PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32139089-7	2020	Conversely, pharmacologic inhibition of exosome secretion with dimethyl amiloride, depletion of exosome from the conditioned media or knockdown of Shh expression abolished the ability of transforming growth factor-beta1-treated HKC-8 cells to induce NRK-49F activation.	5-dimethylamiloride	63-81	transforming growth factor beta 1	Homo sapiens	187-219
2844806-4	1988	This rise in pHi is both Na+- and HCO3- -dependent, does not occur in Cl(-)-depleted cells, and is inhibited by 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid, but not by 5-(n,n-dimethyl)-amiloride, indicating the involvement of Na+-dependent HCO3-/Cl- exchange.	5-dimethylamiloride	173-199	glucose-6-phosphate isomerase 1	Mus musculus	13-16
3184169-3	1988	Following an acid load imposed by a NH4Cl prepulse, pHi was regulated in the absence of HCO3- by a Na+-dependent process inhibitable to a large extent by 1 mM amiloride and 0.1 mM dimethylamiloride.	5-dimethylamiloride	180-197	glucose-6-phosphate isomerase	Bos taurus	52-55
3020026-5	1986	In Na+-free medium, or in presence of the Na+/H+ antiport inhibitors, 5-(N,N-dimethyl)amiloride (DMA) or 5-(N-ethyl-N-isopropyl)amiloride (EIPA), thrombin caused a greater fall of pHi (0.22-0.26 units) that was sustained.	5-dimethylamiloride	70-95	glucose-6-phosphate isomerase	Homo sapiens	180-183
3020026-6	1986	DMA or EIPA could also reverse the alkalinization response to thrombin.	5-dimethylamiloride	0-3	coagulation factor II, thrombin	Homo sapiens	62-70
6208556-5	1984	In comparison, cells incubated with 10 microM MK-685 for 24 hr showed only a slight inhibition of stimulation by EGF.	5-dimethylamiloride	46-52	epidermal growth factor	Mus musculus	113-116
30839176-7	2019	Administering Ang-(1-7) decreased VO2 ; an effect prevented by dimethyl amiloride and furosemide, signifying that Ang-(1-7) inhibits transport-dependent VO2 in TAL.	5-dimethylamiloride	63-81	angiopoietin 1	Homo sapiens	14-22
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	185-203	interleukin 6	Homo sapiens	41-45
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	185-203	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	185-203	tumor necrosis factor	Homo sapiens	57-66
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	185-203	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	259-265
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	205-208	interleukin 6	Homo sapiens	41-45
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	205-208	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	205-208	tumor necrosis factor	Homo sapiens	57-66
32117213-6	2019	The relative expression and secretion of IL-6, IL-8, and TNF-alpha in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs.	5-dimethylamiloride	205-208	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	259-265
30839176-7	2019	Administering Ang-(1-7) decreased VO2 ; an effect prevented by dimethyl amiloride and furosemide, signifying that Ang-(1-7) inhibits transport-dependent VO2 in TAL.	5-dimethylamiloride	63-81	angiopoietin 1	Homo sapiens	114-122
30839176-7	2019	Administering Ang-(1-7) decreased VO2 ; an effect prevented by dimethyl amiloride and furosemide, signifying that Ang-(1-7) inhibits transport-dependent VO2 in TAL.	5-dimethylamiloride	63-81	transaldolase 1	Homo sapiens	160-163
27515813-6	2016	The flux was also decreased a) by inhibition of Na,H-exchangers by amiloride, dimethylamiloride (DMA), S3226 and Hoe694, b) by inhibition of Na,2Cl,K-cotransporter (NKCC1) by bumetanide, and c) by the likely inhibition of HCO3/anion exchange by DIDS.	5-dimethylamiloride	97-100	solute carrier family 12, member 2	Mus musculus	165-170
25715987-11	2015	With furosemide and NHE inhibitor, dimethylamiloride (DMA), increase in tubular flow increased PSF (furosemide+DMA: 2.7 +- 0.5 mmHg, n = 6), and benzamil blocked this (furosemide+DMA+benzamil: -1.1 +- 0.2 mmHg; P < 0.01, n = 6).	5-dimethylamiloride	111-114	solute carrier family 9 member C1	Homo sapiens	20-23
