PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2556473-8	1989	The IL-1-induced rise in pHi is both sodium dependent and amiloride sensitive, indicative of activation of the Na+/H+ antiport.	Amiloride	58-67	glucose-6-phosphate isomerase 1	Mus musculus	25-28	
35538691-6	2022	Low pHe reduced intracellular pH (pHi), while amiloride treatment, which is known to reduce pHi, induced c-Src phosphorylation through AhR.	Amiloride	46-55	glucose-6-phosphate isomerase 1	Mus musculus	92-95	
2574175-4	1989	These pHi changes were dependent on extracellular Na+ and inhibited by amiloride.	Amiloride	71-80	glucose-6-phosphate isomerase 1	Mus musculus	6-9	
16336655-1	2005	BACKGROUND: Amiloride derivatives, commonly used for their diuretic and antihypertensive properties, can also cause a sustained but reversible decrease of intracellular pH (pHi).	Amiloride	12-21	glucose-6-phosphate isomerase 1	Mus musculus	173-176	
2835488-6	1988	In the presence of amiloride (0.1 mM) or the absence of Na+, application of ACh caused a significant decrease in pHi and removal of amiloride or replacement with Na+-containing saline, respectively, rapidly increased the pHi.	Amiloride	19-28	glucose-6-phosphate isomerase 1	Mus musculus	113-116	
2835488-6	1988	In the presence of amiloride (0.1 mM) or the absence of Na+, application of ACh caused a significant decrease in pHi and removal of amiloride or replacement with Na+-containing saline, respectively, rapidly increased the pHi.	Amiloride	19-28	glucose-6-phosphate isomerase 1	Mus musculus	221-224	
2883187-3	1987	The recovery of pHi to its resting value was blocked by the removal of extracellular Na+, by the addition of extra-cellular H+, and by the addition of analogs of amiloride selective for inhibition of Na+/H+ exchange.	Amiloride	162-171	glucose-6-phosphate isomerase 1	Mus musculus	16-19	
23428-13	1977	Amiloride (10(-4)M) reversibly reduced the rate of pH(i) recovery to much the same extent as removal of external Na.	Amiloride	0-9	glucose-6-phosphate isomerase 1	Mus musculus	51-56	
3254411-15	1988	In HCO3- -free solution pHi recovery was completely blocked when either Na+ was removed or when amiloride was applied indicating an exclusive activation of the Na+-H+ exchanger.	Amiloride	96-105	glucose-6-phosphate isomerase 1	Mus musculus	24-27	
2835488-6	1988	In the presence of amiloride (0.1 mM) or the absence of Na+, application of ACh caused a significant decrease in pHi and removal of amiloride or replacement with Na+-containing saline, respectively, rapidly increased the pHi.	Amiloride	132-141	glucose-6-phosphate isomerase 1	Mus musculus	221-224	
3367375-4	1988	After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange.	Amiloride	122-131	glucose-6-phosphate isomerase 1	Mus musculus	48-51	
3367375-6	1988	The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump.	Amiloride	99-108	glucose-6-phosphate isomerase 1	Mus musculus	22-25	
6338733-4	1983	Amiloride, a specific blocker of the transmembrane sodium proton exchange, has been used to demonstrate that this mechanism is also operative in the beta-cell membrane in the control of pHi.	Amiloride	0-9	glucose-6-phosphate isomerase 1	Mus musculus	186-189	
8554515-5	1995	Recovery of pHi in L1210 cells after a nigericin- or NH4(+)-mediated acid load in HCO3(-)-free buffers was mediated by Na+/H+ antiporter activity, in addition to a minor Na(+)-independent and amiloride-insensitive pathway.	Amiloride	192-201	glucose-6-phosphate isomerase 1	Mus musculus	12-15	
15193158-6	2004	Islet pHi was altered using amiloride, removal of medium Cl-, and changing medium pH.	Amiloride	28-37	glucose-6-phosphate isomerase 1	Mus musculus	6-9	
12493726-6	2003	The Na(+)-dependent rate of pH(i) recovery was also inhibited by amiloride, indicating H(+) extrusion through NHEs; however, the amiloride sensitivity of the apical membrane was less than that of the basolateral membrane, suggesting the involvement of different types of NHEs in the two membranes.	Amiloride	65-74	glucose-6-phosphate isomerase 1	Mus musculus	28-33	
