PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
11232243-2	2000	An anti-CD95 antibody caused apoptosis associated with intracellular GSH depletion, a significant increase in 86Rb+ efflux, and a decrease in cell volume compared with control cells.	Rubidium-86	110-115	Fas cell surface death receptor	Homo sapiens	8-12
11232243-6	2000	Ouabain induced significant 86Rb+ efflux in untreated cells, as well as it seemed to compete with 86Rb+ efflux induced by the anti-CD95 antibody, supporting a role for Na+/K(+)-ATPase in the CD95-mediated 86Rb+ efflux.	Rubidium-86	98-102	Fas cell surface death receptor	Homo sapiens	131-135
11334374-0	2000	Angiotensin II activates a bumetanide sensitive increase in 86RB+ efflux in the rat heart.	Rubidium-86	60-64	angiotensinogen	Rattus norvegicus	0-14
10698206-5	2000	In this study we use 3T3-L1 fibroblasts to show that leptin inhibits Na,K-pump activity, as assessed by ouabain-sensitive 86Rb+ uptake.	Rubidium-86	122-127	leptin	Homo sapiens	53-59
11334374-5	2000	Angiotensin II induced a maximal increase in 86Rb+ efflux rate of 13+/-1.6% (n=12, p<0.0001).	Rubidium-86	45-49	angiotensinogen	Rattus norvegicus	0-14
10347194-6	1999	The expression of mouse KCC3 in Xenopus laevis oocytes reveals the expected functional characteristics of a K+Cl- cotransporter: Cl--dependent uptake of 86Rb+ which is strongly activated by cell swelling and weakly sensitive to furosemide.	Rubidium-86	153-158	solute carrier family 12, member 6	Mus musculus	24-28
10484519-8	1999	These data suggest that TNF-mediated induction of COX-2 protein expression accounted for the lag-time required for this cytokine to inhibit 86Rb uptake in MTAL cells.	Rubidium-86	140-144	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	50-55
10484519-7	1999	The time-dependent inhibition of 86Rb uptake by MTAL cells challenged with TNF was diminished by pretreating cells with NS-398.	Rubidium-86	33-37	tumor necrosis factor	Homo sapiens	75-78
10484519-8	1999	These data suggest that TNF-mediated induction of COX-2 protein expression accounted for the lag-time required for this cytokine to inhibit 86Rb uptake in MTAL cells.	Rubidium-86	140-144	tumor necrosis factor	Homo sapiens	24-27
10440258-6	1999	The inhibitory effect of thrombin on ouabain-sensitive potassium (86Rb) uptake was suppressed in the presence of hirudin (an antagonist for thrombin receptors) but persisted in the presence of amphotericin B (a pseudo ionophore that effectively clamps plasma membrane sodium permeability at a high value).	Rubidium-86	66-70	coagulation factor II, thrombin	Homo sapiens	25-33
10440258-6	1999	The inhibitory effect of thrombin on ouabain-sensitive potassium (86Rb) uptake was suppressed in the presence of hirudin (an antagonist for thrombin receptors) but persisted in the presence of amphotericin B (a pseudo ionophore that effectively clamps plasma membrane sodium permeability at a high value).	Rubidium-86	66-70	coagulation factor II, thrombin	Homo sapiens	140-148
10440258-9	1999	Both genistein and herbimycin (tyrosine kinase inhibitors) suppressed the effect of thrombin on the 86Rb uptake response.	Rubidium-86	100-104	coagulation factor II, thrombin	Homo sapiens	84-92
10362601-2	1999	The activity of NKCC1 was measured as the bumetanide-sensitive efflux of 86Rb+ from intact smooth muscle of the rat aorta.	Rubidium-86	73-78	solute carrier family 12 member 2	Rattus norvegicus	16-21
10198422-5	1999	The NOS2-transfected cells allowed to produce NO continuously (vehicle or D-NAME) exhibited lower rates of ouabain-sensitive 86Rb+ uptake ( approximately 65%), lower levels of Na+-K+-ATPase alpha1-subunit mRNA ( approximately 60%), and reduced rates of de novo Na+-K+-ATPase alpha1-subunit transcription compared with L-NAME-treated cells.	Rubidium-86	125-130	nitric oxide synthase 2	Homo sapiens	4-8
9864342-9	1999	Uptake of 86Rb+ by intact trk1Delta trk2Delta cells was inhibited by extracellular Ca2+ with a Ki within the range observed for the inward current.	Rubidium-86	10-15	Trk1p	Saccharomyces cerevisiae S288C	26-30
9950760-3	1999	Bumetanide inhibited 86Rb efflux in KCC1-HEK cells after cell swelling [inhibition constant (Ki) approximately 190 microM] and pretreatment with NEM (Ki approximately 60 microM).	Rubidium-86	21-25	solute carrier family 12 member 4	Homo sapiens	36-40
9458834-3	1998	ANG II also increased prostaglandin E2 (PGE2) production by the MTAL in a dose-dependent manner and exerted biphasic differential effects on 86Rb uptake, depending on the exposure time of the tubules to the peptide and the doses used.	Rubidium-86	141-145	angiotensinogen	Homo sapiens	0-6
9683454-8	1998	PD-98059, an inhibitor of the ERK cascade, reduced both the increased 86Rb+ efflux and ERK activity.	Rubidium-86	70-74	Eph receptor B1	Rattus norvegicus	30-33
9916138-3	1999	Trypsin and activating peptide (AP or SLIGRL-NH2, corresponding to the PAR-2 tethered ligand) stimulated both an 125I- efflux inhibited by Ca2+-activated Cl- channel inhibitors and a 86Rb+ efflux inhibited by a Ca2+-activated K+ channel inhibitor.	Rubidium-86	183-188	F2R like trypsin receptor 1	Canis lupus familiaris	71-76
9774385-3	1998	However, the 86Rb+-influx mediated by the ATP1AL1-gH,Kbeta heterodimer in HEK 293 cells is at least 1 order of magnitude larger than the maximum ouabain-sensitive proton efflux detected in the same cells.	Rubidium-86	13-18	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	42-49
9774385-7	1998	Finally, 86Rb+ influx through the ATP1AL1-gH,Kbeta complex is comparable to the 1 mM ouabain-sensitive Na+ efflux in the same cells.	Rubidium-86	9-14	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	34-41
9794108-2	1998	Treatment of 3T3-L1 fibroblasts with insulin increased total 86Rb+ (K+) uptake from 0.8 +/- 0.04 to 1.02 +/- 0.05 nmol.mg-1.protein-1.min-1 (p < 0.005).	Rubidium-86	61-66	insulin	Homo sapiens	37-44
9486222-2	1998	The basal net secretory flux of 86Rb+ (as a tracer for K+) across the CRF distal colon (-0.20 +/- 0.04 mu eq.cm-2.h-1) was reversed to an absorptive flux (0.35 +/- 0.05 mu eq.cm-2.h-1) by injecting the rats with the AT1 receptor antagonist, losartan.	Rubidium-86	32-37	angiotensin II receptor, type 1a	Rattus norvegicus	216-219
9446567-3	1998	HgTX1 inhibits 125I-margatoxin binding to rat brain membranes as well as depolarization-induced 86Rb+ flux through homotetrameric Kv1.1, Kv1.	Rubidium-86	96-101	potassium voltage-gated channel subfamily A member 1	Rattus norvegicus	130-135
9446567-3	1998	HgTX1 inhibits 125I-margatoxin binding to rat brain membranes as well as depolarization-induced 86Rb+ flux through homotetrameric Kv1.1, Kv1.	Rubidium-86	96-101	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	130-133
9458834-4	1998	Low-dose ANG II (10(-11) M) increased 86Rb uptake by MTAL tubules after a "short-term" (15 min) challenge, whereas uptake was inhibited after a "long-term" (3 h) incubation period.	Rubidium-86	38-42	angiotensinogen	Homo sapiens	9-15
9458834-5	1998	High-dose ANG II (10(-6) M) inhibited MTAL 86Rb uptake, irrespective of incubation time.	Rubidium-86	43-47	angiotensinogen	Homo sapiens	10-16
9458834-6	1998	Uptake of 86Rb was inhibited by approximately 60% in MTAL tubules that were challenged for 3 h with ANG II.	Rubidium-86	10-14	angiotensinogen	Homo sapiens	100-106
9458834-8	1998	We conclude that ANG II regulates TNF production in the MTAL, an interaction that affects 86Rb uptake via an eicosanoid-dependent mechanism in this nephron segment.	Rubidium-86	90-94	angiotensinogen	Homo sapiens	17-23
9374636-7	1997	This diuretic-sensitive 86Rb influx in the KCC2-9 cells, operationally defined as KCC2 mediated, required external Cl- but not external Na+ and exhibited a high apparent affinity for external Rb+(K+) [Michaelis constant (Km) = 5.2 +/- 0.9 (SE) mM; n = 5] but a low apparent affinity for external Cl- (Km > 50 mM).	Rubidium-86	24-28	solute carrier family 12 member 5	Homo sapiens	43-47
9481677-9	1998	This Na+ gain is in good agreement with the stimulation of Na+ extrusion via Na(+)-K(+)-ATPase plus the actual increase in cell Na+, namely 55 mmol l-1 (10 min)-1, as we determined on the basis of ouabain-sensitive 86Rb+ uptake and by means of Na(+)-sensitive microelectrodes, respectively.	Rubidium-86	215-220	ribosomal protein L4	Rattus norvegicus	148-162