26497614-9	2015	Finally, Ang II-induced exosome release from cardiac fibroblasts and pathological cardiac hypertrophy were dramatically inhibited by GW4869 and DMA in mice.	5-dimethylamiloride	144-147	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	9-15
19056765-5	2009	Inhibition of DRA activity by niflumic acid was greater than that by DIDS as well as by the NHE inhibitor dimethylamiloride and the carbonic anhydrase inhibitor methazolamide.	5-dimethylamiloride	106-123	solute carrier family 26 member 3	Homo sapiens	14-17
21537843-5	2011	5-(N-ethyl-N-isopropyl) amiloride or dimethylamiloride, NHE inhibitor, abrogated the elevated MCT expression, indicating that MCT followed NHE activation.	5-dimethylamiloride	37-54	solute carrier family 9 member C1	Homo sapiens	56-59
21537843-5	2011	5-(N-ethyl-N-isopropyl) amiloride or dimethylamiloride, NHE inhibitor, abrogated the elevated MCT expression, indicating that MCT followed NHE activation.	5-dimethylamiloride	37-54	solute carrier family 16 member 1	Homo sapiens	94-97
21537843-5	2011	5-(N-ethyl-N-isopropyl) amiloride or dimethylamiloride, NHE inhibitor, abrogated the elevated MCT expression, indicating that MCT followed NHE activation.	5-dimethylamiloride	37-54	solute carrier family 16 member 1	Homo sapiens	126-129
21537843-5	2011	5-(N-ethyl-N-isopropyl) amiloride or dimethylamiloride, NHE inhibitor, abrogated the elevated MCT expression, indicating that MCT followed NHE activation.	5-dimethylamiloride	37-54	solute carrier family 9 member C1	Homo sapiens	139-142
19608532-5	2009	SNP and dimethyl amiloride (DMA), an NHE inhibitor, inhibited pH(i) recovery to a similar degree.	5-dimethylamiloride	8-26	solute carrier family 9 member C1	Homo sapiens	37-40
19608532-5	2009	SNP and dimethyl amiloride (DMA), an NHE inhibitor, inhibited pH(i) recovery to a similar degree.	5-dimethylamiloride	28-31	solute carrier family 9 member C1	Homo sapiens	37-40
25715987-11	2015	With furosemide and NHE inhibitor, dimethylamiloride (DMA), increase in tubular flow increased PSF (furosemide+DMA: 2.7 +- 0.5 mmHg, n = 6), and benzamil blocked this (furosemide+DMA+benzamil: -1.1 +- 0.2 mmHg; P < 0.01, n = 6).	5-dimethylamiloride	54-57	solute carrier family 9 member C1	Homo sapiens	20-23
25715987-11	2015	With furosemide and NHE inhibitor, dimethylamiloride (DMA), increase in tubular flow increased PSF (furosemide+DMA: 2.7 +- 0.5 mmHg, n = 6), and benzamil blocked this (furosemide+DMA+benzamil: -1.1 +- 0.2 mmHg; P < 0.01, n = 6).	5-dimethylamiloride	54-57	insulin like growth factor binding protein 7	Homo sapiens	95-98
25715987-11	2015	With furosemide and NHE inhibitor, dimethylamiloride (DMA), increase in tubular flow increased PSF (furosemide+DMA: 2.7 +- 0.5 mmHg, n = 6), and benzamil blocked this (furosemide+DMA+benzamil: -1.1 +- 0.2 mmHg; P < 0.01, n = 6).	5-dimethylamiloride	111-114	solute carrier family 9 member C1	Homo sapiens	20-23
21865738-6	2011	The stimulation of Na(+)/H(+) exchanger activity by dexamethasone was virtually abrogated by glucocorticoid receptor blocker mefiprestone (1 muM) and NHE3 inhibitor dimethyl amiloride (5 muM), but not prevented by NHE1 inhibitor cariporide (10 muM).	5-dimethylamiloride	165-183	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	150-154
21865738-6	2011	The stimulation of Na(+)/H(+) exchanger activity by dexamethasone was virtually abrogated by glucocorticoid receptor blocker mefiprestone (1 muM) and NHE3 inhibitor dimethyl amiloride (5 muM), but not prevented by NHE1 inhibitor cariporide (10 muM).	5-dimethylamiloride	165-183	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	214-218
19056765-5	2009	Inhibition of DRA activity by niflumic acid was greater than that by DIDS as well as by the NHE inhibitor dimethylamiloride and the carbonic anhydrase inhibitor methazolamide.	5-dimethylamiloride	106-123	solute carrier family 9 member C1	Homo sapiens	92-95
17234953-8	2007	Selective inhibition of NHE-1 using dimethylamiloride significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR.	5-dimethylamiloride	36-53	solute carrier family 9 member A1	Rattus norvegicus	24-29
18413672-7	2008	Thus we also have explored another possible mechanism through which DMA enables/enhances TDP, via the activation of mitochondrial alpha-ketoglutarate dehydrogenase.	5-dimethylamiloride	68-71	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	130-163