12493726-6	2003	The Na(+)-dependent rate of pH(i) recovery was also inhibited by amiloride, indicating H(+) extrusion through NHEs; however, the amiloride sensitivity of the apical membrane was less than that of the basolateral membrane, suggesting the involvement of different types of NHEs in the two membranes.	Amiloride	129-138	glucose-6-phosphate isomerase 1	Mus musculus	28-33	
9501924-10	1997	Our data indicate that the Na+/H+ exchanger is involved in this process, since acid load and pHi-recovery experiments showed the alkalization to be amiloride-sensitive.	Amiloride	148-157	glucose-6-phosphate isomerase 1	Mus musculus	93-96	
9298595-5	1997	Amiloride (1 mM) of 5-(N-ethyl-N-isopropyl)-amiloride (10 microM), two previously reported inhibitors of the Na+/H+ exchangers, mimicked the effects produced by 2H2O on pHi and PtdCho turnover.	Amiloride	0-9	glucose-6-phosphate isomerase 1	Mus musculus	169-172	
9407593-2	1997	Coadministration of amiloride increases the incidence and severity of acetazolamide-induced forelimb malformations and further reduces limb bud pHi.	Amiloride	20-29	glucose-6-phosphate isomerase 1	Mus musculus	144-147	
1311525-2	1992	When the apical Na(+)-H+ antiporter was inhibited in the absence of AVP with removal of luminal Na+ plus addition of 0.5 mM amiloride, a small but significant increase in pHi was observed after luminal NH4Cl-induced acidification of MTAL cells to pHi less than 6.7.	Amiloride	124-133	glucose-6-phosphate isomerase 1	Mus musculus	171-174	
8638256-12	1995	However, treatment with acetazolamide plus amiloride for 15 hr produced a marked reduction of pHi values throughout the forelimb bud.	Amiloride	43-52	glucose-6-phosphate isomerase 1	Mus musculus	94-97	
8381657-0	1993	Therapeutic potential of analogues of amiloride: inhibition of the regulation of intracellular pH as a possible mechanism of tumour selective therapy.	Amiloride	38-47	glucose-6-phosphate isomerase 1	Mus musculus	95-97	
8381657-3	1993	Amiloride and its analogues DMA (5-(N,N-dimethyl)amiloride), MIBA (5-(N-methyl-N-isobutyl)amiloride) and EIPA (5-(N-ethyl-N-isopropyl)amiloride) are known to inhibit the Na+/H+ antiport and therefore decrease the cells ability to regulate pHi.	Amiloride	0-9	glucose-6-phosphate isomerase 1	Mus musculus	239-242	
8393012-3	1993	Na/H exchange was assayed as the Na-dependent, amiloride-sensitive component of pHi recovery from an acid load induced by a pulse of NH3/NH4-containing solution.	Amiloride	47-56	glucose-6-phosphate isomerase 1	Mus musculus	80-83	
8393012-9	1993	In addition, a putative Na/HCO3 cotransport system was monitored as a Na-dependent, amiloride-insensitive pHi recovery mechanisms that was inhibited by 200 microM H2DIDS.	Amiloride	84-93	glucose-6-phosphate isomerase 1	Mus musculus	106-109	
1396416-11	1992	Amiloride, a Na(+)-H+ exchange inhibitor, decreased the pHi of both DBA and C57 astrocytes more in HEPES HBSS than in HCO3- HBSS.	Amiloride	0-9	glucose-6-phosphate isomerase 1	Mus musculus	56-59	
1503904-2	1992	Cell killing is enhanced when these agents are used in combination with compounds (amiloride, 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS)) which inhibit the membrane-based exchangers responsible for the regulation of intracellular pH (pHi).	Amiloride	83-92	glucose-6-phosphate isomerase 1	Mus musculus	247-250	
1588302-9	1992	The rate of cellular NH4+ influx in IP-MTAL due to the apical Ba(2+)-sensitive NH4+ transport pathway was sensitive to reduction in cytosolic pH whether pHi was changed by acidifying the basolateral medium or by inhibition of the apical Na+:H+ exchanger with amiloride at a constant pHo of 7.4.	Amiloride	259-268	glucose-6-phosphate isomerase 1	Mus musculus	153-156	
1311525-2	1992	When the apical Na(+)-H+ antiporter was inhibited in the absence of AVP with removal of luminal Na+ plus addition of 0.5 mM amiloride, a small but significant increase in pHi was observed after luminal NH4Cl-induced acidification of MTAL cells to pHi less than 6.7.	Amiloride	124-133	glucose-6-phosphate isomerase 1	Mus musculus	247-250	
