PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
29754714-6	2018	Depolarization by high K+ buffer or K+ channel blockers resulted in a decrease in the mobility of IL-2Ralpha and MHC glycoproteins, as shown by fluorescence correlation spectroscopy, whereas hyperpolarization by the K+ ionophore valinomycin increased their mobility.	Valinomycin	229-240	interleukin 2 receptor subunit alpha	Homo sapiens	98-108
25849454-8	2015	In a growth assay, Pgp-9 increased resistance to the fungicides ketoconazole, actinomycin D, valinomycin and daunorubicin, but not to the anthelmintic fungicide thiabendazole.	Valinomycin	93-104	PGP	Canis lupus familiaris	19-22
26399642-6	2016	One group of sporadic PD lines was highly susceptible to valinomycin-induced mitochondrial depolarization, emulating the mutant LRRK2 phenotype.	Valinomycin	57-68	leucine rich repeat kinase 2	Homo sapiens	128-133
27129925-0	2016	Stimulation by pro-apoptotic valinomycin of cytosolic NADH/cytochrome c electron transport pathway-Effect of SH reagents.	Valinomycin	29-40	cytochrome c, somatic	Homo sapiens	59-71
27129925-6	2016	Valinomycin at 2nM stimulates both the energy-dependent reversible mitochondrial swelling and the NADH/cyto-c oxidation pathway.	Valinomycin	0-11	cytochrome c, somatic	Homo sapiens	103-109
27129925-7	2016	The pro-apoptotic activity of valinomycin, as well as to the dissipation of membrane potential, can be also ascribed to the increased activity of the NADH/cyto-c oxidation pathway useful as an additional source of energy for apoptosis.	Valinomycin	30-41	cytochrome c, somatic	Homo sapiens	155-161
27129925-8	2016	It can be speculated that the activation of the NADH/cyto-c system coupled to valinomycin-induced mitochondrial osmotic swelling may represent a strategy to activate apoptosis in confined solid tumours.	Valinomycin	78-89	cytochrome c, somatic	Homo sapiens	53-59
25990245-7	2016	The excess release of azurophilic granules in Hv1/VSOP-deficient neutrophils was suppressed by inhibiting NADPH oxidase activity and, in part, by valinomycin, a potassium ionophore.	Valinomycin	146-157	hepatitis virus (MHV-2) susceptibility	Mus musculus	46-49
29518371-8	2018	High intracellular K+ concentrations suppressed NTAPP-induced IL-8 mRNA expression, and the K+ ionophore valinomycin (Val) enhanced the induction of IL-8 mRNA.	Valinomycin	105-116	C-X-C motif chemokine ligand 8	Homo sapiens	149-153
29518371-8	2018	High intracellular K+ concentrations suppressed NTAPP-induced IL-8 mRNA expression, and the K+ ionophore valinomycin (Val) enhanced the induction of IL-8 mRNA.	Valinomycin	118-121	C-X-C motif chemokine ligand 8	Homo sapiens	149-153
29518371-10	2018	NTAPP-induced ERK activation was inhibited in the presence of high concentrations of extracellular K+ and enhanced in the presence of Val.	Valinomycin	134-137	mitogen-activated protein kinase 1	Homo sapiens	14-17
29019679-2	2017	Specifically, we benchmark density fitting (DF)-MP2 for as many as 168 atoms (in valinomycin) and show that speed-ups between 3 and 3.8 times can be achieved when compared to the MOLPRO package run on a single CPU.	Valinomycin	81-92	tryptase pseudogene 1	Homo sapiens	48-51
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	55-66	latexin	Homo sapiens	71-74
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	55-66	latexin	Homo sapiens	90-93
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	55-66	latexin	Homo sapiens	90-93
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	94-105	latexin	Homo sapiens	90-93
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	94-105	latexin	Homo sapiens	90-93
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	94-105	latexin	Homo sapiens	90-93
26865218-3	2016	METHODS AND RESULTS: Coadministration of quercetin and valinomycin (50 muM quercetin/0.05 muM valinomycin) reduced intracellular reactive oxygen species content and increased cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) of Caco-2 cells compared to valinomycin-only (0.05 muM) treatment.	Valinomycin	94-105	latexin	Homo sapiens	90-93
