Clinical doses of amikacin provide more effective suppression of the human CFTR-G542X stop mutation than gentamicin in a transgenic CF mouse model-Reference-Cited by-同舟云学术

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Clinical doses of amikacin provide more effective suppression of the human CFTR-G542X stop mutation than gentamicin in a transgenic CF mouse model

Published:2006-03-16 Issue:7 Volume:84 Page:573-582
ISSN:0946-2716
Container-title:Journal of Molecular Medicine
language:en
Short-container-title:J Mol Med

Author:

Du Ming,Keeling Kim M.,Fan Liming,Liu Xiaoli,Kovaçs Timea,Sorscher Eric,Bedwell David M.

Publisher

Springer Science and Business Media LLC

Subject

Genetics (clinical),Drug Discovery,Molecular Medicine

Link

http://link.springer.com/content/pdf/10.1007/s00109-006-0045-5.pdf

Reference50 articles.

1. Krawczak M, Ball EV, Fenton I, Stenson PD, Abeysinghe S, Thomas N, Cooper DN (2000) Human gene mutation database—a biomedical information and research resource. Hum Mutat 15:45–51

2. Fearon K, McClendon V, Bonetti B, Bedwell DM (1994) Premature translation termination mutations are efficiently suppressed in a highly conserved region of yeast Ste6p, a member of the ATP-binding cassette (ABC) transporter family. J Biol Chem 269:17802–17808

3. Bonetti B, Fu L, Moon J, Bedwell DM (1995) The efficiency of translation termination is determined by a synergistic interplay between upstream and downstream sequences in Saccharomyces cerevisiae. J Mol Biol 251:334–345

4. Manuvakhova M, Keeling K, Bedwell DM (2000) Aminoglycoside antibiotics mediate context-dependent suppression of termination codons in a mammalian translation system. RNA 6:1044–1055

5. Keeling KM, Bedwell DM (2002) Clinically relevant aminoglycosides can suppress disease-associated premature stop mutations in the IDUA and P53 cDNAs in a mammalian translation system. J Mol Med 80:367–376

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