PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31736966-0	2019	Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients.	Naltrexone	0-10	transient receptor potential cation channel subfamily M member 3	Homo sapiens	29-70	
31736966-5	2019	Naltrexone hydrochloride (NTX) acts as an antagonist to the muOR thus negating the inhibitory function of this opioid receptor on TRPM3.	Naltrexone	0-24	transient receptor potential cation channel subfamily M member 3	Homo sapiens	130-135	
31736966-5	2019	Naltrexone hydrochloride (NTX) acts as an antagonist to the muOR thus negating the inhibitory function of this opioid receptor on TRPM3.	Naltrexone	26-29	transient receptor potential cation channel subfamily M member 3	Homo sapiens	130-135	
31736966-6	2019	Therefore, understanding the mechanism of action for NTX in regulating and modulating TRPM3 channel function in NK cells will provide important information for the development of effective therapeutic interventions for ME/CFS.	Naltrexone	53-56	transient receptor potential cation channel subfamily M member 3	Homo sapiens	86-91	
31736966-9	2019	Importantly, TRPM3 channel activity was restored in IL-2 stimulated NK cells isolated from ME/CFS patients after incubation for 24 h with NTX.	Naltrexone	138-141	transient receptor potential cation channel subfamily M member 3	Homo sapiens	13-18	
31736966-10	2019	Moreover, we demonstrated that NTX does not act as an agonist by directly coupling on the TRPM3 ion channel gating.	Naltrexone	31-34	transient receptor potential cation channel subfamily M member 3	Homo sapiens	90-95	
31736966-11	2019	The opioid antagonist NTX has the potential to negate the inhibitory function of opioid receptors on TRPM3 in NK cells from ME/CFS patients, resulting in calcium signals remodeling, which will in turn affect cell functions, supporting the hypothesis that NTX may have potential for use as a treatment for ME/CFS.	Naltrexone	22-25	transient receptor potential cation channel subfamily M member 3	Homo sapiens	101-106	
31736966-11	2019	The opioid antagonist NTX has the potential to negate the inhibitory function of opioid receptors on TRPM3 in NK cells from ME/CFS patients, resulting in calcium signals remodeling, which will in turn affect cell functions, supporting the hypothesis that NTX may have potential for use as a treatment for ME/CFS.	Naltrexone	255-258	transient receptor potential cation channel subfamily M member 3	Homo sapiens	101-106	
34326841-0	2021	Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment.	Naltrexone	42-52	transient receptor potential cation channel subfamily M member 3	Homo sapiens	116-157	
34326841-3	2021	Naltrexone hydrochloride (NTX) acts as an antagonist to the mu (mu)-opioid receptor thus negating its inhibitory function on TRPM3.	Naltrexone	0-24	transient receptor potential cation channel subfamily M member 3	Homo sapiens	125-130	
34326841-3	2021	Naltrexone hydrochloride (NTX) acts as an antagonist to the mu (mu)-opioid receptor thus negating its inhibitory function on TRPM3.	Naltrexone	26-29	transient receptor potential cation channel subfamily M member 3	Homo sapiens	125-130	
35172836-0	2022	Impaired TRPM3-dependent calcium influx and restoration using Naltrexone in natural killer cells of myalgic encephalomyelitis/chronic fatigue syndrome patients.	Naltrexone	62-72	transient receptor potential cation channel subfamily M member 3	Homo sapiens	9-14	
35172836-7	2022	Naltrexone hydrochloride (NTX), a microOR antagonist, negates the inhibitory action of microOR on TRPM3 function.	Naltrexone	0-24	transient receptor potential cation channel subfamily M member 3	Homo sapiens	98-103	
35172836-7	2022	Naltrexone hydrochloride (NTX), a microOR antagonist, negates the inhibitory action of microOR on TRPM3 function.	Naltrexone	26-29	transient receptor potential cation channel subfamily M member 3	Homo sapiens	98-103	
35172836-8	2022	Importantly, it has recently been reported that NTX restores impaired TRPM3 function in NK cells of ME/CFS patients.	Naltrexone	48-51	transient receptor potential cation channel subfamily M member 3	Homo sapiens	70-75	
35172836-10	2022	The effect of overnight (24 h) NTX in vitro treatment on TRPM3-dependent Ca2+ influx was determined.	Naltrexone	31-34	transient receptor potential cation channel subfamily M member 3	Homo sapiens	57-62	
35172836-12	2022	Overnight treatment of NK cells with NTX significantly improved TRPM3-dependent Ca2+ influx in ME/CFS patients.	Naltrexone	37-40	transient receptor potential cation channel subfamily M member 3	Homo sapiens	64-69	
35172836-14	2022	CONCLUSION: TRPM3-dependent Ca2+ influx was restored in ME/CFS patients following overnight treatment of isolated NK cells with NTX in vitro.	Naltrexone	128-131	transient receptor potential cation channel subfamily M member 3	Homo sapiens	12-17