25678443-5	2015	This effect is mimicked by cell membrane depolarization induced by an increase in the extracellular K(+) concentration or by application of the Na(+) ionophore gramicidin, but is abolished by stabilization of the membrane potential using the K(+) ionophore valinomycin, by extracellular Mg(2+), which is known to inhibit P2X7R-dependent effects, or by replacing Na(+) by the less P2X7R-permeable Tris(+) ion.	Valinomycin	257-268	purinergic receptor P2X 7	Homo sapiens	321-326
25678443-5	2015	This effect is mimicked by cell membrane depolarization induced by an increase in the extracellular K(+) concentration or by application of the Na(+) ionophore gramicidin, but is abolished by stabilization of the membrane potential using the K(+) ionophore valinomycin, by extracellular Mg(2+), which is known to inhibit P2X7R-dependent effects, or by replacing Na(+) by the less P2X7R-permeable Tris(+) ion.	Valinomycin	257-268	purinergic receptor P2X 7	Homo sapiens	380-385
21739274-1	2011	In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside.	Valinomycin	3-14	cytochrome c, somatic	Homo sapiens	124-136
25088558-6	2014	Cells exposed to severe and irreparable mitochondrial damage agents such as valinomycin can undergo PINK1-Parkin-dependent apoptosis.	Valinomycin	76-87	PTEN induced kinase 1	Homo sapiens	100-105
25088558-7	2014	The proapoptotic response elicited by valinomycin is associated with the degradation of Mcl-1.	Valinomycin	38-49	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	88-93
23688429-4	2013	Valinomycin treatment which depolarizes the membrane potential, abolished mitochondrial localization of the 35 kDa PGC-1alpha.	Valinomycin	0-11	PPARG coactivator 1 alpha	Homo sapiens	115-125
23037694-5	2012	We previously showed that valinomycin, a potassium selective ionophore, also caused release of cytochrome c from mitochondria without inducing PT.	Valinomycin	26-37	cytochrome c, somatic	Homo sapiens	95-107
21739274-0	2011	Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis.	Valinomycin	0-11	cytochrome c, somatic	Homo sapiens	61-73
21739274-0	2011	Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis.	Valinomycin	0-11	cytochrome c, somatic	Homo sapiens	98-110
21739274-1	2011	In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside.	Valinomycin	3-14	cytochrome c, somatic	Homo sapiens	138-144
21739274-1	2011	In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside.	Valinomycin	3-14	sulfite oxidase	Homo sapiens	150-165
21739274-1	2011	In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside.	Valinomycin	3-14	sulfite oxidase	Homo sapiens	167-170
21739274-1	2011	In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside.	Valinomycin	3-14	anti-Mullerian hormone	Homo sapiens	193-233
21739274-8	2011	Rather than to the dissipation of membrane potential, the pro-apoptotic property of valinomycin can be ascribed to both the release of cyto-c from mitochondria to cytosol and the increased rate of cytosolic NADH coupled with an increased availability of energy in the form of glycolytic ATP, useful for the correct execution of apoptotic program.	Valinomycin	84-95	cytochrome c, somatic	Homo sapiens	135-141
22282962-7	2011	Nigericin and valinomycin decreased the concentrations of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, and IL-17 in the culture medium with IC50 values less than 0.01 ng/ml.	Valinomycin	14-25	interferon gamma	Homo sapiens	58-80
22282962-7	2011	Nigericin and valinomycin decreased the concentrations of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, and IL-17 in the culture medium with IC50 values less than 0.01 ng/ml.	Valinomycin	14-25	tumor necrosis factor	Homo sapiens	82-115
22282962-7	2011	Nigericin and valinomycin decreased the concentrations of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, and IL-17 in the culture medium with IC50 values less than 0.01 ng/ml.	Valinomycin	14-25	interleukin 10	Homo sapiens	117-136
22282962-7	2011	Nigericin and valinomycin decreased the concentrations of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, and IL-17 in the culture medium with IC50 values less than 0.01 ng/ml.	Valinomycin	14-25	interleukin 17A	Homo sapiens	142-147
19366603-7	2009	The effects of p13 on ROS are mimicked by the K(+) ionophore valinomycin, while the protonophore FCCP decreases ROS, indicating that depolarization induced by K(+) vs. H(+) currents has different effects on mitochondrial ROS production, possibly because of their opposite effects on matrix pH (alkalinization and acidification, respectively).	Valinomycin	61-72	H3 histone pseudogene 6	Homo sapiens	15-18
