 Volume:130 Page:67-76
ISSN:0022-3476
Container-title:The Journal of Pediatrics
language:en
Short-container-title:The Journal of Pediatrics

Author:

Tyni Tiina,Palotie Aarno,Viinikka Lasse,Valanne Leena,Salo Matti K.,von Döbeln Ulrika,Jackson Sandra,Wanders Ronald,Venizelos Nikolaos,Pihko Helena

Publisher

Elsevier BV

Subject

Pediatrics, Perinatology, and Child Health

Reference41 articles.

1. Sudden infant death and long-chain 3-hydroxyacyl-CoA dehydrogenase;Wanders;Lancet,1989

2. Novel fatty acid β-oxidation enzymes in rat liver mitochondria. II. Purification and properties of enoyl-coenzyme A (CoA) hydratase/3-hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase trifunctional protein;Uchida;J Biol Chem,1992

3. Human liver long-chain 3-hydroxyacyl–coenzyme A dehydrogenase is a multifunctional membrane-bound beta-oxidation enzyme of mitochondria;Carpenter;Biochem Biophys Res Commun,1992

4. Structural analysis of cDNAs for subunits of human mitochondrial fatty acid β-oxidation trifunctional protein;Kamijo;Biochem Biophys Res Commun,1994

5. Two α subunit donor splice site mutations cause human trifunctional protein deficiency;Brackett;J Clin Invest,1995

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