PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
10050042-3	1999	The GlcNAc residue linked to the Manalpha1-3 branch of BA-2 is lacking in BA-1 and the removal of this GlcNAc residue is not part of the usual biosynthetic pathway for N-linked sugar chains, suggesting the existence of an N-acetyl-beta-D-hexosaminidase.	Sugars	177-182	bone area 2	Mus musculus	55-59
6308221-8	1983	Muscle paralysed by Ba2+ responded to caffeine (25 mM) or K+ (100-200 mM) with a contracture.	Caffeine	38-46	bone area 2	Mus musculus	20-23
6308221-9	1983	The Ca2+ channel blocker verapamil did not prevent paralysis and, in fact, enhanced Ba2+ depression of tetani.	Verapamil	25-34	bone area 2	Mus musculus	84-87
29741368-2	2018	Substitution of divalent Ba2+ by trivalent Sb3+ leads to an increase in interstitial fluoride-ion concentration, which enhances the ionic conductivity of the Ba1- xSb xF2+ x (0.1 <= x <= 0.4) system.	Fluorides	85-93	bone area 2	Mus musculus	25-28
32144179-7	2020	Functionally, deletion of Bbeta2 and maintained Drp1 Ser637 phosphorylation improved mitochondrial respiratory capacity, Ca2+ homeostasis, and attenuated superoxide production in response to ischemia and excitotoxicity in vitro and ex vivo Lastly, deletion of Bbeta2 rescued excessive stroke damage associated with dephosphorylation of Drp1 S637 and mitochondrial fission.	Superoxides	154-164	bone area 2	Mus musculus	26-32
10050042-10	1999	BA-2-PA was detected in all the PA-sugar chain fractions prepared from Hexa, Hexb, and both Hexa and Hexb (double knockout) gene-disrupted mice, but BA-1 was not found in the fractions from Hexb gene-disrupted and double knockout mice.	Sugars	35-40	bone area 2	Mus musculus	0-7
2242386-4	1990	Furosemide, an inhibitor of Na+, K+, Cl- co-transport, reduced the 86Rb+ influx and the effect was partly additive to the effect of 2 mM Ba2+.	Furosemide	0-10	bone area 2	Mus musculus	137-140
10050042-3	1999	The GlcNAc residue linked to the Manalpha1-3 branch of BA-2 is lacking in BA-1 and the removal of this GlcNAc residue is not part of the usual biosynthetic pathway for N-linked sugar chains, suggesting the existence of an N-acetyl-beta-D-hexosaminidase.	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	4-10	bone area 2	Mus musculus	55-59
10050042-3	1999	The GlcNAc residue linked to the Manalpha1-3 branch of BA-2 is lacking in BA-1 and the removal of this GlcNAc residue is not part of the usual biosynthetic pathway for N-linked sugar chains, suggesting the existence of an N-acetyl-beta-D-hexosaminidase.	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	103-109	bone area 2	Mus musculus	55-59
10050042-3	1999	The GlcNAc residue linked to the Manalpha1-3 branch of BA-2 is lacking in BA-1 and the removal of this GlcNAc residue is not part of the usual biosynthetic pathway for N-linked sugar chains, suggesting the existence of an N-acetyl-beta-D-hexosaminidase.	Nitrogen	7-8	bone area 2	Mus musculus	55-59
2100304-11	1990	Quinine (0.5-2 mM) blocked the outward currents in embryonic cells and Ba2+ (2 mM) blocked both outward and inward currents in neonatal myelinating cells leaving quinine-sensitive outward currents of the embryonic type.	Quinine	162-169	bone area 2	Mus musculus	71-74
2242386-2	1990	Ba2+ (2 mM) significantly reduced the ouabain-resistant 86Rb+ influx, without affecting the ouabain-sensitive influx.	Rubidium-86	56-61	bone area 2	Mus musculus	0-3
2242386-3	1990	D-Glucose (20 mM) reduced the 86Rb+ influx in the absence of Ba2+ (2 mM) but not in the presence of the cation.	Glucose	0-9	bone area 2	Mus musculus	61-64
9604006-1	1998	We previously detected a fucosylagalactobiantenna with a bisecting GlcNAc residue (BA-2) and one lacking the GlcNAc residue linked to the Manalpha1-3 residue of BA-2 (BA-1), which were enriched specifically in mouse brain [Shimizu, H., Ochiai, K., Ikenaka, K., Mikoshiba, K., and Hase, S. (1993) J. Biochem.	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	67-73	bone area 2	Mus musculus	83-87
9359588-2	1997	Opioid agonists selective for either mu (Tyr-D-Ala-Gly-Mephe-Gly-ol; DAMGO) or delta (Tyr-D-Pen-Gly-Phe-D-Pen-OH; DPDPE) receptors inhibited high-threshold Ba2+ currents.	Enkephalin, Ala(2)-MePhe(4)-Gly(5)-	41-67	bone area 2	Mus musculus	156-159
9359588-6	1997	In contrast, the L-type Ca2+ channel blocker nifedipine inhibited high threshold Ba2+ currents by 15% and failed to block the inhibitory effect of DAMGO or DPDPE.	Nifedipine	45-55	bone area 2	Mus musculus	81-84