20388708-6	2010	Overexpression of wild-type Hax-1 or its uncleavable mutant form protects the mitochondria against GrB or valinomycin-mediated depolarization.	Valinomycin	106-117	HCLS1 associated protein X-1	Homo sapiens	28-33
21329808-7	2011	Indeed, we found several bioactive drugs, such as pyrvinium pamoate, valinomycin, and rottlerin, that selectively suppressed 2DG-induced GRP78 promoter activity as versipelostatin and biguanide did.	Valinomycin	69-80	heat shock protein family A (Hsp70) member 5	Homo sapiens	137-142
16831863-8	2006	We find that suppression of expression of Src in developing osteoclasts results in decreased vesicular acidification, which is rescued by valinomycin, consistent with the loss of chloride conductance in the proton pump-containing vesicles.	Valinomycin	138-149	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	42-45
19218587-2	2009	Our previous study showed that valinomycin also caused the release of cytochrome c from mitochondria but without inducing this PT (Shinohara, Y., Almofti, M. R., Yamamoto, T., Ishida, T., Kita, F., Kanzaki, H., Ohnishi, M., Yamashita, K., Shimizu, S., and Terada, H. (2002) Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin.	Valinomycin	31-42	cytochrome c, somatic	Homo sapiens	70-82
17595513-8	2007	Treatment with 1 nM valinomycin indeed decreased forward scatter and increased annexin V binding.	Valinomycin	20-31	annexin A5	Homo sapiens	79-88
16857314-9	2006	Valinomycin-treated CHO cells underwent several apoptotic events, including phosphatidylserine (PS) membrane translocation, caspase-3 activation, and mitochondrial membrane depolarization during the first few hours of exposure.	Valinomycin	0-11	caspase-3	Cricetulus griseus	124-133
19456150-9	2009	The factors affecting ion selectivity revealed herein help to rationalize why valinomycin and the KcsA ion channels are highly K(+)-selective, whereas the NaK channel is nonselective.	Valinomycin	78-89	TANK binding kinase 1	Homo sapiens	155-158
18645223-4	2008	Using immunocytochemistry we observed redistribution, enhanced upon treatment with camptothecin or valinomycin, of CIDEa to nucleus.	Valinomycin	99-110	cell death inducing DFFA like effector a	Homo sapiens	115-120
17234684-3	2007	Generation of a valinomycin-mediated potassium-diffusion potential induced the reduction of cytochrome b in the reconstituted bc1 complex in the presence of sodium ascorbate.	Valinomycin	16-27	cytochrome b	Bos taurus	92-104
16891388-7	2006	Interestingly, K(+) inhibitors or membrane depolarization (induced by valinomycin in high-K(+) medium) decreased alpha-, beta-, and gamma-ENaC and CFTR mRNA.	Valinomycin	70-81	CF transmembrane conductance regulator	Homo sapiens	147-151
16720572-6	2006	By using isoform-specific peptides, we found that the effects of K(ATP) channel openers, PKG, or valinomycin were mediated by a PKCepsilon.	Valinomycin	97-108	protein kinase C epsilon	Homo sapiens	128-138
12841327-4	2002	CsA-sensitive mitochondrial swelling, depolarization, and the release of Ca2+ and Cyt.c were induced by low concentrations of arachidonic acid, triiodothyronine (T3), or 6-hydroxdopamine but not by valinomycin and high concentrations of the fatty acid or T3.	Valinomycin	198-209	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3
16595926-0	2006	Selective cytotoxic activity of valinomycin against HT-29 Human colon carcinoma cells via down-regulation of GRP78.	Valinomycin	32-43	heat shock protein family A (Hsp70) member 5	Homo sapiens	109-114
16595926-4	2006	We found that valinomycin prevents UPR-induced protein expression, such as GRP78 and GRP94.	Valinomycin	14-25	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-80
16595926-4	2006	We found that valinomycin prevents UPR-induced protein expression, such as GRP78 and GRP94.	Valinomycin	14-25	heat shock protein 90 beta family member 1	Homo sapiens	85-90
15876477-3	2005	In this paper, we show that valinomycin-induced apoptosis involves two different pathways in human NK cells: the predominant one is caspase-3 independent and the other caspase-3 dependent.	Valinomycin	28-39	caspase 3	Homo sapiens	132-141
