PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12226741-0 2002 Aminoglycoside suppression of a premature stop mutation in a Cftr-/- mouse carrying a human CFTR-G542X transgene. Aminoglycosides 0-14 CF transmembrane conductance regulator Homo sapiens 92-96 24251786-0 2014 Synthetic aminoglycosides efficiently suppress cystic fibrosis transmembrane conductance regulator nonsense mutations and are enhanced by ivacaftor. Aminoglycosides 10-25 CF transmembrane conductance regulator Homo sapiens 47-98 24251786-9 2014 These results provide evidence that NB124 and other synthetic aminoglycosides provide a 10-fold improvement in therapeutic index over gentamicin and other first-generation aminoglycosides, providing a promising treatment for a wide array of CFTR nonsense mutations. Aminoglycosides 62-77 CF transmembrane conductance regulator Homo sapiens 241-245 21779978-0 2011 Suppression of CFTR premature termination codons and rescue of CFTR protein and function by the synthetic aminoglycoside NB54. Aminoglycosides 106-120 CF transmembrane conductance regulator Homo sapiens 15-19 21779978-0 2011 Suppression of CFTR premature termination codons and rescue of CFTR protein and function by the synthetic aminoglycoside NB54. Aminoglycosides 106-120 CF transmembrane conductance regulator Homo sapiens 63-67 32640650-4 2020 Aminoglycoside and PTC124 derivatives have been used for the read-through of PTCs to restore the full-length CFTR protein. Aminoglycosides 0-14 CF transmembrane conductance regulator Homo sapiens 109-113 20829696-7 2010 Aminoglycosides and the novel small molecule ataluren induce translational readthrough of nonsense mutations in CFTR and other genetic diseases in vitro and in vivo and have shown activity in proof of concept trials, and ataluren is now being studied in confirmatory trials. Aminoglycosides 0-15 CF transmembrane conductance regulator Homo sapiens 112-116 15510065-6 2004 Clinical studies also provided evidence that the aminoglycoside gentamicin can suppress these CFTR premature stop mutations in affected patients. Aminoglycosides 49-63 CF transmembrane conductance regulator Homo sapiens 94-98 10712334-2 2000 It has been shown in vitro, that aminoglycoside antibiotics can increase the frequency of erroneous insertion of nonsense codons hence permitting the translation of CFTR alleles carrying missense mutations to continue reading to the end of the gene. Aminoglycosides 33-47 CF transmembrane conductance regulator Homo sapiens 165-169 9359706-3 1997 We reported that the aminoglycoside antibiotics G-418 and gentamicin can suppress two premature stop mutations [a stop codon in place of glycine residue 542 (G542X) and arginine residue 553 (R553X)] when expressed from a CFTR cDNA in HeLa cells. Aminoglycosides 21-35 CF transmembrane conductance regulator Homo sapiens 221-225 34272367-7 2021 SRI-41315 also potentiates aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity. Aminoglycosides 27-41 CF transmembrane conductance regulator Homo sapiens 100-104 8597960-0 1996 Aminoglycoside antibiotics restore CFTR function by overcoming premature stop mutations. Aminoglycosides 0-14 CF transmembrane conductance regulator Homo sapiens 35-39 8597960-5 1996 Aminoglycoside treatment resulted in the expression of full-length CFTR and restored its cyclic AMP-activated chloride channel activity. Aminoglycosides 0-14 CF transmembrane conductance regulator Homo sapiens 67-71 8597960-6 1996 Another aminoglycoside, gentamicin, also promoted the expression of full-length CFTR. Aminoglycosides 8-22 CF transmembrane conductance regulator Homo sapiens 80-84 8597960-7 1996 These results suggest that treatment with aminoglycosides may provide a means of restoring CFTR function in patients with this class of mutation. Aminoglycosides 42-57 CF transmembrane conductance regulator Homo sapiens 91-95