Clinically relevant aminoglycosides can suppress disease-associated premature stop mutations in the IDUA and P53 cDNAS in a mammalian translation system

Journal of Molecular Medicine

Volumn 80, Issue 6, 2002, Pages 367-376

  Keeling, Kim M ^a   Bedwell, David M ^a  

^a University of Alabama at Birmingham   (United States)

Author keywords

Aminoglycoside; Readthrough; Suppression; Termination; Translation

Indexed keywords

AMIKACIN; AMINOGLYCOSIDE; COMPLEMENTARY DNA; GENTAMICIN; PROTEIN; PROTEIN IDUA; PROTEIN P53; TOBRAMYCIN; UNCLASSIFIED DRUG; ANTIINFECTIVE AGENT; LEVO IDURONIDASE;

ANIMAL CELL; ARTICLE; BIOASSAY; CONTROLLED STUDY; DRUG EFFECT; DRUG EFFICACY; GENE CONSTRUCT; LYSOSOME STORAGE DISEASE; MUTATION; NONHUMAN; RNA TRANSLATION; STOP CODON; ANIMAL; CELL CULTURE; GENETICS; HUMAN; HURLER SYNDROME; MAMMAL; METHODOLOGY; MOLECULAR BIOLOGY; PLASMID; PROTEIN SYNTHESIS; RAT; REPORTER GENE;

AMIKACIN; AMINOGLYCOSIDES; ANIMAL; ANTIBIOTICS, AMINOGLYCOSIDE; CELLS, CULTURED; CODON, NONSENSE; DNA, COMPLEMENTARY; GENES, REPORTER; GENTAMICINS; HUMAN; IDURONIDASE; MAMMALS; MOLECULAR BIOLOGY; MUCOPOLYSACCHARIDOSIS I; MUTATION; PLASMIDS; PROTEIN P53; RATS; TOBRAMYCIN; TRANSLATION, GENETIC; ANIMALS; ANTI-BACTERIAL AGENTS; HUMANS; PROTEIN BIOSYNTHESIS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0035997219     PISSN: 09462716     EISSN: None     Source Type: Journal    
DOI: 10.1007/s00109-001-0317-z     Document Type: Article

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