15876477-3	2005	In this paper, we show that valinomycin-induced apoptosis involves two different pathways in human NK cells: the predominant one is caspase-3 independent and the other caspase-3 dependent.	Valinomycin	28-39	caspase 3	Homo sapiens	168-177
15835751-8	2005	The known P-gp-activating compounds verapamil, progesterone, and valinomycin revealed the typical bell-shaped activity/concentration profiles in P388/ADR rafts, indicative for activation at low compound concentrations and inhibition at concentrations >10 to 100 microM.	Valinomycin	65-76	phosphoglycolate phosphatase	Mus musculus	10-14
14985103-3	2004	In the case of cyclosporin A, vinblastine or valinomycin, this up-shift was found to be concomitant with the near-complete suppression of labeling with other mAbs specific for Pgp epitopes overlapping with UIC2, while pre-treatment with verapamil or Tween 80 brings about a modest suppression.	Valinomycin	45-56	ATP binding cassette subfamily B member 1	Homo sapiens	176-179
14565686-13	2003	Em hyperpolarization (valinomycin-clamp) reduced V-ATPase activity, causing an acidic shift in baseline pHi under steady-state conditions and slowing pHi recovery from NH4Cl prepulse acid-loads.	Valinomycin	22-33	glucose-6-phosphate isomerase	Oryctolagus cuniculus	104-107
14565686-13	2003	Em hyperpolarization (valinomycin-clamp) reduced V-ATPase activity, causing an acidic shift in baseline pHi under steady-state conditions and slowing pHi recovery from NH4Cl prepulse acid-loads.	Valinomycin	22-33	glucose-6-phosphate isomerase	Oryctolagus cuniculus	150-153
16554024-2	2006	Among these compounds, the yeast expressing hTAPL exhibits high sensitivity to valinomycin, a monovalent cation ionophore.	Valinomycin	79-90	ATP binding cassette subfamily B member 9	Homo sapiens	44-49
16554024-3	2006	A mutation in Walker A motif, which lost ATP-binding activity of hTAPL, eliminated the enhanced sensitivity to valinomycin.	Valinomycin	111-122	ATP binding cassette subfamily B member 9	Homo sapiens	65-70
16554024-4	2006	These findings suggest that the transport activity of hTAPL is important for conferring high valinomycin-sensitive phenotype to yeast.	Valinomycin	93-104	ATP binding cassette subfamily B member 9	Homo sapiens	54-59
16100048-5	2005	Menadione (2 micromol/L) and valinomycin (10 nmol/L) induced similar ROS formation in wild-type (WT) and Cx43+/- cardiomyocytes.	Valinomycin	29-40	gap junction protein, alpha 1	Mus musculus	105-109
15268937-8	2004	Uptake of Mg2+ into corA expressing cells was strongly stimulated by nigericin, which increased the membrane potential DeltaPsi at the expense of DeltapH, and drastically reduced by valinomycin, which decreased the membrane potential DeltaPsi.	Valinomycin	182-193	mucin 7, secreted	Homo sapiens	10-13
12392554-0	2002	Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin.	Valinomycin	85-96	cytochrome c, somatic	Homo sapiens	61-73
12392554-5	2002	However, valinomycin did induce a significant release of cytochrome c, and thus it may be a nice tool to study the processes of mitochondrial cytochrome c release.	Valinomycin	9-20	cytochrome c, somatic	Homo sapiens	57-69
12392554-5	2002	However, valinomycin did induce a significant release of cytochrome c, and thus it may be a nice tool to study the processes of mitochondrial cytochrome c release.	Valinomycin	9-20	cytochrome c, somatic	Homo sapiens	142-154
12101027-8	2002	After the neuronatin-beta gene was transfected into and expressed in the 1.9 cells, they regained wild type PC12 levels of resistance to nigericin, rotenone and valinomycin.	Valinomycin	161-172	neuronatin	Rattus norvegicus	10-20
12841327-4	2002	CsA-sensitive mitochondrial swelling, depolarization, and the release of Ca2+ and Cyt.c were induced by low concentrations of arachidonic acid, triiodothyronine (T3), or 6-hydroxdopamine but not by valinomycin and high concentrations of the fatty acid or T3.	Valinomycin	198-209	cytochrome c, somatic	Homo sapiens	82-87
11710806-4	2001	We have found substantial changes in the above-mentioned Cd2+ effects on mitochondria treated in sequence with 100 microM of Ca2+, Sr2+, Mn2+ or Ba2+(Me2+) and 7.5 microM RR, as well as the alterations in Cd2+ action on the uptake of 137Cs+ by succinate-energized mitochondria in the presence or absence of valinomycin in acetate medium (50 mM Tris-acetate and 140 mM sucrose) with or without Ca2+ or RR.	Valinomycin	307-318	Cd2 molecule	Rattus norvegicus	57-60
