Novel Mutations Mapping to the Fourth Sodium Channel Domain of Nav1.7 Result in Variable Clinical Manifestations of Primary Erythromelalgia-Reference-Cited by-同舟云学术

Novel Mutations Mapping to the Fourth Sodium Channel Domain of Nav1.7 Result in Variable Clinical Manifestations of Primary Erythromelalgia

Published:2013-01-06 Issue:2 Volume:15 Page:265-278
ISSN:1535-1084
Container-title:NeuroMolecular Medicine
language:en
Short-container-title:Neuromol Med

Author:

Cregg Roman,Laguda Bisola,Werdehausen Robert,Cox James J.,Linley John E.,Ramirez Juan D.,Bodi Istvan,Markiewicz Michael,Howell Kevin J.,Chen Ya-Chun,Agnew Karen,Houlden Henry,Lunn Michael P.,Bennett David L. H.,Wood John N.,Kinali Maria

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Neurology,Molecular Medicine

Link

http://link.springer.com/content/pdf/10.1007/s12017-012-8216-8.pdf

Reference46 articles.

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3. Charalambous, K., & Wallace, B. A. (2011). NaChBac: The long lost sodium channel ancestor. Biochemistry, 50, 6742–6752.

4. Cheng, X., Dib-Hajj, S. D., Tyrrell, L., & Waxman, S. G. (2008). Mutation I136 V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade. Molecular Pain, 4, 1.

5. Cheng, X., Dib-Hajj, S. D., Tyrrell, L., Wright, D. A., Fischer, T. Z., & Waxman, S. G. (2010). Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders. Molecular Pain, 6, 24.

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