PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
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	
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	
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	
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	
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	
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	
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	
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	
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