11743742-6	2001	Remarkably, we have also identified several compounds-valinomycin, norverapamil, reserpine, nobiletin, emetine, gallopamil, fluphenazine-that uniquely inhibit P-gp function with affinities comparable to benchmark P-gp inhibitors despite a lack of effect on CYP3A4 function at physiologically relevant concentrations.	Valinomycin	54-65	phosphoglycolate phosphatase	Homo sapiens	159-163
11743742-6	2001	Remarkably, we have also identified several compounds-valinomycin, norverapamil, reserpine, nobiletin, emetine, gallopamil, fluphenazine-that uniquely inhibit P-gp function with affinities comparable to benchmark P-gp inhibitors despite a lack of effect on CYP3A4 function at physiologically relevant concentrations.	Valinomycin	54-65	phosphoglycolate phosphatase	Homo sapiens	213-217
11743742-6	2001	Remarkably, we have also identified several compounds-valinomycin, norverapamil, reserpine, nobiletin, emetine, gallopamil, fluphenazine-that uniquely inhibit P-gp function with affinities comparable to benchmark P-gp inhibitors despite a lack of effect on CYP3A4 function at physiologically relevant concentrations.	Valinomycin	54-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	257-263
11743742-7	2001	Indeed, valinomycin inhibits P-gp with an IC(50) similar to cyclosporin A yet apparently does not affect CYP3A4 function, and emetine and nobiletin are also specific for interaction with P-gp.	Valinomycin	8-19	phosphoglycolate phosphatase	Homo sapiens	29-33
11743742-7	2001	Indeed, valinomycin inhibits P-gp with an IC(50) similar to cyclosporin A yet apparently does not affect CYP3A4 function, and emetine and nobiletin are also specific for interaction with P-gp.	Valinomycin	8-19	phosphoglycolate phosphatase	Homo sapiens	187-191
11641429-4	2001	In contrast, valinomycin-induced cytochrome c-EGFP release occurred slowly over several hours.	Valinomycin	13-24	cytochrome c, somatic	Homo sapiens	33-45
11641429-5	2001	Unlike staurosporine, the valinomycin-induced cytochrome c release was not associated with translocation of the proapoptotic Bax protein to the mitochondria, and was not accompanied by co-release of the proapoptotic Smac protein.	Valinomycin	26-37	cytochrome c, somatic	Homo sapiens	46-58
11426445-6	2001	Prolonged exposure to valinomycin induced significant matrix swelling, and per se also caused release of cytochrome c from mitochondria.	Valinomycin	22-33	cytochrome c, somatic	Homo sapiens	105-117
11426445-7	2001	In contrast to staurosporine, however, valinomycin-induced cytochrome c release and cell death were not associated with caspase-3 activation and insensitive to Bcl-xL overexpression.	Valinomycin	39-50	cytochrome c, somatic	Homo sapiens	59-71
10874038-5	2000	Chloride permeability of reconstituted vesicles was assessed using a valinomycin dependent chloride efflux assay, demonstrating increased vesicular chloride permeability with CLIC-1 compared with control.	Valinomycin	69-80	chloride intracellular channel 1	Bos taurus	175-181
11406104-5	2001	Changes of inorganic anions in the extravesicular medium and of membrane potential by valinomycin altered the initial uptake activity of L-carnitine by OCTN2.	Valinomycin	86-97	solute carrier family 22 member 5	Homo sapiens	152-157
11072136-5	2000	However, valinomycin-induced caspase-3 elevation was only prevented by lithium pretreatment while both lithium and valproate attenuated valinomycin-induced LDH release.	Valinomycin	9-20	caspase 3	Homo sapiens	29-38
10729188-3	2000	Yeast cells expressing P-gp were valinomycin resistant.	Valinomycin	33-44	ATP binding cassette subfamily B member 1	Homo sapiens	23-27
10194338-15	1999	Interestingly, relative valinomycin resistance and growth of the 9.3/hu MDR 1 strains are found to strongly depend on the ionic composition of the growth medium.	Valinomycin	24-35	GTPase-activating protein MDR1	Saccharomyces cerevisiae S288C	72-77
10718344-8	2000	Also, modifying the membrane potential with valinomycin (hyperpolarization) or either gramicidin or KCl (depolarization) demonstrated a strong relationship between PtdSer synthesis and annexin V-FITC reactivity in CD95-treated cells.	Valinomycin	44-55	annexin A5	Homo sapiens	185-194