18172614-4	2008	On the other hand, in the presence of dimethylamiloride (DMA), a specific inhibitor of the Na+-H+ exchanger, endothelin-1 produced negative inotropy.	5-dimethylamiloride	38-55	endothelin 1	Mus musculus	109-121
18172614-4	2008	On the other hand, in the presence of dimethylamiloride (DMA), a specific inhibitor of the Na+-H+ exchanger, endothelin-1 produced negative inotropy.	5-dimethylamiloride	57-60	endothelin 1	Mus musculus	109-121
18172614-5	2008	In cardiomyocytes, in the presence of DMA, endothelin-1 produced a decrease in peak amplitude of the Ca2+ transient.	5-dimethylamiloride	38-41	endothelin 1	Mus musculus	43-55
17599909-8	2007	Dimethylamiloride, a classic blocker of Na(+)/H(+) exchange, did not affect pH(c) but increased insulin secretion in NHE1 mutant islets, indicating unspecific effects.	5-dimethylamiloride	0-17	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	117-121
16619256-5	2006	Secondly, the [Ca2+]i increase by progesterone was dependent on Ca2+ influx, and the acidification was blocked by Na+/H+ exchange (NHE) inhibitor, 3-methylsulphonyl-4-piperidinobenzoyl, guanidine hydrochloride (HOE-694) but not by 5-(N,N-dimethyl)-amiloride (DMA).	5-dimethylamiloride	231-257	solute carrier family 9 member C1	Homo sapiens	114-129
17095754-6	2007	The subsequent RVI was strongly inhibited with the Na(+)/H(+) exchanger 1 (NHE1)-specific concentration of HOE642 and completely by 500 muM dimethyl-amiloride (DMA), which also inhibits NHE4.	5-dimethylamiloride	160-163	sodium/hydrogen exchanger 1	Oryctolagus cuniculus	75-79
16619256-5	2006	Secondly, the [Ca2+]i increase by progesterone was dependent on Ca2+ influx, and the acidification was blocked by Na+/H+ exchange (NHE) inhibitor, 3-methylsulphonyl-4-piperidinobenzoyl, guanidine hydrochloride (HOE-694) but not by 5-(N,N-dimethyl)-amiloride (DMA).	5-dimethylamiloride	231-257	solute carrier family 9 member C1	Homo sapiens	131-134
16619256-5	2006	Secondly, the [Ca2+]i increase by progesterone was dependent on Ca2+ influx, and the acidification was blocked by Na+/H+ exchange (NHE) inhibitor, 3-methylsulphonyl-4-piperidinobenzoyl, guanidine hydrochloride (HOE-694) but not by 5-(N,N-dimethyl)-amiloride (DMA).	5-dimethylamiloride	259-262	solute carrier family 9 member C1	Homo sapiens	114-129
16619256-5	2006	Secondly, the [Ca2+]i increase by progesterone was dependent on Ca2+ influx, and the acidification was blocked by Na+/H+ exchange (NHE) inhibitor, 3-methylsulphonyl-4-piperidinobenzoyl, guanidine hydrochloride (HOE-694) but not by 5-(N,N-dimethyl)-amiloride (DMA).	5-dimethylamiloride	259-262	solute carrier family 9 member C1	Homo sapiens	131-134
12881227-3	2004	5-(N,N-dimethyl)-amiloride (50 microM; DMA), a concentration that selectively inhibits the NHE isoforms NHE1 and NHE2, but not NHE3, did not affect DBS.	5-dimethylamiloride	0-26	solute carrier family 9 member A2	Rattus norvegicus	113-117
16556652-7	2006	The changes in luminal and PV pH and [CO2] were also inhibited by the Na+-H+ exchanger-1 (NHE1) inhibitor dimethylamiloride, but not by the NHE3 inhibitor S3226.	5-dimethylamiloride	106-123	solute carrier family 9 member A1	Rattus norvegicus	70-88
16556652-7	2006	The changes in luminal and PV pH and [CO2] were also inhibited by the Na+-H+ exchanger-1 (NHE1) inhibitor dimethylamiloride, but not by the NHE3 inhibitor S3226.	5-dimethylamiloride	106-123	solute carrier family 9 member A1	Rattus norvegicus	90-94
16800927-0	2006	[Effect of the NHE-1-specific inhibitor DMA on pHi, proliferation and apoptosis of HL-60/ADM cells in vitro].	5-dimethylamiloride	40-43	solute carrier family 9 member A1	Homo sapiens	15-20
16800927-1	2006	The aim of this study was to evaluate the effect of dimethyl amiloride (DMA), a specific inhibitor of Na(+)/H(+) exchanger-1 (NHE-1), on intracellular pH value (pHi), proliferation and apoptosis of HL-60/ADM cells in vitro.	5-dimethylamiloride	52-70	solute carrier family 9 member A1	Homo sapiens	102-124