9414032-10	1997	In conclusion, the phenylephrine stimulated increase in 86Rb+ efflux in the rat heart is not specifically linked to only one of the alpha1-adrenoceptor subtypes, but involves the alpha1B- and the alpha1D-adrenoceptor subtypes, and probably the alpha1A-adrenoceptor subtype as well.	Rubidium-86	56-61	adrenoceptor alpha 1D	Rattus norvegicus	196-216
9414032-10	1997	In conclusion, the phenylephrine stimulated increase in 86Rb+ efflux in the rat heart is not specifically linked to only one of the alpha1-adrenoceptor subtypes, but involves the alpha1B- and the alpha1D-adrenoceptor subtypes, and probably the alpha1A-adrenoceptor subtype as well.	Rubidium-86	56-61	adrenoceptor alpha 1A	Rattus norvegicus	244-264
9337640-7	1997	Thrombin (0.1-0.6 i.u./ml) stimulated an increase in 86Rb+ efflux from the platelets in a concentration-dependent manner.	Rubidium-86	53-58	coagulation factor II, thrombin	Homo sapiens	0-8
9337640-16	1997	These findings suggest that 86Rb+ efflux from platelets stimulated by thrombin and ionomycin occurs via two types of KCa channel: SKCa and KCh channels.	Rubidium-86	28-33	coagulation factor II, thrombin	Homo sapiens	70-78
9452948-5	1997	The ouabain-sensitive component of 86Rb influx was also higher in K(+)-(Kin = 0.62 +/- 0.05 h-1) than in Rb(+)-medium (Kin = 0.54 +/- 0.05 h-1, P < 0.05).	Rubidium-86	35-39	Kin17 DNA and RNA binding protein	Homo sapiens	72-75
9452948-5	1997	The ouabain-sensitive component of 86Rb influx was also higher in K(+)-(Kin = 0.62 +/- 0.05 h-1) than in Rb(+)-medium (Kin = 0.54 +/- 0.05 h-1, P < 0.05).	Rubidium-86	35-39	Kin17 DNA and RNA binding protein	Homo sapiens	119-122
9282914-6	1997	In addition, concentrations of (+/-)-epibatidine, similar to those necessary to induce maximal 86Rb+ efflux, evoked spontaneous release of SP from these cells, which was blocked by mecamylamine.	Rubidium-86	95-100	tachykinin precursor 1	Homo sapiens	139-141
9374636-7	1997	This diuretic-sensitive 86Rb influx in the KCC2-9 cells, operationally defined as KCC2 mediated, required external Cl- but not external Na+ and exhibited a high apparent affinity for external Rb+(K+) [Michaelis constant (Km) = 5.2 +/- 0.9 (SE) mM; n = 5] but a low apparent affinity for external Cl- (Km > 50 mM).	Rubidium-86	24-28	solute carrier family 12 member 5	Homo sapiens	82-86
9128849-14	1997	We conclude that whereas the alpha 1-adrenoceptor-stimulated increase in 86Rb+ influx rate is mediated via the alpha 1A-adrenoceptor subtype only, both alpha 1A- and alpha 1B-adrenoceptor subtypes are involved in the increase in IP3 mass.	Rubidium-86	73-78	adrenoceptor alpha 1A	Rattus norvegicus	111-132
9159841-7	1997	After 60 minutes the ouabain-sensitive 86Rb uptake (cpm/10(4) cells) was increased from 6650 +/- 796 in control cells to 9763 +/- 1212 in HPMC exposed to 100 mU/mL insulin (1.5-fold increase; n = 4, P < 0.05).	Rubidium-86	39-43	insulin	Homo sapiens	164-171
9038823-5	1997	The apical localization of BSC2 in the CP was confirmed by 86Rb+ uptakes in primary cultures of CP cells grown on permeable filters and confocal immunofluorescence microscopy.	Rubidium-86	59-64	solute carrier family 12 member 2	Rattus norvegicus	27-31
9446185-1	1997	The uptake of 86Rb+ ions by human erythrocytes as the measure of inhibition or stimulation of Na+, K(+)-ATPase by synthetic brassinolides, steroid fytohormonal promotors, was determined.	Rubidium-86	14-19	dynein axonemal heavy chain 8	Homo sapiens	104-110
8853415-9	1996	Moreover, whereas the acid extrusion activity mediated by the pump shows a marked pH dependence, the 86Rb+ uptake activity present in the cells expressing the ATP1AL1-gH-K beta complex cannot be stimulated by acute lowering of pHi.	Rubidium-86	101-106	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	159-166
8877285-11	1996	In addition, ET-1 transiently enhanced 86Rb(+)-efflux from 86Rb(+)-prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca2+ suggesting that ET-1 does not elicit insulin secretion by inhibition of the potassium permeability.	Rubidium-86	39-46	endothelin 1	Mus musculus	13-17
8876673-5	1996	Compared with parental cotransport-deficient cells, transfected clones expressing the exogenous NKCC1 gene responded like typical BALB/c 3T3 cells to 12-O-tetradecanoylphorbol-13-acetate: loop diuretic-sensitive 86Rb+ flux was inhibited, cell volume was decreased, and cell growth was stimulated.	Rubidium-86	212-217	solute carrier family 12, member 2	Mus musculus	96-101
8760039-4	1996	In a suspension of rat kidney cortical tubules, activation of PKC by 10(-7) M PDBu increased the level of phosphorylation of the Na(+)-K(+)-ATPase alpha-subunit and stimulated the ouabain-sensitive 86Rb uptake by 47 and 42%, respectively.	Rubidium-86	198-202	protein kinase C, gamma	Rattus norvegicus	62-65
8584442-3	1996	In primary cultures of rabbit proximal tubule, porcine aortic endothelial cells, and rat vascular smooth muscle cells, expression of the second isoform BSC2 was demonstrated by Northern blot analysis and bumetanide-sensitive 86Rb+ uptake studies.	Rubidium-86	225-230	solute carrier family 12 member 2	Rattus norvegicus	152-156
8877285-11	1996	In addition, ET-1 transiently enhanced 86Rb(+)-efflux from 86Rb(+)-prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca2+ suggesting that ET-1 does not elicit insulin secretion by inhibition of the potassium permeability.	Rubidium-86	39-46	endothelin 1	Mus musculus	194-198
9044903-6	1996	The combination of IL-1 alpha and TNF-alpha reduced the 86Rb uptake to 41% bf control.	Rubidium-86	56-60	interleukin 1 alpha	Mus musculus	19-29
9044903-6	1996	The combination of IL-1 alpha and TNF-alpha reduced the 86Rb uptake to 41% bf control.	Rubidium-86	56-60	tumor necrosis factor	Mus musculus	34-43
8621717-1	1996	We have recently described an ATP-driven, valinomycin-dependent 86Rb+uptake into proteoliposomes reconstituted with mammalian P-glycoprotein (Eytan, G. D., Borgnia, M. J., Regev, R., and Assaraf, Y. G. (1994) J. Biol.	Rubidium-86	64-69	ATP binding cassette subfamily B member 1	Homo sapiens	126-140
8621717-4	1996	P-glycoprotein mediated the ATP-dependent uptake of 86Rb+-ionophore complex into the proteoliposomes, where the radioactive cation was accumulated, thus, circumventing the obstacle posed by the hydrophobicity of P-glycoprotein substrates in transport studies.	Rubidium-86	52-57	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
8621717-4	1996	P-glycoprotein mediated the ATP-dependent uptake of 86Rb+-ionophore complex into the proteoliposomes, where the radioactive cation was accumulated, thus, circumventing the obstacle posed by the hydrophobicity of P-glycoprotein substrates in transport studies.	Rubidium-86	52-57	ATP binding cassette subfamily B member 1	Homo sapiens	212-226
8621717-6	1996	The amount of 86Rb+ ions transported within 1 min via the ATP- and valinomycin-dependent P-glycoprotein was equivalent to an intravesicular cation concentration of 8 mM.	Rubidium-86	14-19	ATP binding cassette subfamily B member 1	Homo sapiens	89-103
8927619-5	1996	Similarly, GRP increased 86Rb+ efflux from 86Rb(+)-prelabeled islets both in the presence and in the absence of extracellular Ca2+ (p < 0.001).	Rubidium-86	43-50	gastrin releasing peptide	Mus musculus	11-14
8927619-6	1996	In contrast to GRP-induced insulin secretion, the GRP-induced 86Rb+ efflux was sustained throughout the stimulation period, suggesting that increased K+ conductance may be involved in the vanishing effect of GRP on insulin secretion.	Rubidium-86	62-67	gastrin releasing peptide	Mus musculus	50-53
8927619-6	1996	In contrast to GRP-induced insulin secretion, the GRP-induced 86Rb+ efflux was sustained throughout the stimulation period, suggesting that increased K+ conductance may be involved in the vanishing effect of GRP on insulin secretion.	Rubidium-86	62-67	gastrin releasing peptide	Mus musculus	50-53
8584416-5	1995	86Rb and 36Cl uptake experiments confirmed the presence of a bumetanide- and a NPPB-sensitive Cl- pathway, the latter being approximately three times more important than the former (Na/K/2Cl cotransporter).	Rubidium-86	0-4	natriuretic peptide B	Homo sapiens	79-83