10718344-8	2000	Also, modifying the membrane potential with valinomycin (hyperpolarization) or either gramicidin or KCl (depolarization) demonstrated a strong relationship between PtdSer synthesis and annexin V-FITC reactivity in CD95-treated cells.	Valinomycin	44-55	Fas cell surface death receptor	Homo sapiens	214-218
11674717-8	1999	The linear precursor of the valinomycin analogue 30 ([L-Val-D-Man-D-Val-L-Lac](3)) was entirely synthesized on resin and cyclized in solution.	Valinomycin	28-39	lactase	Homo sapiens	74-77
10098900-7	1999	Uptake of 137-Cs by succinate-energized mitochondria in the presence of 10(-8) M of valinomycin was substantially decreased in experiments with 10 microM of the complexes than with Cd2+.	Valinomycin	84-95	Cd2 molecule	Rattus norvegicus	181-184
9920900-4	1999	Both the ionophores nigericin and valinomycin inhibited QacA-mediated export of ethidium, indicating an electrogenic drug/nH+ (n >/= 2) antiport mechanism.	Valinomycin	34-45	QacA	Staphylococcus aureus	56-60
10418988-4	1999	Both MA-10 Leydig tumor cell steroidogenesis and mitochondrial import of StAR were inhibited by m-CCCP or valinomycin at concentrations which had only minimal effects on P450scc activity.	Valinomycin	106-117	steroidogenic acute regulatory protein	Mus musculus	73-77
9312089-6	1997	When the purified ATPase was reconstituted into liposomes prepared from Enterococcus faecalis phospholipids, ATP-driven Na+ uptake was observed; uptake was blocked by nitrate, destruxin B, and monensin, but it accelerated by carbonyl cyanide m-chlorophenylhydrazone and valinomycin.	Valinomycin	270-281	ATPase	Enterococcus faecalis	18-24
9688604-2	1998	We studied pyruvate, alpha-ketoisovalerate, alpha-ketoisocaproate, and phenylpyruvate uniport via the uncoupling protein (UCP1) as a GDP-sensitive swelling in K+ salts induced by valinomycin or by monensin and carbonyl cyanide-p-(trifluoromethoxy)phenylhydrazone in Na+ salts.	Valinomycin	179-190	uncoupling protein 1	Homo sapiens	122-126
9581870-12	1998	Potassium ionophorvalinomycin, considered to select against mineralizing osteoprogenitors at 30 degrees C, showed on day 10 in the absence of DEX a relative increase in truncated Src protein compared to both DEX-stimulated and nonstimulated cultures in the absence of valinomycin.	Valinomycin	18-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-182
9581870-13	1998	On day 7 of DEX stimulation, the presence of valinomycin resulted in low p54/52src.	Valinomycin	45-56	interferon induced protein with tetratricopeptide repeats 2	Homo sapiens	73-76
9581870-16	1998	On day 7, p32-34 did not change under DEX, but valinomycin selected cells with less phoshpotyrosine-containing p32-34.	Valinomycin	47-58	inhibitor of growth family member 2	Homo sapiens	111-114
9702339-4	1998	The K(+)-uptake by the arcA mutant is also inhibited by N,N"-dicyclohexylcarbodiimide and has a variable stoichiometry of N,N"-dicyclohexylcarbodiimide-sensitive ion fluxes and does not significantly change in the presence of valinomycin and with varying temperature, whereas the intracellular activity of K+ ions is lower.	Valinomycin	226-237	arginine deiminase	Escherichia coli	23-27
9595303-10	1997	Valinomycin in part released the inhibition of the vanadate-induced Ca2+ influx by known K(Ca) inhibitors (quinine, oligomycin, 4-aminopyridine) but not by inhibitors of the Ca2+ channel (Cu2+, HS-reagents, organic Ca2+ channel blockers).	Valinomycin	0-11	casein kappa	Homo sapiens	89-94
9358731-0	1997	The crystal and molecular structure of a valinomycin analogue cyclo[(D-Val-L-Lac-L-Ala-D-Hyi)2(D-Val-L-Lac-L-Val-D-Hyi)].	Valinomycin	41-52	lactase	Homo sapiens	77-80
9358731-0	1997	The crystal and molecular structure of a valinomycin analogue cyclo[(D-Val-L-Lac-L-Ala-D-Hyi)2(D-Val-L-Lac-L-Val-D-Hyi)].	Valinomycin	41-52	lactase	Homo sapiens	103-106
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.	Valinomycin	23-34	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	83-97
9247172-5	1997	Yeast cells transformed with the Pgp expression plasmid acquire increased resistance to valinomycin, suggesting that the expressed Pgp is properly folded and functional.	Valinomycin	88-99	ATP binding cassette subfamily B member 1	Homo sapiens	33-36
