✦ LIBER ✦

Structural Basis of an Inherited hERG1 Long QT Mutant

✍ Scribed by Cordero-Morales, Julio F.; Jogini, Vishwanath; Lewis, Anthony; Vasquez, Valeria; Medovoy, David; Tristani-Firouzi, Martin; Perozo, Eduardo

Book ID: 122318312
Publisher: Biophysical Society
Year: 2011
Tongue: English
Weight: 40 KB
Volume: 100
Category: Article
ISSN: 0006-3495
DOI: 10.1016/j.bpj.2010.12.2517

No coin nor oath required. For personal study only.

📜 SIMILAR VOLUMES

Perturbation of sodium channel structure

Perturbation of sodium channel structure by an inherited Long QT Syndrome mutation

✍ Glaaser, Ian W.; Osteen, Jeremiah D.; Puckerin, Akil; Sampson, Kevin J.; Jin, Xi 📂 Article 📅 2012 🏛 Nature Publishing Group 🌐 English ⚖ 821 KB

The structural basis of drug induced lon

The structural basis of drug induced long QT syndrome

✍ John Mitcheson 📂 Article 📅 2007 🏛 Elsevier Science 🌐 English ⚖ 68 KB

Disopyramide is an effective inhibitor o

Disopyramide is an effective inhibitor of mutant HERG K+ channels involved in variant 1 short QT syndrome

✍ Mark J. McPate; Rona S. Duncan; Harry J. Witchel; Jules C. Hancox 📂 Article 📅 2006 🏛 Elsevier Science 🌐 English ⚖ 126 KB

An NMR investigation of the structure, f

An NMR investigation of the structure, function and role of the hERG channel selectivity filter in the long QT syndrome

✍ Gravel, Andrée E.; Arnold, Alexandre A.; Dufourc, Erick J.; Marcotte, Isabelle 📂 Article 📅 2013 🏛 Elsevier Science 🌐 English ⚖ 859 KB

Molecular basis of very long chain acyl-

Molecular basis of very long chain acyl-CoA dehydrogenase deficiency in three Israeli patients: Identification of a complex mutant allele with P65L and K247Q mutations, the former being an exonic mutation causing exon 3 skipping

✍ Hiroh Watanabe; Kenji E. Orii; Toshiyuki Fukao; Xiang-Qian Song; Toshifumi Aoyam 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 343 KB 👁 3 views

Very long chain acyl-CoA dehydrogenase (VLCAD) deficiency is a life-threatening disorder of mitochondrial fatty acid beta-oxidation. We identified four novel mutations in three unrelated patients. All patients had the severe childhood form of VLCAD deficiency with early onset and high mortality. Imm