8786359-8	1995	Accordingly, secretin increased total 86Rb uptake more than the Ca(2+)-mobilizing agonists and the apparent coupling between the NaK2Cl cotransport and the Na+ pump.	Rubidium-86	38-42	secretin	Homo sapiens	13-21
7561853-1	1995	The effect of endothelins (ET-1 and ET-3) on 86Rb+ uptake as a measure of K+ uptake was investigated in cultured rat brain capillary endothelium.	Rubidium-86	45-50	endothelin 1	Rattus norvegicus	14-25
7561853-1	1995	The effect of endothelins (ET-1 and ET-3) on 86Rb+ uptake as a measure of K+ uptake was investigated in cultured rat brain capillary endothelium.	Rubidium-86	45-50	endothelin 1	Rattus norvegicus	27-40
8005795-5	1994	The 86Rb uptake in the SCK tumor slightly increased 30 min after an IP injection of 50 mg/kg PTX.	Rubidium-86	4-8	SHC adaptor protein 2	Homo sapiens	23-26
7485470-6	1995	The functional properties of the stable alpha/beta-complex were studied by 86Rb+ uptake and demonstrated that ATP1AL1 is a novel human K(+)-dependent ATPase [apparent half-constant activation/(K1/2) for K+ approximately 375 microM)].	Rubidium-86	75-80	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	110-117
7762637-3	1995	We show here that IGF-I increases 42K and 86Rb uptake and the efflux of 22Na in isolated rat soleus muscle.	Rubidium-86	42-46	insulin-like growth factor 1	Rattus norvegicus	18-23
7772716-9	1994	Taken together the results show that the hypothalamic NKA inhibitor blocks NKA of isolated human lymphocytes with high potency at nanomolar concentrations without toxicity; concentrations exceeding the ones required to block 86Rb-uptake reduce cell viability, probably due to leak formation across the NKA molecule.	Rubidium-86	225-229	tachykinin precursor 1	Homo sapiens	54-57
7496041-1	1995	Cells expressing a recombinant human voltage-activated potassium channel (K-channel), Kv1.5, have been used in a functional assay that measures depolarization-stimulated 86Rb+ efflux as an indicator of K-channel function.	Rubidium-86	170-175	potassium voltage-gated channel subfamily A member 5	Homo sapiens	86-91
7631748-3	1995	Insulin rapidly increased ion pump activity [ouabain-sensitive 86Rb+(K+) uptake] in 3T3-L1 fibroblasts and adipocytes without changing the plasma membrane concentration of alpha 1- or alpha 2-subunits as determined by subcellular membrane fractionation and immunoblotting or by [3H]ouabain binding to intact cells.	Rubidium-86	63-68	insulin	Homo sapiens	0-7
7631748-6	1995	Insulin increased both ouabain-sensitive and bumetanide-sensitive 86Rb+(K+) uptake.	Rubidium-86	66-71	insulin	Homo sapiens	0-7
7607721-3	1995	Angiotensin II and endothelin-1 increased ouabain-inhibitable 86Rb+ uptake more in SHR than WKY cells, whereas no effects were obtained with sodium nitroprusside, 8-bromo-cGMP, or iloprost.	Rubidium-86	62-67	angiotensinogen	Rattus norvegicus	0-14
7607721-3	1995	Angiotensin II and endothelin-1 increased ouabain-inhibitable 86Rb+ uptake more in SHR than WKY cells, whereas no effects were obtained with sodium nitroprusside, 8-bromo-cGMP, or iloprost.	Rubidium-86	62-67	endothelin 1	Rattus norvegicus	19-31
7782936-7	1995	Insulin also stimulates ouabain-sensitive 86Rb+ uptake (Na(+)-K+ pump activity) and does not inhibit VSM contraction in the presence of ouabain.	Rubidium-86	42-47	insulin	Canis lupus familiaris	0-7
8574808-4	1995	Anti-ouabain rabbit antiserum and anti-digoxin Fab fragments induced a significantly greater percentage change in 86Rb uptake in the erythrocytes than the two control sera (ANOVA followed by multiple comparison by the Games-Howell test).	Rubidium-86	114-118	FA complementation group B	Homo sapiens	47-50
7523400-2	1994	The peptide ionophores valinomycin and gramicidin D, which are known substrates of P-glycoprotein, served to monitor the P-glycoprotein activity indirectly as the ATP-dependent uptake of 86Rb+ mediated by these ionophores.	Rubidium-86	187-192	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	83-97
7523400-2	1994	The peptide ionophores valinomycin and gramicidin D, which are known substrates of P-glycoprotein, served to monitor the P-glycoprotein activity indirectly as the ATP-dependent uptake of 86Rb+ mediated by these ionophores.	Rubidium-86	187-192	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	121-135
7523400-6	1994	Maximal ATP-dependent 86Rb+ uptake occurred at 50 nM gramicidin D and at 500 nM valinomycin thus possibly reflecting higher affinity of P-glycoprotein for gramicidin D. Nigericin, which does not participate in the multidrug resistance phenomenon, did not support an ATP-dependent uptake of 86Rb+.	Rubidium-86	22-27	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-150
7523400-6	1994	Maximal ATP-dependent 86Rb+ uptake occurred at 50 nM gramicidin D and at 500 nM valinomycin thus possibly reflecting higher affinity of P-glycoprotein for gramicidin D. Nigericin, which does not participate in the multidrug resistance phenomenon, did not support an ATP-dependent uptake of 86Rb+.	Rubidium-86	290-295	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-150
7523400-9	1994	The ATP-dependent component of 86Rb+ uptake occurred neither with liposomes nor with proteoliposomes reconstituted with proteins extracted from sinusoidal vesicles that lack P-glycoprotein.	Rubidium-86	31-36	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	174-188
7943288-2	1994	This study shows that when furosemide- and bumetanide-inhibitable 86Rb+ uptake is measured in the skeletal muscle-like BC3H1 cell line, insulin and insulin-like growth factor I (IGF-I) activate a loop diuretic-sensitive K+ and Cl- transport system but have no effect on Na(+)-K(+)-ATPase.	Rubidium-86	66-71	insulin-like growth factor 1	Mus musculus	148-176
7943288-2	1994	This study shows that when furosemide- and bumetanide-inhibitable 86Rb+ uptake is measured in the skeletal muscle-like BC3H1 cell line, insulin and insulin-like growth factor I (IGF-I) activate a loop diuretic-sensitive K+ and Cl- transport system but have no effect on Na(+)-K(+)-ATPase.	Rubidium-86	66-71	insulin-like growth factor 1	Mus musculus	178-183
8023889-7	1994	These data demonstrate that a prostanoid produced by mTALH cells mediates the inhibitory effect of LPS and TNF on 86Rb uptake and imply that endogenous TNF inhibits ion fluxes in the mTALH via a prostaglandin-dependent mechanism.	Rubidium-86	114-118	tumor necrosis factor	Oryctolagus cuniculus	107-110
7949236-8	1994	We have also demonstrated that insulin enhances the 86Rb uptake and stimulates the Na, K-ATPase activity in HPMC but on the other hand is capable of reducing the phospholipids secretion from HPMC.	Rubidium-86	52-56	insulin	Homo sapiens	31-38
8195155-13	1994	ADP was less active than ATP at initiating the post-translational maturation and release of IL-1 beta and AMP, GTP, and UTP were totally inactive, ATP, nigericin, A204, and lasalocid promoted a rapid and complete loss of the potassium analog 86Rb+ from cells that were preloaded with this cation; valinomycin-treated cells released only a portion of the radiolabeled cation.	Rubidium-86	242-247	interleukin 1 beta	Mus musculus	92-101
7512618-0	1994	Evidence that prostaglandin E2 can block calcium-activated 86Rb efflux from rat brain synaptosomes via a protein kinase C-dependent mechanism.	Rubidium-86	59-63	protein kinase C, gamma	Rattus norvegicus	105-121
8148397-6	1994	Ca(2+)-activated 86Rb efflux was inhibited by pretreatment with calmodulin (CaM) antagonist, W7.	Rubidium-86	17-21	calmodulin 1	Homo sapiens	76-79
7508733-1	1993	In this report, it is shown that the platelet-activating factor (PAF) induced, in human B lymphoblastoid cells, 86Rb+ influx and efflux suggesting that it activated a K+ channel.	Rubidium-86	112-117	PCNA clamp associated factor	Homo sapiens	37-63
8148397-6	1994	Ca(2+)-activated 86Rb efflux was inhibited by pretreatment with calmodulin (CaM) antagonist, W7.	Rubidium-86	17-21	calmodulin 1	Homo sapiens	64-74
8238476-3	1993	The fast-activating noninactivating Kv1.5 channel, but not the rapidly inactivating Kv1.4 channel, prevented dexamethasone-induced increases in intracellular volume and inhibited Na(+)-K(+)-ATPase activity by 25%, as measured by 86Rb+ uptake.	Rubidium-86	229-234	potassium voltage-gated channel subfamily A member 5	Homo sapiens	36-41