9247172-5	1997	Yeast cells transformed with the Pgp expression plasmid acquire increased resistance to valinomycin, suggesting that the expressed Pgp is properly folded and functional.	Valinomycin	88-99	ATP binding cassette subfamily B member 1	Homo sapiens	131-134
9208926-1	1997	The activity of the Cl(-)-conductive pathways, their regulation by protein kinase A (PKA) and their relationship to the cystic fibrosis transmembrane regulator (CFTR) protein were assessed in rat kidney cortical brush-border-membrane vesicles (cBBMV) and outer medullary vesicles (OMV) by measuring the rate of valinomycin-induced microsomal swelling by light scattering in the presence of an inward Cl- gradient.	Valinomycin	311-322	CF transmembrane conductance regulator	Rattus norvegicus	161-165
9208926-8	1997	Two anti-CFTR mAbs inhibited PKA-activated valinomycin-induced swelling in cBBMV and OMV, while immunoblot analysis of the corresponding proteins with the same antibodies indicated the presence of a 170-kDa protein.	Valinomycin	43-54	CF transmembrane conductance regulator	Rattus norvegicus	9-13
9208926-8	1997	Two anti-CFTR mAbs inhibited PKA-activated valinomycin-induced swelling in cBBMV and OMV, while immunoblot analysis of the corresponding proteins with the same antibodies indicated the presence of a 170-kDa protein.	Valinomycin	43-54	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	29-32
8815210-7	1996	We describe a "profile migration" method in which dilute red cell suspensions in low-K+ media were permeabilized to K+ with a high concentration of valinomycin, rendering PCl the main rate-limiting factor for cell dehydration.	Valinomycin	148-159	PHD finger protein 1	Homo sapiens	171-174
8626756-4	1996	MRP and Mdr3 expression produced pleiotropic effects on drug resistance in this mutant, as corresponding VASY2563 transformants also acquired resistance to the anti-fungal agent FK506 and to the K+/H+ ionophore valinomycin.	Valinomycin	211-222	ATP binding cassette subfamily C member 3	Homo sapiens	0-3
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.	Valinomycin	42-53	ATP binding cassette subfamily B member 1	Homo sapiens	126-140
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.	Valinomycin	67-78	ATP binding cassette subfamily B member 1	Homo sapiens	89-103
7563015-8	1995	When cells with normal chloride content were depolarized (135 mM medium potassium + 10 microM valinomycin), cAMP activated electrogenic chloride uptake permselective for Cl- approximately Br- > NO3- > I-.	Valinomycin	94-105	NBL1, DAN family BMP antagonist	Homo sapiens	197-200
9287320-6	1997	For some other drugs (e.g. valinomycin or calcein acetoxymethylester) activation of the MDR1-ATPase for any of the mutants was indistinguishable from that of the wild-type protein.	Valinomycin	27-38	ATP binding cassette subfamily B member 1	Homo sapiens	88-92
9287320-6	1997	For some other drugs (e.g. valinomycin or calcein acetoxymethylester) activation of the MDR1-ATPase for any of the mutants was indistinguishable from that of the wild-type protein.	Valinomycin	27-38	dynein axonemal heavy chain 8	Homo sapiens	93-99
8647905-3	1996	Hyperpolarization of the parental and neomycin control transfected cells by valinomycin significantly increased the radioresistance of these cells to such an extent that there was no longer a significant difference in the survival of the valinomycin treated and irradiated control cells compared to similarly irradiated Bcl-2 transfected cells.	Valinomycin	76-87	BCL2 apoptosis regulator	Homo sapiens	320-325
8670194-6	1996	Administration of the K+ ionophore, valinomycin, abolished the action of CCK-OPE.	Valinomycin	36-47	cholecystokinin	Homo sapiens	73-76
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.	Valinomycin	23-34	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+.	Valinomycin	80-91	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-150
8304443-3	1994	Valinomycin (2 microM), a K+ ionophore, inhibited both basal and TEA-induced Prl secretion.	Valinomycin	0-11	prolactin	Rattus norvegicus	77-80
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.	Valinomycin	297-308	interleukin 1 beta	Mus musculus	92-101