16800927-1	2006	The aim of this study was to evaluate the effect of dimethyl amiloride (DMA), a specific inhibitor of Na(+)/H(+) exchanger-1 (NHE-1), on intracellular pH value (pHi), proliferation and apoptosis of HL-60/ADM cells in vitro.	5-dimethylamiloride	52-70	solute carrier family 9 member A1	Homo sapiens	126-131
16800927-1	2006	The aim of this study was to evaluate the effect of dimethyl amiloride (DMA), a specific inhibitor of Na(+)/H(+) exchanger-1 (NHE-1), on intracellular pH value (pHi), proliferation and apoptosis of HL-60/ADM cells in vitro.	5-dimethylamiloride	72-75	solute carrier family 9 member A1	Homo sapiens	102-124
16800927-1	2006	The aim of this study was to evaluate the effect of dimethyl amiloride (DMA), a specific inhibitor of Na(+)/H(+) exchanger-1 (NHE-1), on intracellular pH value (pHi), proliferation and apoptosis of HL-60/ADM cells in vitro.	5-dimethylamiloride	72-75	solute carrier family 9 member A1	Homo sapiens	126-131
16800927-6	2006	It is concluded that by causing intracellular acidification, the NHE-1-specific inhibitor DMA inhibits proliferation of HL-60/ADM cells and induces apoptosis of HL-60/ADM cells, and the degree of this growth inhibition of HL-60/ADM cells is higher than that of HL-60 cells.	5-dimethylamiloride	90-93	solute carrier family 9 member A1	Homo sapiens	65-70
16336655-2	2005	Using dimethyl amiloride (DMA) on normal rodent pancreatic islets, we previously demonstrated the critical influence of islet pHi on insulin secretion.	5-dimethylamiloride	6-24	glucose-6-phosphate isomerase 1	Mus musculus	126-129
16336655-2	2005	Using dimethyl amiloride (DMA) on normal rodent pancreatic islets, we previously demonstrated the critical influence of islet pHi on insulin secretion.	5-dimethylamiloride	26-29	glucose-6-phosphate isomerase 1	Mus musculus	126-129
15802363-3	2005	A carbonic anhydrase inhibitor, acetazolamide, and dimethylamiloride, an inhibitor of the Na(+)/H(+) antiporter NHE1, delayed the recoveries of pH, phosphocreatine, and P(i) for >10 min, but the rate of recovery, once initiated, was unchanged.	5-dimethylamiloride	51-68	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	90-111
15802363-3	2005	A carbonic anhydrase inhibitor, acetazolamide, and dimethylamiloride, an inhibitor of the Na(+)/H(+) antiporter NHE1, delayed the recoveries of pH, phosphocreatine, and P(i) for >10 min, but the rate of recovery, once initiated, was unchanged.	5-dimethylamiloride	51-68	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	112-116
15499081-9	2005	Dimethyl amiloride (0.1 mM), an inhibitor of the basolateral sodium-hydrogen exchanger 1, also inhibited CO(2)-augumented DBS, although S-3226, a specific inhibitor of apical sodium-hydrogen exchanger 3, did not.	5-dimethylamiloride	0-18	solute carrier family 9 member A1	Rattus norvegicus	61-88
15020300-7	2004	Effects of ET-1 were prevented by cotreatment with either Ro31-8425, a PKC inhibitor, or dimethylamiloride, an inhibitor of the Na(+)/H(+) exchanger.	5-dimethylamiloride	89-106	endothelin 1	Rattus norvegicus	11-15
16538461-2	2006	This study reports the Kfc in the isolated lungs of normal chickens and in the lungs of chickens given the edemogenic agents oleic acid (OA) or dimethyl amiloride (DMA).	5-dimethylamiloride	144-162	TAO kinase 3	Gallus gallus	23-26
16538461-2	2006	This study reports the Kfc in the isolated lungs of normal chickens and in the lungs of chickens given the edemogenic agents oleic acid (OA) or dimethyl amiloride (DMA).	5-dimethylamiloride	164-167	TAO kinase 3	Gallus gallus	23-26
12881227-3	2004	5-(N,N-dimethyl)-amiloride (50 microM; DMA), a concentration that selectively inhibits the NHE isoforms NHE1 and NHE2, but not NHE3, did not affect DBS.	5-dimethylamiloride	0-26	solute carrier family 9 member A1	Rattus norvegicus	104-108
12107065-5	2002	The ANG II-induced cell sodium increase and (86)Rb uptake increase were reduced by dimethylamiloride (DMA; 10 microM).	5-dimethylamiloride	83-100	angiogenin	Oryctolagus cuniculus	4-7
12702745-2	2003	Maximal inhibitory concentrations of bumetanide and dimethylamiloride, which respectively block Cl- and HCO3- secretion in porcine airways, induced the formation of dense "plastered" mucus on the airway surface, depletion of periciliary fluid and collapse of cilia.	5-dimethylamiloride	52-69	HCO3	Sus scrofa	104-108