7508733-1	1993	In this report, it is shown that the platelet-activating factor (PAF) induced, in human B lymphoblastoid cells, 86Rb+ influx and efflux suggesting that it activated a K+ channel.	Rubidium-86	112-117	PCNA clamp associated factor	Homo sapiens	65-68
7508020-4	1993	The inhibitory activity of this factor on 86Rb uptake could be neutralized by antidigoxin antibodies (Fab fragments) and provided, for the first time, direct evidence of an association between digoxin-like immunoreactivity and biological digitalis-like activity.	Rubidium-86	42-46	FA complementation group B	Homo sapiens	102-105
8417825-3	1993	injections of 25 micrograms/kg IL-1 alpha, the tumor blood perfusion, as measured with the 86Rb uptake method, significantly declined, reaching minimum blood perfusion in 3-5 h. Although the tumor blood perfusion started to rise thereafter, the recovery was still incomplete 1 day later.	Rubidium-86	91-95	interleukin 1 alpha	Mus musculus	31-41
8474012-6	1993	Functional nAChR ion channels of the ganglia-type are expressed by IMR-32 cells, as assessed by the abilities of nicotinic agonists to stimulate 86Rb+ efflux, the relatively higher sensitivity of those responses to blockade by mecamylamine than by d-tubocurarine, and the inability of alpha-bungarotoxin to antagonize nAChR function.	Rubidium-86	145-150	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	11-16
7508036-2	1993	OLF was identified by its ability (a) to inhibit ouabain-sensitive 86Rb uptake into human erythrocytes, (b) to displace [3H]ouabain binding, and (c) to inhibit purified dog kidney Na-K-ATPase.	Rubidium-86	67-71	transmembrane O-mannosyltransferase targeting cadherins 1	Homo sapiens	0-3
8366769-8	1993	86Rb+ efflux as an indicator for closing K+ channels which leads to a depolarization of the beta-cell membrane and which is a prerequisite for Ca++ influx was inhibited by activin A at a low glucose concentration (3.0 mM).	Rubidium-86	0-5	inhibin subunit beta A	Rattus norvegicus	172-181
1338036-6	1992	The rate of basal cellular 86Rb+ uptake (cpm x 10(3).g wet weight-1.min-1) was not significantly different between control (77.7 +/- 2.9) and endotoxic soleus muscles (76.1 +/- 3.9).	Rubidium-86	27-32	Body weight QTL 17	Rattus norvegicus	59-67
8434816-5	1993	In contrast, application of bradykinin at a constant shear stress of 1 dyn/cm2 produced a transient increase in 86Rb+ efflux that was followed by a sustained elevated phase during which time efflux gradually returned to pre-stimulus levels.	Rubidium-86	112-117	kininogen 1	Bos taurus	28-38
1284494-3	1992	GIP (5 nM) neither inhibited 86Rb+ efflux at 3 mM glucose nor modulated 86Rb+ efflux that was inhibited by 5.6 mM glucose or stimulated by the calcium ionophore A23187.	Rubidium-86	72-76	gastric inhibitory polypeptide	Mus musculus	0-3
1569072-10	1992	Ang II-treated cells also exhibited a 90% increase in bumetanide-sensitive 86Rb uptake over control cells.	Rubidium-86	75-79	angiogenin	Homo sapiens	0-3
1322364-5	1992	Angiotensin II caused rapid increases in both steady-state Na+, K(+)-ATPase activity (ouabain-sensitive 86Rb uptake) and intracellular [Na+].	Rubidium-86	104-108	angiotensinogen	Homo sapiens	0-14
1312727-5	1992	Ouabain-sensitive 86Rb uptake of aortas of rats receiving 80-100, 160-180, and 240-260 ng/kg.min-1 of ANG II for 24 hr was 26.6 +/- 3.5, 28.8 +/- 3.4, and 29.1 +/- 2.6 nmol/mg dry wt.15 min-1 (mean +/- SD, n = 7-12), respectively, compared with 25.2 +/- 3.8 in controls (n = 23, P less than 0.01).	Rubidium-86	18-22	angiotensinogen	Rattus norvegicus	102-108
1311522-7	1992	Monensin-stimulated ouabain-sensitive 86Rb uptake was inhibited by PTH in a dose-dependent manner, with 10(-7) M PTH being maximally inhibitory.	Rubidium-86	38-42	parathyroid hormone	Rattus norvegicus	67-70
1311522-7	1992	Monensin-stimulated ouabain-sensitive 86Rb uptake was inhibited by PTH in a dose-dependent manner, with 10(-7) M PTH being maximally inhibitory.	Rubidium-86	38-42	parathyroid hormone	Rattus norvegicus	113-116
1311245-5	1992	Angiotensin-II (AII) inhibited the ouabain-sensitive 86Rb uptake by glomerulosa cells.	Rubidium-86	53-57	angiotensinogen	Rattus norvegicus	0-14
1311245-5	1992	Angiotensin-II (AII) inhibited the ouabain-sensitive 86Rb uptake by glomerulosa cells.	Rubidium-86	53-57	angiotensinogen	Rattus norvegicus	16-19
1370600-9	1992	ATP-induced 86Rb efflux showed a sigmoid dependence on the concentration of ATP and Hill analysis gave K1/2 of 90 and 130 microM and n values of 2.5 and 2.5 for KCl and NaCl media, respectively.	Rubidium-86	12-16	keratin 1	Homo sapiens	103-113
1725864-4	1991	The diazoxide-induced 86Rb+ efflux was not affected by galanin, indicating that galanin activates ATP-regulated K+ channels in rat islets.	Rubidium-86	22-26	galanin and GMAP prepropeptide	Mus musculus	80-87
1725864-5	1991	In mouse islets prelabelled with 86Rb+, galanin (10(-6) M) decreased 86Rb+ efflux.	Rubidium-86	33-38	galanin and GMAP prepropeptide	Mus musculus	40-47
1725864-5	1991	In mouse islets prelabelled with 86Rb+, galanin (10(-6) M) decreased 86Rb+ efflux.	Rubidium-86	69-74	galanin and GMAP prepropeptide	Mus musculus	40-47
1791921-4	1991	ET stimulated 86Rb+ efflux with an EC50 of 5.9 nM.	Rubidium-86	14-19	endothelin 1	Rattus norvegicus	0-2
1666367-5	1991	CCK-8 stimulated the 86Rb+ efflux (reflecting K+ movements) from prelabelled islets, which probably reflects an indirect effect of CCK-8 due to opening of Ca(2+)-activated K+ channels.	Rubidium-86	21-26	cholecystokinin	Rattus norvegicus	0-3
1666367-5	1991	CCK-8 stimulated the 86Rb+ efflux (reflecting K+ movements) from prelabelled islets, which probably reflects an indirect effect of CCK-8 due to opening of Ca(2+)-activated K+ channels.	Rubidium-86	21-26	cholecystokinin	Rattus norvegicus	131-134
1791921-5	1991	ET-stimulated 86Rb+ efflux was insensitive to Ca2+ channel blockade, however it was reduced by 68% in Ca(2+)-free buffer, suggesting a sizable dependence on an extracellular source of Ca2+ influx through non voltage-operated Ca2+ channels.	Rubidium-86	14-19	endothelin 1	Rattus norvegicus	0-2
1791921-7	1991	ET-stimulated 86Rb+ efflux was insensitive to glyburide suggesting that efflux is not through ATP-sensitive K+ channels.	Rubidium-86	14-19	endothelin 1	Rattus norvegicus	0-2
1791921-9	1991	Pre-incubation with the protein kinase C (PKC) inhibitor, staurosporine, inhibited 86Rb+ efflux by 66%, suggesting the involvement of PKC activation in ET-mediated 86Rb+ efflux.	Rubidium-86	83-87	endothelin 1	Rattus norvegicus	152-154
1791921-9	1991	Pre-incubation with the protein kinase C (PKC) inhibitor, staurosporine, inhibited 86Rb+ efflux by 66%, suggesting the involvement of PKC activation in ET-mediated 86Rb+ efflux.	Rubidium-86	164-168	endothelin 1	Rattus norvegicus	152-154
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
2022640-5	1991	Overexpression of the Ha-ras proto-oncogene causes only a marginal increase in total 86Rb+ uptake.	Rubidium-86	85-90	Harvey rat sarcoma virus oncogene	Mus musculus	22-28
2020021-4	1991	86Rb+ uptake into MTAL tubules in suspension was significant only after exposure of tubules to AVP.	Rubidium-86	0-5	arginine vasopressin	Mus musculus	95-98
1987779-9	1991	In this study, neurotensin was found to enhance dramatically the Ba2(+)- and tetraethylammonium chloride-sensitive K(+)-efflux rate (measured with 86Rb+) in the presence of ouabain and bumetanide, with basal efflux increasing 4.5 +/- 0.5-fold with 10 nM neurotensin.	Rubidium-86	147-152	neurotensin	Homo sapiens	15-26
12106193-11	1991	We now demonstrate, using 86Rb+ influx assays and single channel patch-clamp recording, that both endothelins-ET-3 and ET-1-can also open a charybdotoxin-sensitive, calcium-activated K+ channel of 15 - 40 pS in glial cells.	Rubidium-86	26-31	endothelin 3	Homo sapiens	110-114
12106193-11	1991	We now demonstrate, using 86Rb+ influx assays and single channel patch-clamp recording, that both endothelins-ET-3 and ET-1-can also open a charybdotoxin-sensitive, calcium-activated K+ channel of 15 - 40 pS in glial cells.	Rubidium-86	26-31	endothelin 1	Homo sapiens	119-123
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.	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.	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