9134988-2	1997	Low concentrations (< nM) of most opioid receptor agonists decrease the K+ conductance (gK) in cultures of dissociated mouse dorsal root ganglion neurons regardless of the presence of Ba2+ However, low concentrations of etorphine, in contrast to all other opioids tested, decreased gK only in the absence of Ba2+.	Etorphine	223-232	bone area 2	Mus musculus	311-314
9134988-3	1997	In the presence of Ba2+, pM-nM etorphine elicited dose-dependent increases, instead of decreases in gK.	Etorphine	31-40	bone area 2	Mus musculus	19-22
9134988-4	1997	Higher concentrations of etorphine (> nM) not only increased gK but, in addition, appreciably increased a delayed-onset inward Ca2+ current during pulsed depolarization regardless of the presence of Ba2+.	Etorphine	25-34	bone area 2	Mus musculus	202-205
2242386-4	1990	Furosemide, an inhibitor of Na+, K+, Cl- co-transport, reduced the 86Rb+ influx and the effect was partly additive to the effect of 2 mM Ba2+.	Rubidium-86	67-72	bone area 2	Mus musculus	137-140
2242386-5	1990	When the islets were preincubated with Ba2+ (2 mM) the specific effect of 1 mM furosemide on the 86Rb+ influx was reduced, whereas, in acute experiments, Ba2+ (2 mM) did not affect the specific effect of furosemide on 86Rb+ influx.	Furosemide	79-89	bone area 2	Mus musculus	39-42
2242386-5	1990	When the islets were preincubated with Ba2+ (2 mM) the specific effect of 1 mM furosemide on the 86Rb+ influx was reduced, whereas, in acute experiments, Ba2+ (2 mM) did not affect the specific effect of furosemide on 86Rb+ influx.	Rubidium-86	97-102	bone area 2	Mus musculus	39-42
2242386-5	1990	When the islets were preincubated with Ba2+ (2 mM) the specific effect of 1 mM furosemide on the 86Rb+ influx was reduced, whereas, in acute experiments, Ba2+ (2 mM) did not affect the specific effect of furosemide on 86Rb+ influx.	Furosemide	204-214	bone area 2	Mus musculus	39-42
2242386-5	1990	When the islets were preincubated with Ba2+ (2 mM) the specific effect of 1 mM furosemide on the 86Rb+ influx was reduced, whereas, in acute experiments, Ba2+ (2 mM) did not affect the specific effect of furosemide on 86Rb+ influx.	Rubidium-86	218-223	bone area 2	Mus musculus	39-42
2242386-6	1990	86Rb+ efflux from preloaded islets was significantly reduced by 2 mM Ba2+ and during the first 5 min of ion efflux the effect of the combination of 2 mM Ba2+ and 1 mM furosemide was stronger than the effect of Ba2+ alone.	Rubidium-86	0-5	bone area 2	Mus musculus	69-72
2242386-6	1990	86Rb+ efflux from preloaded islets was significantly reduced by 2 mM Ba2+ and during the first 5 min of ion efflux the effect of the combination of 2 mM Ba2+ and 1 mM furosemide was stronger than the effect of Ba2+ alone.	Rubidium-86	0-5	bone area 2	Mus musculus	153-156
2242386-6	1990	86Rb+ efflux from preloaded islets was significantly reduced by 2 mM Ba2+ and during the first 5 min of ion efflux the effect of the combination of 2 mM Ba2+ and 1 mM furosemide was stronger than the effect of Ba2+ alone.	Rubidium-86	0-5	bone area 2	Mus musculus	153-156
2242386-6	1990	86Rb+ efflux from preloaded islets was significantly reduced by 2 mM Ba2+ and during the first 5 min of ion efflux the effect of the combination of 2 mM Ba2+ and 1 mM furosemide was stronger than the effect of Ba2+ alone.	Furosemide	167-177	bone area 2	Mus musculus	69-72
2242386-7	1990	The data show that Ba2+ reduces 86Rb+ fluxes in the beta-cells and suggest that this is mainly mediated by inhibition of K+ channels in the beta-cell plasma membrane.	Rubidium-86	32-37	bone area 2	Mus musculus	19-22
2372542-2	1990	Plasma membranes were solubilized in cholate/urea and reconstituted with Ba2(+)-precipitated asolectin (soybean phospholipid free of anionic phospholipids) replenished with different acidic phospholipids.	Phospholipids	112-124	bone area 2	Mus musculus	73-76
2372542-4	1990	However, three acidic lipids [cardiolipin greater than phosphatidic acid (PA) greater than phosphatidylinositol] were capable of restoring transport activity (in the order given) to proteoliposomes made from Ba2(+)-precipitated asolectin, while other acidic phospholipids (phosphatidylserine and phosphatidylglycerol) were much less active in this respect.	Cardiolipins	30-41	bone area 2	Mus musculus	208-211