14645139-3	2003	Addition of 5-(N,N-dimethyl)-amiloride, an inhibitor of Na+/H+ exchanger, prolonged DHA-induced acidification as a function of time, indicating that the exchanger is implicated in pHi recovery.	5-dimethylamiloride	12-38	glucose-6-phosphate isomerase	Homo sapiens	180-183
12107065-5	2002	The ANG II-induced cell sodium increase and (86)Rb uptake increase were reduced by dimethylamiloride (DMA; 10 microM).	5-dimethylamiloride	102-105	angiogenin	Oryctolagus cuniculus	4-7
12034348-3	2002	Dimethyl amiloride (DMA) was used to study sodium/proton exchanger (NHE) activity in cells growing at different cell densities.	5-dimethylamiloride	0-18	solute carrier family 9 member C1	Homo sapiens	68-71
12034348-4	2002	Exposing cells at low density to dust induced an initial release of acid not involving NHE, followed by a sustained DMA-sensitive NHE activation.	5-dimethylamiloride	116-119	solute carrier family 9 member C1	Homo sapiens	130-133
12046895-3	2002	Here we report that the Vpu ion channel is inhibited by the amiloride derivatives 5-(N,N-hexamethylene)amiloride and 5-(N,N-dimethyl)amiloride but not by amiloride itself, nor by amantadine.	5-dimethylamiloride	117-142	Vpu	Human immunodeficiency virus 1	24-27
11832447-5	2002	The effects of mucosal 5-(N,N-dimethyl)-amiloride (DMA), which inhibits NHE2 and/or NHE3, and wortmannin, which inhibits phosphatidylinositol 3-kinase, on CO2-stimulated Na+ absorption were measured in the Ussing chamber.	5-dimethylamiloride	51-54	solute carrier family 9 member A2	Rattus norvegicus	72-76
11832447-5	2002	The effects of mucosal 5-(N,N-dimethyl)-amiloride (DMA), which inhibits NHE2 and/or NHE3, and wortmannin, which inhibits phosphatidylinositol 3-kinase, on CO2-stimulated Na+ absorption were measured in the Ussing chamber.	5-dimethylamiloride	51-54	solute carrier family 9 member A3	Rattus norvegicus	84-88
11832447-10	2002	DMA inhibition indicated that NHE3 mediates CO2-stimulated Na+ absorption.	5-dimethylamiloride	0-3	solute carrier family 9 member A3	Rattus norvegicus	30-34
11930639-5	2002	In situ cell death detection kit (TUNEL) was used for studying the effect of specific NHE-1 inhibitor-dimethyl amiloride (DMA) on the apoptosis of muscle cells which had intracellular acidification.	5-dimethylamiloride	102-120	solute carrier family 9 member A1	Rattus norvegicus	86-91
9425602-7	1997	Inhibition kinetics of NHE1 by amiloride, 5-(N,N-dimethyl)amiloride (DMA), 5-(N-hexamethyl)amiloride (HMA) and 5-(N-ethyl-N-isopropyl)amiloride (EIPA) were largely unchanged.	5-dimethylamiloride	42-67	solute carrier family 9 member A1	Homo sapiens	23-27
9657902-4	1998	Inhibition of NHE with 100 microM dimethylamiloride (DMA) rapidly decreased pHi by 0.37 units.	5-dimethylamiloride	34-51	glucose-6-phosphate isomerase	Bos taurus	76-79
9657902-4	1998	Inhibition of NHE with 100 microM dimethylamiloride (DMA) rapidly decreased pHi by 0.37 units.	5-dimethylamiloride	53-56	glucose-6-phosphate isomerase	Bos taurus	76-79
9565666-5	1998	This DMA-sensitive Li+ pathway, but not SLC, was significantly enhanced by hyperosmolar cell shrinkage, which is a characteristic feature of NHE.	5-dimethylamiloride	5-8	solute carrier family 9 member C1	Homo sapiens	141-144
9565666-6	1998	In conclusion, DMA-sensitive Li+ pathways, possibly mediated by NHE, are present in erythrocytes and coexist with the DMA-insensitive, SLC.	5-dimethylamiloride	15-18	solute carrier family 9 member C1	Homo sapiens	64-67
9565666-6	1998	In conclusion, DMA-sensitive Li+ pathways, possibly mediated by NHE, are present in erythrocytes and coexist with the DMA-insensitive, SLC.	5-dimethylamiloride	15-18	C-C motif chemokine ligand 21	Homo sapiens	135-138
11356638-7	2001	Expression of ICAM-1 mRNA was markedly increased in the vehicle-treated CMECs 3 h after reoxygenation, and this was significantly inhibited by treatment with cariporide, DMA, or Ca2+-free buffer.	5-dimethylamiloride	170-173	intercellular adhesion molecule 1	Rattus norvegicus	14-20