2242386-7	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
2174063-4	1990	ANP reduced bumetanide-sensitive 86Rb+ influx under isotonic as well as under hypertonic conditions.	Rubidium-86	33-38	natriuretic peptide A	Homo sapiens	0-3
2174063-6	1990	Furthermore, efflux of 86Rb+ and 22Na+ was greatly reduced in the presence of bumetanide and ANP.	Rubidium-86	23-28	natriuretic peptide A	Homo sapiens	93-96
2224845-4	1990	When the SCK tumors of A/J mice were heated at 42.5 degrees C for 1 h, the tumor vessels became most thermotolerant at 18 h postheating, as measured with the 86Rb uptake method.	Rubidium-86	158-162	SHC (Src homology 2 domain containing) transforming protein 2	Mus musculus	9-12
2388254-7	1990	Efflux of 86Rb+ from BAEC monolayers was stimulated by both bradykinin and ionomycin.	Rubidium-86	10-15	kininogen 1	Bos taurus	60-70
2172559-2	1990	When myocytes were exposed to xanthine plus xanthine oxidase, there were time-dependent inhibitions of ouabain-sensitive 86Rb+ uptake and (Na+ + K+)-ATPase activity that could be prevented by allopurinol, or by catalase and superoxide dismutase; suggesting the involvements of H2O2 or oxygen free radicals in the inhibition of the pump.	Rubidium-86	121-126	catalase	Rattus norvegicus	211-219
2388254-9	1990	Thus, 86Rb+ efflux stimulated by bradykinin and ionomycin has the same pharmacological sensitivity as the bradykinin- and Ca2(+)-activated membrane currents.	Rubidium-86	6-11	kininogen 1	Bos taurus	33-43
2388254-9	1990	Thus, 86Rb+ efflux stimulated by bradykinin and ionomycin has the same pharmacological sensitivity as the bradykinin- and Ca2(+)-activated membrane currents.	Rubidium-86	6-11	kininogen 1	Bos taurus	106-116
2388254-10	1990	The results confirm that bradykinin-stimulated 86Rb+ efflux occurs via Ca2(+)-activated K+ channels.	Rubidium-86	47-52	kininogen 1	Bos taurus	25-35
2360657-3	1990	Ba2(+)-sensitive 86Rb+ uptake was completely blocked by 10 microM [Ca2+]i.	Rubidium-86	17-22	carbonic anhydrase 2	Oryctolagus cuniculus	67-70
2360657-5	1990	Thus 0.1 microM [Ca2+]i produced a maximal inhibition of 86Rb+ uptake at pH greater than 7.4 but had no effect at pH less than 7.0.	Rubidium-86	57-62	carbonic anhydrase 2	Oryctolagus cuniculus	17-20
2904889-2	1988	86Rb+ efflux is stimulated by somatostatin in a dose-dependent manner.	Rubidium-86	0-4	somatostatin	Rattus norvegicus	30-42
2333983-10	1990	Concentration-dependent stimulation of Na(+)-K(+)-Cl- cotransport-mediated 86Rb+ influx was induced by two vasoconstrictors, angiotensin II (ANG II) and arginine vasopressin (AVP), and by a vasodilator, atrial natriuretic peptide (ANP).	Rubidium-86	75-80	angiotensinogen	Rattus norvegicus	125-139
2333983-10	1990	Concentration-dependent stimulation of Na(+)-K(+)-Cl- cotransport-mediated 86Rb+ influx was induced by two vasoconstrictors, angiotensin II (ANG II) and arginine vasopressin (AVP), and by a vasodilator, atrial natriuretic peptide (ANP).	Rubidium-86	75-80	angiotensinogen	Rattus norvegicus	141-147
2333983-10	1990	Concentration-dependent stimulation of Na(+)-K(+)-Cl- cotransport-mediated 86Rb+ influx was induced by two vasoconstrictors, angiotensin II (ANG II) and arginine vasopressin (AVP), and by a vasodilator, atrial natriuretic peptide (ANP).	Rubidium-86	75-80	arginine vasopressin	Rattus norvegicus	162-173
2333983-10	1990	Concentration-dependent stimulation of Na(+)-K(+)-Cl- cotransport-mediated 86Rb+ influx was induced by two vasoconstrictors, angiotensin II (ANG II) and arginine vasopressin (AVP), and by a vasodilator, atrial natriuretic peptide (ANP).	Rubidium-86	75-80	natriuretic peptide A	Rattus norvegicus	203-229
1688561-11	1990	The monoclonal AMOG antibody that blocks adhesion was shown to interact with Na,K-ATPase in intact cultured astrocytes by its ability to increase ouabain-inhibitable 86Rb+ uptake.	Rubidium-86	166-171	ATPase Na+/K+ transporting subunit beta 2	Rattus norvegicus	15-19
2790380-11	1989	NECA and R-PIA shortened the action potential duration and increased the rate constant of the efflux of 86Rb in a concentration-dependent manner with no differences in potency; the effects were competitively antagonized by 8-phenyltheophylline.	Rubidium-86	104-108	ribose-5-phosphate isomerase	Cavia porcellus	9-14
7806016-8	1994	Finally, in pre-labelled perifused islets, peptide YY caused a small and transient increase in the 86Rb+ efflux (p < 0.001), but only in the absence of extracellular Ca2+.	Rubidium-86	99-104	peptide YY	Mus musculus	43-53
2539125-2	1989	Addition of ANP to culture medium stimulated 86Rb+ uptake in bovine endothelial cells with a concomitant increase in cGMP contents.	Rubidium-86	45-50	natriuretic peptide A	Bos taurus	12-15
2924525-8	1989	Inhibition of ouabain-sensitive 86Rb uptake of cells occurred in the plasma of rats with malignant hypertension when an angiotensin II antagonist was added to the reaction mixture.	Rubidium-86	32-36	angiotensinogen	Rattus norvegicus	120-134
2904889-1	1988	Somatostatin, an hyperglycemia-inducing hormone, was studied in rat insulinoma (RINm5F) cells using 86Rb+ efflux techniques.	Rubidium-86	100-104	somatostatin	Rattus norvegicus	0-12
2904889-6	1988	86Rb+ efflux studies show that somatostatin activates an ATP-dependent K+ channel.	Rubidium-86	0-5	somatostatin	Rattus norvegicus	31-43
2845805-8	1988	The dose-response curve for HF inhibition of LLC-PK1 86Rb+ uptake showed a sigmoidal shape consistent with an allosteric binding reaction.	Rubidium-86	53-58	prokineticin 1	Homo sapiens	49-52
2853084-4	1988	However the Na,K-ATPase mediated 86Rb uptake was always positively correlated with basal blood insulin levels and the insulin sensitivity index.	Rubidium-86	33-37	insulin	Homo sapiens	95-102
2826993-6	1987	The similarities in the characteristics of the high affinity [3H]ouabain-binding sites and the sites involved in the inhibition of 86Rb uptake and stimulation of NAT activity indicate that an alpha +-like Na+,K+-ATPase mediates the inhibitory effects of ouabain on the adrenergic induction of pineal NAT activity.	Rubidium-86	131-135	N-acetyltransferase 1	Rattus norvegicus	300-303
2904889-4	1988	Somatostatin-induced 86Rb+ efflux is abolished by the hypoglycemia-inducing sulfonylurea, glibenclamide, a known blocker of ATP-regulated K+ channels.	Rubidium-86	21-26	somatostatin	Rattus norvegicus	0-12
2451537-1	1988	We study bradykinin-stimulated K+ efflux in Madin-Darby canine kidney (MDCK) cells using 86Rb as an isotopic tracer.	Rubidium-86	89-93	kininogen 1	Canis lupus familiaris	9-19
3346341-4	1988	When the rate of 86Rb+ efflux (as a tracer for K+) was measured from each of the three cell lines, a furosemide- and TPA-inhibitable component of efflux was clearly evident in parental and TNR-9 cells but was virtually absent in TNR-2 cells.	Rubidium-86	17-22	tenascin R	Mus musculus	189-192
3346341-5	1988	86Rb+ influx measurements indicated the presence in parental 3T3 cells and the TNR-9 line of a substantial furosemide-sensitive flux that could be inhibited by TPA.	Rubidium-86	0-5	tenascin R	Mus musculus	79-82
3346341-7	1988	In both parental 3T3 and 3T3-TNR-2 cells, most of the furosemide-sensitive 86Rb+ influx is dependent on extracellular Na+ and Cl-.	Rubidium-86	75-80	tenascin R	Mus musculus	29-32
2447103-1	1988	Purified colony stimulating factor (CSF-1) stimulates the Na+,K+-ATPase activity of murine bone marrow-derived macrophages (BMM) and resident peritoneal macrophages (RPM) measured as ouabain-sensitive 86Rb+ uptake.	Rubidium-86	201-206	colony stimulating factor 1 (macrophage)	Mus musculus	36-41
3427468-2	1987	We found NGF to cause an immediate increase in electrogenic Na-K pump activity as determined by electrogenic component of membrane potential (Em) and ouabain-sensitive 86Rb uptake.	Rubidium-86	168-172	nerve growth factor	Rattus norvegicus	9-12
3042025-0	1988	Furosemide and Ca2+ affect 86Rb+ efflux from pancreatic beta-cells by different mechanisms.	Rubidium-86	27-32	carbonic anhydrase 2	Mus musculus	15-18
3136667-2	1988	In the present study, measurement of BK-induced changes in fura-2 fluorescence and 86Rb+ efflux were used to monitor changes in cytosolic Ca2+ and K+ permeability in cultured bovine aortic endothelial cells.	Rubidium-86	83-88	kininogen 1	Bos taurus	37-39