1311525-6	1992	In the absence of AVP, addition of 0.5 mM amiloride to the luminal perfusate reduced steady-state pHi by 0.40 +/- 0.07 units, whereas exposure of the basolateral membrane to the same concentration of amiloride had no effect on pHi (delta pHi = 0.01 +/- 0.01 units).	Amiloride	42-51	glucose-6-phosphate isomerase 1	Mus musculus	98-101	
1311525-6	1992	In the absence of AVP, addition of 0.5 mM amiloride to the luminal perfusate reduced steady-state pHi by 0.40 +/- 0.07 units, whereas exposure of the basolateral membrane to the same concentration of amiloride had no effect on pHi (delta pHi = 0.01 +/- 0.01 units).	Amiloride	42-51	glucose-6-phosphate isomerase 1	Mus musculus	227-230	
1311525-6	1992	In the absence of AVP, addition of 0.5 mM amiloride to the luminal perfusate reduced steady-state pHi by 0.40 +/- 0.07 units, whereas exposure of the basolateral membrane to the same concentration of amiloride had no effect on pHi (delta pHi = 0.01 +/- 0.01 units).	Amiloride	42-51	glucose-6-phosphate isomerase 1	Mus musculus	227-230	
1311525-7	1992	AVP reduced the magnitude of cell acidification on exposure of apical membranes to amiloride (delta pHi = 0.16 +/- 0.03) but increased the pHi response to basolateral amiloride (delta pHi = 0.09 +/- 0.00).	Amiloride	167-176	glucose-6-phosphate isomerase 1	Mus musculus	139-142	
1311525-7	1992	AVP reduced the magnitude of cell acidification on exposure of apical membranes to amiloride (delta pHi = 0.16 +/- 0.03) but increased the pHi response to basolateral amiloride (delta pHi = 0.09 +/- 0.00).	Amiloride	167-176	glucose-6-phosphate isomerase 1	Mus musculus	139-142	
1964210-7	1990	This Na(+)-induced increase in pHi was almost completely inhibited by 0.5 mmol/l amiloride and was associated with a rapid, amiloride-sensitive increase in aNai.	Amiloride	81-90	glucose-6-phosphate isomerase 1	Mus musculus	31-34	
1914146-6	1991	Recovery of pHi after NH4Cl prepulse was markedly inhibited in low-Na+ and in amiloride-containing HEPES HBSS.	Amiloride	78-87	glucose-6-phosphate isomerase 1	Mus musculus	12-15	
1847362-2	1991	We investigated the possible relationship between changes in the thermal response of SCK mouse mammary tumor cells in vitro and changes in intracellular pH (pHi) due to amiloride in the present study.	Amiloride	169-178	glucose-6-phosphate isomerase 1	Mus musculus	157-160	
1847362-6	1991	The presence of 0.5 mM amiloride significantly reduced pHi in both pH 7.2 and 6.6 medium.	Amiloride	23-32	glucose-6-phosphate isomerase 1	Mus musculus	55-58	
1847362-8	1991	The combined effect of heat and amiloride in reducing the pHi of SCK cells was additive.	Amiloride	32-41	glucose-6-phosphate isomerase 1	Mus musculus	58-61	
1847362-9	1991	These results suggest that the effects of amiloride on the thermal response of SCK cells might be mediated in part by a decrease in pHi.	Amiloride	42-51	glucose-6-phosphate isomerase 1	Mus musculus	132-135	
1964210-7	1990	This Na(+)-induced increase in pHi was almost completely inhibited by 0.5 mmol/l amiloride and was associated with a rapid, amiloride-sensitive increase in aNai.	Amiloride	124-133	glucose-6-phosphate isomerase 1	Mus musculus	31-34	
2156445-6	1990	Recovery of pHi was dependent on luminal Na+ (apparent Km = 13.2 +/- 3.2 mM) and was inhibited by amiloride (apparent Ki = 10.6 microM), consistent with the activity of an apical Na(+)-H+ antiporter.	Amiloride	98-107	glucose-6-phosphate isomerase 1	Mus musculus	12-15	
2107748-5	1990	Steady-state pHi of BC3H-1 cells in NHB acidified reversibly on exposure to 0.5 mM 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS; 1.4 +/- 0.3 x 10(-4) pH/s), 1 mM amiloride (2.0 +/- 0.7 x 10(-4) pH/s), or Na-free solution (8.3 +/- 2.4 x 10(-4) pH/s) and alkalinized upon exposure to Cl-free solutions (9.7 +/- 2.2 x 10(-4) pH/s).	Amiloride	172-181	glucose-6-phosphate isomerase 1	Mus musculus	13-16	
2107748-7	1990	This new steady-state pHi acidified very slowly upon exposure to 1 mM amiloride (0.3 +/- 0.1 x 10(-4) pH/s), acidified more rapidly upon exposure to 0.5 mM DIDS (5.9 +/- 0.6 x 10(-4) pH/s) or Na-free solutions (9.8 +/- 1.0 x 10(-4) pH/s), and alkalinized on exposure to Cl-free solutions (24.5 +/- 1.3 x 10(-4) pH/s).	Amiloride	70-79	glucose-6-phosphate isomerase 1	Mus musculus	22-25