11356638-8	2001	In addition, enhanced ICAM-I protein expression on the cell surface of CMECs 8 h after reoxygenation was attenuated by treatment with cariporide, DMA, or Ca2+-free buffer.	5-dimethylamiloride	146-149	intercellular adhesion molecule 1	Rattus norvegicus	22-26
10942720-10	2000	Because the gp120-induced cell physiological changes were partially inhibited by dimethylamiloride (an inhibitor of Na(+)/H(+) exchange), our findings suggest that modification of human astrocyte Na(+)/H(+) exchange activity may provide a means of addressing some of the neurological complications of HIV infection.	5-dimethylamiloride	81-98	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	12-17
10362546-6	1999	When GRP94 was present in the medium, and thus accessible to both receptor-mediated and fluid phase internalization pathways, internalization was modestly inhibited in the presence of yeast mannan, a competitive inhibitor of mannose/fucose receptor activity, and substantially inhibited by dimethylamiloride, an inhibitor of macropinocytosis.	5-dimethylamiloride	290-307	heat shock protein 90, beta (Grp94), member 1	Mus musculus	5-10
9887007-8	1999	Interventions that load the cells with protons without affecting superfusate pH (NH4Cl prepulse, nigericin with low superfusate K+ concentration, DMA, and DIDS) all decreased pHi, supporting our contention that the dye was faithfully measuring pHi.	5-dimethylamiloride	146-149	glucose-6-phosphate isomerase	Rattus norvegicus	175-178
9657902-6	1998	Following acid loading in NaCl Ringers with a 20 mm NH4Cl prepulse, pHi recovery was partially inhibited by exposure to either Na-free (NMGCl) Ringers, 100 microM DMA or 20 microM bafilomycin A1.	5-dimethylamiloride	163-166	glucose-6-phosphate isomerase	Bos taurus	68-71
9425602-7	1997	Inhibition kinetics of NHE1 by amiloride, 5-(N,N-dimethyl)amiloride (DMA), 5-(N-hexamethyl)amiloride (HMA) and 5-(N-ethyl-N-isopropyl)amiloride (EIPA) were largely unchanged.	5-dimethylamiloride	69-72	solute carrier family 9 member A1	Homo sapiens	23-27
8760301-3	1996	We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak.	5-dimethylamiloride	245-273	colony stimulating factor 1	Homo sapiens	85-90
9453461-12	1997	Moreover, NPY caused a 22Na+ influx into the cells of about 1.6-fold over the basal value which was inhibited by amiloride and 5-(N,N-dimethyl)-amiloride, known Na+/Ca2+ exchange inhibitors.	5-dimethylamiloride	127-153	neuropeptide Y	Rattus norvegicus	10-13
8978356-5	1997	In groups 1-4, luminal 5-(N,N-dimethyl)-amiloride (DMA) was administered at doses of 100 nmol/L, 5 mumol/L, and 0.7 mmol/L to inhibit NHE1, NHE2, and NHE3, respectively.	5-dimethylamiloride	23-49	solute carrier family 9 member A3	Homo sapiens	150-154
8910773-2	1996	Long-term G-CSF-dependent proliferation was found to be completely inhibited by interferon-gamma (IFN-gamma), cyclic AMP, and dimethylamiloride and partially inhibited by IFN-alpha and lipopolysaccharide.	5-dimethylamiloride	126-143	colony stimulating factor 3 (granulocyte)	Mus musculus	10-15
9139940-6	1997	Treatment with T3 increased the rate of fall in pHi on exposure of the papillary muscles to DMA; when the buffer capacity was taken into account, the T3 treatment-induced increase in this rate corresponded well with the treatment-induced, DMA-inhibitable estimate of Na+ uptake.	5-dimethylamiloride	92-95	glucose-6-phosphate isomerase	Oryctolagus cuniculus	48-51
14646543-6	1997	The Na+/H+ antiporter inhibitor of 5-(N,N"-dimethyl)-amiloride inhibited the dexamethasone-induced increase in pHi and apoptosis of thymocytes.	5-dimethylamiloride	35-62	glucose-6-phosphate isomerase	Homo sapiens	111-114
8945936-6	1996	In control myocytes dialyzed with pHp 6.0, block of Na+/H+ exchange with 5-(N,N-dimethyl)-amiloride (DMA) or Na(+)-free external solution further reduced I(to) density compared with pHp 6.0 alone, whereas these treatments had less effect on acid-dialyzed cells from diabetic rats.	5-dimethylamiloride	101-104	FXYD domain-containing ion transport regulator 6	Rattus norvegicus	182-185
8945936-7	1996	Dialysis with pHp to 6.0 did not alter IK1 in either group of cells compared with standard pHp 7.2, but when done in the presence of DMA or Na(+)-free conditions, IK1 density in both groups was significantly reduced by nearly the same amount.	5-dimethylamiloride	133-136	potassium calcium-activated channel subfamily N member 4	Rattus norvegicus	163-166