2424505-3	1986	The increase of Ca2+ concentration within this range recruits a larger fraction of the vesicles to the active (permeable to 86Rb+) state.	Rubidium-86	124-129	carbonic anhydrase 2	Homo sapiens	16-19
3123696-13	1987	Calmodulin antagonists selectively inhibited 86Rb+ influx via the cotransporter.	Rubidium-86	45-50	calmodulin 1	Homo sapiens	0-10
3095627-3	1986	Permeability to small cations of liver plasma membrane vesicles of control and CCl4-dosed rats was tested by two independent methods: 1) Ca2+ efflux after passive loading in 1 mM Ca2+, and 2) 86Rb+ uptake driven by valinomycin-induced K+ diffusion potential after 100 mM KCl-equilibrated vesicles were stripped of external K+ by cation exchange.	Rubidium-86	192-197	C-C motif chemokine ligand 4	Rattus norvegicus	79-83
3095627-6	1986	86Rb+ uptake by CCl4 vesicles was 47% of control.	Rubidium-86	0-5	C-C motif chemokine ligand 4	Rattus norvegicus	16-20
2424505-4	1986	The apparent rate of 86Rb+ transport through each individual channel was found to increase, however, with Ca2+ concentration.	Rubidium-86	21-26	carbonic anhydrase 2	Homo sapiens	106-109
3717330-6	1986	Maximal concentrations (100 nM) of bradykinin and vasopressin increase the initial rate of bumetanide-sensitive 86Rb influx by approximately 60 and 70% (50% effective concentration approximately 1 and 0.6 nM, respectively).	Rubidium-86	112-116	kininogen 1	Bos taurus	35-45
2423536-6	1986	The structurally related peptides litorin, gastrin-releasing peptide, and neuromedin B also stimulated ouabain-sensitive 86Rb+ uptake; the relative potencies of these peptides in stimulating the Na+/K+ pump were comparable to their potencies in increasing DNA synthesis (Zachary, I., and E. Rozengurt, 1985, Proc.	Rubidium-86	121-126	gastrin releasing peptide	Mus musculus	43-68
2423536-6	1986	The structurally related peptides litorin, gastrin-releasing peptide, and neuromedin B also stimulated ouabain-sensitive 86Rb+ uptake; the relative potencies of these peptides in stimulating the Na+/K+ pump were comparable to their potencies in increasing DNA synthesis (Zachary, I., and E. Rozengurt, 1985, Proc.	Rubidium-86	121-126	neuromedin B	Mus musculus	74-86
2421725-3	1986	Addition of calmodulin further enhanced the Ca2+ activating effect on 86Rb+ uptake (K+ channel activity).	Rubidium-86	70-75	calmodulin 1	Homo sapiens	12-22
2420200-10	1986	86Rb+ efflux across the basolateral membrane was accelerated two- to threefold by addition of either VIP or A23187.	Rubidium-86	0-4	vasoactive intestinal peptide	Homo sapiens	101-104
3000466-4	1985	Sertoli cells showed efflux of 86Rb+ with t1/2 of approximately 11 min and an active ATPase in plasma membranes.	Rubidium-86	31-36	brachyury 2	Rattus norvegicus	42-70
4063359-2	1985	In the presence of external Ca2+ the sodium ionophore monensin greatly increased cellular Na+ content (and decreased K+ content) although 86Rb uptake, reflecting Na+-pump activity was increased.	Rubidium-86	138-142	carbonic anhydrase 2	Rattus norvegicus	28-31
3019770-3	1986	"Quiescent" CTL clones stimulated with IL-2 showed an increase of 48-380% in ouabain-sensitive 86Rb uptake.	Rubidium-86	95-99	interleukin 2	Homo sapiens	39-43
2998364-0	1985	CSF-1 stimulates Na+K+-ATPase mediated 86Rb+ uptake in mouse bone marrow-derived macrophages.	Rubidium-86	39-44	colony stimulating factor 1 (macrophage)	Mus musculus	0-5
2998364-4	1985	A purified colony stimulating factor (CSF-1) was shown to stimulate the ouabain-sensitive 86Rb+ uptake in a dose-dependent manner.	Rubidium-86	90-95	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	11-36
2998364-4	1985	A purified colony stimulating factor (CSF-1) was shown to stimulate the ouabain-sensitive 86Rb+ uptake in a dose-dependent manner.	Rubidium-86	90-95	colony stimulating factor 1 (macrophage)	Mus musculus	38-43
2998364-5	1985	Such colony stimulating factor stimulation of 86Rb+ (K+) influx was rapid, with a maximal effect seen 10 minutes after growth factor addition followed by a gradual decrease.	Rubidium-86	46-51	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	5-30
6328908-4	1984	AII also stimulated ouabain-sensitive 86Rb+ uptake by cultured aortic smooth muscle and brain microvessel cells.	Rubidium-86	38-43	angiotensinogen	Homo sapiens	0-3
3926504-5	1985	The ouabain-suppressible component of 86Rb+ influx in erythrocytes obtained 15 min after the administration of insulin was virtually doubled compared to erythrocytes obtained before insulin suggesting increased activity of the sodium pump of erythrocytes.	Rubidium-86	38-43	insulin	Homo sapiens	111-118
6487622-2	1984	Enterotoxin was shown to cause a rapid loss of intracellular 86Rb+ (Mr approx.	Rubidium-86	61-66	cpe	Clostridium perfringens	0-11
6487622-4	1984	The enterotoxin-induced release of intracellular 86Rb+ preceded the loss of two larger labels, 51Cr label (Mr approx.	Rubidium-86	49-54	cpe	Clostridium perfringens	4-15
6086680-0	1984	Initiation of DNA synthesis by human thrombin: relationships between receptor binding, enzymic activity, and stimulation of 86Rb+ influx.	Rubidium-86	124-129	coagulation factor II, thrombin	Homo sapiens	37-45
6086680-7	1984	High concentrations of either gamma-thrombin or nitro-alpha-thrombin, however, stimulate both early and late 86RB+ uptake but do not initiate DNA synthesis.	Rubidium-86	109-114	coagulation factor II, thrombin	Homo sapiens	36-44
6086680-7	1984	High concentrations of either gamma-thrombin or nitro-alpha-thrombin, however, stimulate both early and late 86RB+ uptake but do not initiate DNA synthesis.	Rubidium-86	109-114	coagulation factor II, thrombin	Homo sapiens	60-68
6311844-2	1983	This pump activation, measured by ouabain-sensitive 86Rb+ uptake, appeared susceptible to the phospholipid-interacting drugs tetracaine and quinacrine, to the antioxydant nordihydroguaiaretic acid (NDGA), and to the calmodulin antagonist trifluoperazine, while much less susceptible to the methylation inhibitor-3-deazaadenosine.	Rubidium-86	52-57	calmodulin 1	Homo sapiens	216-226
6630302-6	1983	86Rb+ transport studies demonstrated that in this system ouabain-sensitive K+ uptake via the Na, K-ATPase was stimulated by thrombin during both an early and a late period.	Rubidium-86	0-5	coagulation factor II	Mus musculus	124-132
6365716-0	1984	Radioactive 86rubidium influx into red blood cells in essential hypertension in relation to the plasma renin activity.	Rubidium-86	12-22	renin	Homo sapiens	103-108
185297-3	1976	The guinea pig hepatoma (line-1) treated with anti-Forssman antibody (TA) and GPC sequentially released 86Rb, 14C from 14C aminoidobutyric acid and failed to exclude trypan blue.	Rubidium-86	104-108	glycophorin C (Gerbich blood group)	Homo sapiens	78-81
6306227-2	1983	Ouabain-sensitive 86Rb+ uptake in slices of lactating rabbit mammary gland significantly increased after 20 min or 1 hr of incubation with ovine prolactin (NIH-P-S12; 1 microgram/ml.).	Rubidium-86	18-23	prolactin	Oryctolagus cuniculus	145-154
6284772-6	1982	On the other hand, the decrease in the rate of uptake of rubidium-86, an analogue of K+, by treated-induced cells was significantly enhanced over that observed with untreated-induced cells, suggesting that alpha-galactosidase plus neuraminidase modification of the cell surface was affecting at least one of the early events occurring in the Friend erythroleukemic cell differentiation program.	Rubidium-86	57-68	neuraminidase 1	Homo sapiens	231-244
366104-2	1978	Both phenylephrine and angiotensin II caused transient increases in 86Rb efflux from liver slices.	Rubidium-86	68-72	angiotensinogen	Homo sapiens	23-37
147030-2	1978	Monovalent cation active transport, measured by ouabain-inhibitable 86Rb+ uptake, was significantly increased (21.9 +/- 7.3% SE) in tissue slices exposed to insulin (100 mU/ml) for 15 min.	Rubidium-86	68-73	insulin	Homo sapiens	157-164
6293005-0	1982	Secretin exerts inhibition of the 8BrcAMP-stimulated 86Rb influx into avian red blood cells.	Rubidium-86	53-57	secretin	Homo sapiens	0-8
6293005-3	1982	Secretin caused a 50% inhibition of the 8BrcAMP-stimulated 86Rb influx into red blood cells from goose at a concentration of 8.5 X 10(-6) M, while furosemide and bumetanide caused a 50% inhibition at concentrations of 7 X 10(-6) M and 9 X 10(-8) M, respectively.	Rubidium-86	59-63	secretin	Homo sapiens	0-8
6280182-7	1982	AII and AIII nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [Sar1, Ileu5, Ala8]AII had no effect.	Rubidium-86	46-51	angiotensinogen	Rattus norvegicus	0-3
6280182-7	1982	AII and AIII nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [Sar1, Ileu5, Ala8]AII had no effect.	Rubidium-86	46-51	angiotensinogen	Rattus norvegicus	8-11
6115784-11	1981	SRIF-induced enhancement of 86Rb efflux was antagonized by TEA or quinine.	Rubidium-86	28-32	somatostatin	Mus musculus	0-4
7250123-9	1981	In this respect, particularly striking was the parallelism found between 86Rb+ leakage and inhibition of protein synthesis by treatment with different genetic variants of thionins (alpha 1 purothionin, alpha 2 purothionin, beta purothionin from wheat; hordothionin from barley), as well as with the viscotoxins, which are homologous polypeptides from the European mistletoe.	Rubidium-86	73-78	alpha-1-purothionin	Triticum aestivum	181-221
7030323-2	1981	A recently developed technique for the measurement of plasma-membrane and mitochondrial-membrane potentials in intact cells by using the distribution of 86Rb+ and [3H]methyltriphenylphosphonium+ has enabled us to characterize a novel insulin effect on fat-cell mitochondria.	Rubidium-86	153-158	insulin	Homo sapiens	234-241
20599770-0	2010	86Rb+ efflux mediated by alpha4beta2*-nicotinic acetylcholine receptors with high and low-sensitivity to stimulation by acetylcholine display similar agonist-induced desensitization.	Rubidium-86	0-4	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	38-71
1082887-5	1976	86Rb+ efflux was increased by 27% in rat thymic lymphocytes and by 78% in human blood lymphocytes following PHA treatment.	Rubidium-86	0-5	lamin B receptor	Homo sapiens	108-111
1110239-5	1975	After 3 min of 86-Rb administration, EM significantly exceeded ETB (P is less than 0.05) due to the more rapid decline with time of ETB.	Rubidium-86	15-20	endothelin receptor type B	Canis lupus familiaris	132-135
27496272-6	2016	Ouabain 10pM stimulated NKA-mediated 86Rb uptake and phosphorylation of EGFR, Src, and ERK1/2.	Rubidium-86	37-41	tachykinin precursor 1	Homo sapiens	24-27
22101002-6	2012	Additional studies showed that TNF produced by mTAL cells inhibits 86Rb uptake, an in vitro correlate of natriuresis, in an autocrine- and COX-2-dependent manner.	Rubidium-86	67-71	tumor necrosis factor	Homo sapiens	31-34
22101002-6	2012	Additional studies showed that TNF produced by mTAL cells inhibits 86Rb uptake, an in vitro correlate of natriuresis, in an autocrine- and COX-2-dependent manner.	Rubidium-86	67-71	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	139-144
31445709-4	2019	In the living cells, Shh-N recombinant inhibited the SCH28080-sensitive 86Rb+-uptake.	Rubidium-86	72-77	sonic hedgehog signaling molecule	Homo sapiens	21-26
24393035-5	2014	Thirdly, in ES (embryonic stem) cells lacking SPAK/OSR1 activity, endogenous phosphorylation of KCC isoforms at Site-2 is abolished and these cells display elevated basal activity of 86Rb+ uptake that was not markedly stimulated further by hypotonic high K+ conditions, consistent with KCC3A activation.	Rubidium-86	183-188	serine/threonine kinase 39	Homo sapiens	46-50
24393035-5	2014	Thirdly, in ES (embryonic stem) cells lacking SPAK/OSR1 activity, endogenous phosphorylation of KCC isoforms at Site-2 is abolished and these cells display elevated basal activity of 86Rb+ uptake that was not markedly stimulated further by hypotonic high K+ conditions, consistent with KCC3A activation.	Rubidium-86	183-188	solute carrier family 12 member 6	Homo sapiens	286-291
19232517-5	2009	CIP1 co-purified with KCC2 in pull-down experiments and significantly increased KCC2 transport activity, as determined by 86Rb+ flux measurements.	Rubidium-86	122-127	solute carrier family 12, member 9	Rattus norvegicus	0-4
19232517-5	2009	CIP1 co-purified with KCC2 in pull-down experiments and significantly increased KCC2 transport activity, as determined by 86Rb+ flux measurements.	Rubidium-86	122-127	solute carrier family 12 member 5	Rattus norvegicus	22-26
19232517-5	2009	CIP1 co-purified with KCC2 in pull-down experiments and significantly increased KCC2 transport activity, as determined by 86Rb+ flux measurements.	Rubidium-86	122-127	solute carrier family 12 member 5	Rattus norvegicus	80-84
16014898-6	2005	In A549 human lung epithelial cells and in mouse primary alveolar type II cells, thrombin blocked ouabain-sensitive Na+,K+-ATPase-mediated 86Rb+ uptake, without altering amiloride-sensitive sodium currents.	Rubidium-86	139-144	coagulation factor II	Mus musculus	81-89
18194436-1	2008	The effects of the endogenous cannabinoid anandamide [arachidonylethanolamide (AEA)] on the function of nicotinic acetylcholine receptor (nAChR) were investigated using the 86Rb+ efflux assay in thalamic synaptosomes.	Rubidium-86	173-178	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	138-143
15709110-5	2005	Stichodactyla helianthus peptide (ShK), isolated from S. helianthus venom and a known high-affinity blocker of Kv1.1 and Kv1.3 channels, was found to potently inhibit 86Rb+ efflux from CHO-K1.hKv3.2b (IC50 approximately 0.6 nM).	Rubidium-86	167-172	sedoheptulokinase	Homo sapiens	34-37
16135750-8	2005	Furthermore, transfection of MONaKA inhibits 86Rb+ uptake via the Na,K-ATPase in intact cells.	Rubidium-86	45-50	PX domain containing serine/threonine kinase	Mus musculus	29-35
15899883-4	2005	NKCC1 activity was measured as bumetanide-sensitive 86Rb uptake or basolateral to apical 86Rb flux in primary cultures of human tracheal epithelial cells or in Calu-3 airway epithelial cells grown on Transwell filter inserts.	Rubidium-86	52-56	solute carrier family 12 member 2	Homo sapiens	0-5
15899883-4	2005	NKCC1 activity was measured as bumetanide-sensitive 86Rb uptake or basolateral to apical 86Rb flux in primary cultures of human tracheal epithelial cells or in Calu-3 airway epithelial cells grown on Transwell filter inserts.	Rubidium-86	89-93	solute carrier family 12 member 2	Homo sapiens	0-5
15647390-0	2005	CD63 interacts with the carboxy terminus of the colonic H+-K+-ATPase to decrease [corrected] plasma membrane localization and 86Rb+ uptake.	Rubidium-86	126-131	CD63 antigen	Mus musculus	0-4
16000700-6	2005	PTH decreased 86Rb uptake significantly in OK-WT but not in OKH cells.	Rubidium-86	14-18	parathyroid hormone	Mus musculus	0-3
16000700-7	2005	PTH also significantly inhibited 86Rb uptake in OKH cells that were transfected with full-length NHERF-1 or NHERF-1 with mutated PDZ 2 but not in OKH cells that were transfected with mutated PDZ 1.	Rubidium-86	33-37	parathyroid hormone	Mus musculus	0-3
16000700-7	2005	PTH also significantly inhibited 86Rb uptake in OKH cells that were transfected with full-length NHERF-1 or NHERF-1 with mutated PDZ 2 but not in OKH cells that were transfected with mutated PDZ 1.	Rubidium-86	33-37	solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1	Mus musculus	97-104
16000700-7	2005	PTH also significantly inhibited 86Rb uptake in OKH cells that were transfected with full-length NHERF-1 or NHERF-1 with mutated PDZ 2 but not in OKH cells that were transfected with mutated PDZ 1.	Rubidium-86	33-37	solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1	Mus musculus	108-115
15304508-6	2004	ATP-induced efflux of 86Rb+ from erythrocytes was inhibited by extracellular Na+ and oxidized ATP, as well as by KN-62, an antagonist specific for the human P2X7 receptor.	Rubidium-86	22-27	purinergic receptor P2X 7	Homo sapiens	157-170
15569257-5	2004	Based on agonist profiles and sensitivity to the antagonist dihydro-beta-erythroidine (DHbetaE), the predominant alpha4beta2 nAchR expressed in the mmalpha4beta2 cells exhibits a pharmacology that most resembles the DHbetaE-sensitive component of 86Rb+ efflux from mouse brain synaptosomes.	Rubidium-86	247-252	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	125-130
15672465-7	2004	Monolayers exposed to 10 nM prolactin for 24 hr revealed an inhibition of 40% in ouabain-sensitive 86Rb+ uptake, a sensitive measure of pump-mediated transport.	Rubidium-86	99-104	prolactin	Homo sapiens	28-37