8760301-3	1996	We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak.	5-dimethylamiloride	275-278	colony stimulating factor 1	Homo sapiens	85-90
7713887-7	1995	After inhibition of the Na+/H+ exchanger by dimethylamiloride, glucose produced a marked and sustained fall in pHi in HEPES buffer.	5-dimethylamiloride	44-61	glucose-6-phosphate isomerase 1	Mus musculus	111-114
8672233-5	1996	The results indicate that both fish and human Ang II stimulate the DMA-sensitive Na+/H+ antiporter present in eel intestinal cells by means of a mammalian AT1-like receptor.	5-dimethylamiloride	67-70	angiotensinogen	Homo sapiens	46-52
8805791-6	1996	Specifically, inhibition of the Na+/H+ exchanger with dimethylamiloride or HOE694 delayed the return of physiologic pH(i) after reperfusion and prevented reperfusion-induced cell killing to both cultured myocytes and perfused papillary muscle.	5-dimethylamiloride	54-71	glucose-6-phosphate isomerase	Homo sapiens	116-118
7503797-6	1995	The proton release induced by either ferricyanide or diferric transferrin was inhibited by about 35% at a near optimal amiloride concentration of 0.2 mM or at a dimethylamiloride concentration of 0.075 mM.	5-dimethylamiloride	161-178	transferrin	Homo sapiens	62-73
8388419-4	1993	When Na+/H+ exchange was blocked with 10 microM DMA, the pHi of NKC bound to NK-sensitive K562 target cells progressively decreased for 3 to 4 min, then stabilized at 0.1 to 0.15 pH units below the pHi of NKU.	5-dimethylamiloride	48-51	glucose-6-phosphate isomerase	Homo sapiens	57-60
7604180-7	1995	This basolateral Na(+)-dependent pHi recovery in the presence of HCO3-/CO2 was reduced, but present, in experiments where dimethylamiloride (DMA, 100 microM) or the stilbene derivative DIDS (500 microM) was in basolateral fluid.	5-dimethylamiloride	122-139	glucose-6-phosphate isomerase	Homo sapiens	33-36
7604180-7	1995	This basolateral Na(+)-dependent pHi recovery in the presence of HCO3-/CO2 was reduced, but present, in experiments where dimethylamiloride (DMA, 100 microM) or the stilbene derivative DIDS (500 microM) was in basolateral fluid.	5-dimethylamiloride	141-144	glucose-6-phosphate isomerase	Homo sapiens	33-36
8315350-6	1993	The response to fMLP did not change with the duration of incubation and, as with neutrophils, cytoplasmic realkalinization was blocked by dimethylamiloride (20 microM).	5-dimethylamiloride	138-155	formyl peptide receptor 1	Homo sapiens	16-20
8315350-8	1993	In addition, monocytes isolated from the blood of a patient with X-linked chronic granulomatous disease (CGD) underwent fMLP-induced acidification that was unmasked further by coincubation with dimethylamiloride, in a manner quantitatively similar to that of normal monocytes, despite the inability of the CGD cells to produce superoxide.	5-dimethylamiloride	194-211	formyl peptide receptor 1	Homo sapiens	120-124
8315350-9	1993	The chemotactic factor-induced cytoplasmic pH responses of monocytes/macrophages remained constant as the cells matured in vitro and exhibited a dimethylamiloride-independent acidification and dependent alkalinization, as did the response in neutrophils.	5-dimethylamiloride	145-162	glucose-6-phosphate isomerase	Homo sapiens	43-45
7507013-5	1994	In contrast, the amiloride derivative 5-(N,N-dimethyl)-amiloride, more specific for Na+/H+ exchanges, slightly increased the IL-3-enhanced release.	5-dimethylamiloride	38-64	interleukin 3	Homo sapiens	125-129
8388419-4	1993	When Na+/H+ exchange was blocked with 10 microM DMA, the pHi of NKC bound to NK-sensitive K562 target cells progressively decreased for 3 to 4 min, then stabilized at 0.1 to 0.15 pH units below the pHi of NKU.	5-dimethylamiloride	48-51	glucose-6-phosphate isomerase	Homo sapiens	198-201
8388419-8	1993	Manipulations of HCO3- and DMA that clamped NKC pHi at values ranging from 6.8 to 7.2 failed to significantly influence NK cell cytolytic function.	5-dimethylamiloride	27-30	glucose-6-phosphate isomerase	Homo sapiens	48-51