15071352-3	2004	HPLC chromatographic separation of cardiac extracts showed that RIA-determined OLF activity coincided with the elution profile of exogenous ouabain and with the ability to inhibit 86Rb uptake in human erythrocytes.	Rubidium-86	180-184	transmembrane O-mannosyltransferase targeting cadherins 1	Homo sapiens	79-82
15210579-4	2004	2 Both ATP and the nucleotide analogue 2"-3"-O-(4-benzoylbenzoyl)-ATP (BzATP) induced an 86Rb+ efflux, which was completely inhibited by the isoquinoline derivative 1-(N,O-bis[5-isoquinolinesulphonyl]-N-methyl-l-tyrosyl)-4-phenylpiperazine (KN-62), a potent P2X7 receptor antagonist.	Rubidium-86	89-93	purinergic receptor P2X 7	Homo sapiens	258-271
15111021-7	2004	86Rb+ efflux with higher sensitivity to acetylcholine and cytisine-sensitive [125I]-epibatidine binding are predominantly alpha4beta2-nAChR.	Rubidium-86	0-4	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	134-139
32585787-7	2004	86Rb+ efflux with higher sensitivity to acetylcholine and cytisine-sensitive [125I]-epibatidine binding are predominantly alpha4beta2-nAChR.	Rubidium-86	0-5	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	134-139
15071352-7	2004	In hearts subjected to 15 minutes of aerobic perfusion followed by 15 minutes of global myocardial ischemia OLF concentration was remarkably increased (8.59 +/- 1.13 versus 4.58 +/- 0.57 pmol/g wet weight by RIA, P < 0.01; an increase after ischemia was confirmed by the assay of 86Rb uptake).	Rubidium-86	283-287	transmembrane O-mannosyltransferase targeting cadherins 1	Homo sapiens	108-111
14570699-10	2004	Inhibition of PKC-epsilon activation prevented a decline in Na+-K+-ATPase activity and reduced decreases in ouabain-sensitive 86Rb+ uptake.	Rubidium-86	126-131	protein kinase C epsilon	Homo sapiens	14-25
14500754-6	2003	Nicotinic receptor-mediated function measured with the 86Rb+ efflux assay was evident only in the NGF-treated cells, and it had a pharmacological profile that was, again, nearly identical to that of the heterologously expressed alpha3beta4 receptor subtype.	Rubidium-86	55-59	nerve growth factor	Rattus norvegicus	98-101
12668585-3	2003	Treatment of adrenalectomized rats with aldosterone for 7 days resulted in a 63% increase in NKCC1 activity as measured by bumetanide-sensitive efflux of 86Rb+.	Rubidium-86	154-159	solute carrier family 12 member 2	Rattus norvegicus	93-98
12766617-3	2003	Mouse strains expressing the A variant have, in general, greater nAChR-mediated 86Rb+ efflux in response to nicotine than strains with the T variant.	Rubidium-86	80-84	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	65-70
12766617-5	2003	METHODS: We have used the 86Rb+ efflux method to study the acute effects of ethanol on the function of the alpha4beta2 nAChR in the thalamus in six different mouse strains.	Rubidium-86	26-31	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	119-124
11692276-8	2001	Secondly, total 86Rb+(K+) influx was stimulated markedly when external osmolarity was increased to 600 mosmol/l by mannitol due to an increase via NKCC1 from 55+/-11 to 191+/-2 nmol/106 cells per 15 min, (both n=4, P<0.01).	Rubidium-86	16-21	solute carrier family 12, member 2	Mus musculus	147-152
11821021-2	2002	Tenidap (a) potently potentiated 86Rb+ efflux through hKir2.3 channels expressed in Chinese hamster ovary cells (EC50=402 nM), (b) reversibly and dose-dependently increased whole-cell and macro-patch hKir2.3 currents (maximum whole-cell current response to tenidap was 230+/-27% of control; EC50=1.3 microM.	Rubidium-86	33-38	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	54-61
11926362-1	2002	In this paper, we describe an assay using radioactive rubidium (86Rb) efflux to screen functional human ether-a go-go-related gene (HERG) K+ channels in a high-throughput screening (HTS) format.	Rubidium-86	64-68	potassium voltage-gated channel subfamily H member 2	Homo sapiens	132-136
12490593-2	2003	Magnitudes of acute, nAChR-mediated, specific 86Rb+ efflux responses to 1 mM carbamylcholine were reduced after pretreatment with specific nAChR ligands in effects that depended on pretreatment drug dose, duration of drug pretreatment, and duration of drug-free recovery.	Rubidium-86	46-51	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	21-26
12490593-2	2003	Magnitudes of acute, nAChR-mediated, specific 86Rb+ efflux responses to 1 mM carbamylcholine were reduced after pretreatment with specific nAChR ligands in effects that depended on pretreatment drug dose, duration of drug pretreatment, and duration of drug-free recovery.	Rubidium-86	46-51	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	139-144
11882918-5	2002	In HEK cells transfected with the recombinant vascular K(ATP) channel (Kir6.1 + SUR2B), the compound elicited a concentration-dependent outward current (pEC50 6.8) and in preloaded rat aortic rings it induced a concentration-dependent glibenclamide-sensitive 86Rb+ efflux (pEC50 7.51).	Rubidium-86	259-263	potassium inwardly-rectifying channel, subfamily J, member 8	Rattus norvegicus	71-77
11561100-3	2001	(+/-)-methadone inhibited nicotine-stimulated 86Rb+ efflux from the cells in a concentration-dependent manner with an IC50 value of 1.9 +/- 0.2 microM, indicating that it is a potent nAChR antagonist.	Rubidium-86	46-51	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	183-188
11692276-10	2001	Finally, the ability of both K+ and NH4+ to compete for ouabain-insensitive 86Rb+(K+) influx via NKCC1 was confirmed with similar concentrations for half-maximal influx reduction (K0.5).	Rubidium-86	76-81	solute carrier family 12, member 2	Mus musculus	97-102
11454552-7	2001	Cation flux via NKCC, as measured by 86Rb uptake, was significantly increased in diabetic hearts.	Rubidium-86	37-41	solute carrier family 12 member 1	Homo sapiens	16-20
11557311-5	2001	CuZn-SOD-null lenses showed a doubled basal superoxide concentration, and were more prone to develop photochemical cataract in the present model with more opacification, more hydration, and less 86Rb uptake than lenses from wild-type mice.	Rubidium-86	195-199	superoxide dismutase 1, soluble	Mus musculus	0-8
11192933-2	2000	Moreover, expression of COX-2 was linked to decreases in TNFalpha-mediated 86Rb uptake, an in vitro correlate of natriuresis.	Rubidium-86	75-79	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-29
11274080-8	2001	RESULTS: In the presence of ET-1 (0.1 nM or higher concentration), the rate of ouabain-sensitive potassium (86Rb) uptake was diminished.	Rubidium-86	108-112	endothelin 1	Homo sapiens	28-32
11274080-9	2001	The ET receptor antagonist PD145065 (2 microM) suppressed the inhibitory effect of ET-1 (100 nM) on 86Rb uptake.	Rubidium-86	100-104	endothelin 1	Homo sapiens	83-87
11274080-12	2001	Genistein (150 microM), an inhibitor of tyrosine kinases, abolished the inhibitory effects of ET-1 on lens 86Rb uptake.	Rubidium-86	107-111	endothelin 1	Homo sapiens	94-98
11192933-2	2000	Moreover, expression of COX-2 was linked to decreases in TNFalpha-mediated 86Rb uptake, an in vitro correlate of natriuresis.	Rubidium-86	75-79	tumor necrosis factor	Homo sapiens	57-65
11012899-7	2000	RESULTS: CsA inhibited by 38% the ouabain-sensitive component of 86Rb+ influx mediated by the Na+,K+-ATPase pumps.	Rubidium-86	65-70	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	9-12
11012899-8	2000	CsA also increased by 38% the ouabain-resistant furosemide-sensitive component (Or-Fs) of 86Rb+ influx, reflecting the Na+-K+-Cl- cotransport activity and stimulated the basolateral efflux of 36Cl- from mTAL cells grown on filters.	Rubidium-86	90-95	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	0-3
11012899-11	2000	Adding Ba2+ to the luminal side of cells grown on Petri dishes also prevented the rise in apical 86Rb+ efflux and the increased Or-Fs component of 86Rb+ influx caused by CsA.	Rubidium-86	147-152	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	170-173
10944175-6	2000	In soleus, amylin was found to induce a 45 % stimulation of Na+ efflux, a 43 % increase in 86Rb influx and a rise in intracellular K+.	Rubidium-86	91-95	islet amyloid polypeptide	Rattus norvegicus	11-17