1335727-9	1992	Moreover, although dimethylamiloride and DIDS reduced the rate of recovery to 0.06 +/- 0.02 and 0.18 +/- 0.04 pH units respectively during the 2-min period, the cells returned to the basal pHi within 15 min.	5-dimethylamiloride	19-36	glucose-6-phosphate isomerase	Rattus norvegicus	110-112
1335727-9	1992	Moreover, although dimethylamiloride and DIDS reduced the rate of recovery to 0.06 +/- 0.02 and 0.18 +/- 0.04 pH units respectively during the 2-min period, the cells returned to the basal pHi within 15 min.	5-dimethylamiloride	19-36	glucose-6-phosphate isomerase	Rattus norvegicus	189-192
1322838-4	1992	The effect of bradykinin is completely abolished in the presence of dimethylamiloride (100 mumol/l), which does not modify pHi in the absence of bradykinin.	5-dimethylamiloride	68-85	kininogen 1	Homo sapiens	14-24
1310209-3	1992	In the absence of HCO3-, inhibition of the Na(+)-H+ exchanger by dimethylamiloride (DMA) or removal of extracellular Na+ produced substantial acidification of basal pHi.	5-dimethylamiloride	65-82	glucose-6-phosphate isomerase	Rattus norvegicus	165-168
1320336-7	1992	Restoration of pH(i) was Na+ dependent and inhibited by dimethyl amiloride (concentration that produces half-maximal inhibition, K0.5 = 30 microM), features characteristic of Na(+)-H+ exchange.	5-dimethylamiloride	56-74	glucose-6-phosphate isomerase	Rattus norvegicus	15-20
1310209-3	1992	In the absence of HCO3-, inhibition of the Na(+)-H+ exchanger by dimethylamiloride (DMA) or removal of extracellular Na+ produced substantial acidification of basal pHi.	5-dimethylamiloride	84-87	glucose-6-phosphate isomerase	Rattus norvegicus	165-168
1310209-7	1992	In the absence of HCO3-, Na+ removal or DMA addition blocked greater than 80% of pHi recovery.	5-dimethylamiloride	40-43	glucose-6-phosphate isomerase	Rattus norvegicus	81-84
1310209-8	1992	In the presence of HCO3-, 34% of the pHi recovery rate was inhibited by 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS), 34% by DMA, and 72% by Na+ removal plus DIDS.	5-dimethylamiloride	136-139	glucose-6-phosphate isomerase	Rattus norvegicus	37-40
1645954-2	1991	Inhibition of the Na+/H(+)-antiporter by dimethylamiloride or a reduction of external Na(+)-concentrations attenuates the increases in pHi and [Ca2+]i.	5-dimethylamiloride	41-58	glucose-6-phosphate isomerase	Homo sapiens	135-138
1649743-8	1991	The EGF-induced pHi change was also inhibited by amiloride, dimethyl amiloride, and ethylisopropyl amiloride, inhibitors of the Na+/H+ antiporter.	5-dimethylamiloride	60-78	epidermal growth factor	Gallus gallus	4-7
2170361-4	1990	The response to CSF-1 is maintained for at least 24 h. Inhibition of Na+/H+ exchange with 5-N,N-dimethylamiloride prevents CSF-1-stimulated DNA synthesis and cell growth.	5-dimethylamiloride	90-113	colony stimulating factor 1 (macrophage)	Mus musculus	16-21
2170361-4	1990	The response to CSF-1 is maintained for at least 24 h. Inhibition of Na+/H+ exchange with 5-N,N-dimethylamiloride prevents CSF-1-stimulated DNA synthesis and cell growth.	5-dimethylamiloride	90-113	colony stimulating factor 1 (macrophage)	Mus musculus	123-128
2154448-2	1990	When the activation of the Na+/H+ antiporter which occurs in mitogen-stimulated Swiss 3T3 fibroblasts or murine fibroblasts is completely blocked by dimethylamiloride, there is little or no effect on the phosphorylation of the ribosomal protein S6 or the activation of protein synthesis assayed by [35S]methionine incorporation.	5-dimethylamiloride	149-166	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	27-44
2169700-4	1990	An inhibition of the Na+/H(+)-antiporter by dimethylamiloride or a reduction of the extracellular [Na+] concentration results in a depression of the bombesin induced release of Ca2+ from intracellular stores.	5-dimethylamiloride	44-61	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	21-40
2169700-4	1990	An inhibition of the Na+/H(+)-antiporter by dimethylamiloride or a reduction of the extracellular [Na+] concentration results in a depression of the bombesin induced release of Ca2+ from intracellular stores.	5-dimethylamiloride	44-61	gastrin releasing peptide	Homo sapiens	149-157