8294431-2	1994	The reduction of cytochrome b in the presence of sodium ascorbate was observed on addition of valinomycin to the K(+)-loaded proteoliposomes in a medium containing no external KCl; it was followed by the gradual oxidation.	Valinomycin	94-105	mitochondrially encoded cytochrome b	Homo sapiens	17-29
2511996-4	1989	The monovalent cation ionophores, valinomycin and nigericin (5 microM), enhanced the release of PGI2 from endothelial cells stimulated by ATP or bradykinin.	Valinomycin	34-45	kininogen 1	Bos taurus	145-155
18476229-8	1994	We here report that mobile ionophores such as valinomycin, nonactin, nigericin, monensin, calcimycin, lasalocid inhibit the efflux of anthracycline by P-glycoprotein whereas, channel-forming ionophores such as gramicidin do not.	Valinomycin	46-57	ATP binding cassette subfamily B member 1	Homo sapiens	151-165
7690715-4	1993	KN3/pgp was resistant to valinomycin and actinomycin D, but not to adriamycin.	Valinomycin	25-36	phosphoglycolate phosphatase	Homo sapiens	4-7
7690715-8	1993	These results suggest that human P-glycoprotein functions as an efflux pump of valinomycin and actinomycin D in the membrane of S. pombe.	Valinomycin	79-90	ATP binding cassette subfamily B member 1	Homo sapiens	33-47
8359386-0	1993	Valinomycin pretreatment induced LDL receptor activity in cultured human cells.	Valinomycin	0-11	low density lipoprotein receptor	Homo sapiens	33-45
1378400-17	1992	By demonstrating that valinomycin-induced K+ and H+ fluxes reflect relaxation into the diffusion equilibrium state, the transport rate of UCP can be evaluated as a first-order rate, VH+/CH+, in which the rate, VH+, is related to H(+)-uptake capacity, CH+.	Valinomycin	22-33	uncoupling protein 1	Homo sapiens	138-141
1318017-2	1992	This appears as an inhibition of substrate oxidation (cytochrome c) or reduction (O2) rates which, in the first few turnovers, can be largely removed upon addition of valinomycin, a specific K+ carrier.	Valinomycin	167-178	cytochrome c, somatic	Homo sapiens	54-66
1347948-6	1992	Nevertheless, some, if not all, of the Mdr1 made in yeast was properly folded and functional because it could be photoaffinity labeled specifically with 8-azido-ATP and because cells overexpressing Mdr1 displayed increased resistance towards valinomycin, an ionophore known to interact with Mdr1 in animal cells.	Valinomycin	242-253	GTPase-activating protein MDR1	Saccharomyces cerevisiae S288C	39-43
1347948-6	1992	Nevertheless, some, if not all, of the Mdr1 made in yeast was properly folded and functional because it could be photoaffinity labeled specifically with 8-azido-ATP and because cells overexpressing Mdr1 displayed increased resistance towards valinomycin, an ionophore known to interact with Mdr1 in animal cells.	Valinomycin	242-253	GTPase-activating protein MDR1	Saccharomyces cerevisiae S288C	198-202
1347948-6	1992	Nevertheless, some, if not all, of the Mdr1 made in yeast was properly folded and functional because it could be photoaffinity labeled specifically with 8-azido-ATP and because cells overexpressing Mdr1 displayed increased resistance towards valinomycin, an ionophore known to interact with Mdr1 in animal cells.	Valinomycin	242-253	GTPase-activating protein MDR1	Saccharomyces cerevisiae S288C	198-202
1665913-0	1991	Chlorophyll photosensitized electron transfer reactions in lipid vesicles: enhancement in yield of vectorial electron transfer across the bilayer from reduced cytochrome c to oxidized ferredoxin by addition of valinomycin plus potassium ion.	Valinomycin	210-221	cytochrome c, somatic	Homo sapiens	159-171
1920117-3	1991	The renin secretion stimulated by valinomycin was further increased by inclusion of the H+ ionophore, carbonylcyanide m-chlorophenylhydrazone.	Valinomycin	34-45	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	4-9
2078629-1	1990	The effect of the membrane potential (K(+)-valinomycin system) on the Mg2+, ATP-dependent transport of Ca2+ in inside-out vesicles of myometrium sarcolemma has been studied.	Valinomycin	43-54	mucin 7, secreted	Homo sapiens	70-73
2078629-1	1990	The effect of the membrane potential (K(+)-valinomycin system) on the Mg2+, ATP-dependent transport of Ca2+ in inside-out vesicles of myometrium sarcolemma has been studied.	Valinomycin	43-54	carbonic anhydrase 2	Homo sapiens	103-106
2078629-3	1990	In the presence of valinomycin (5.10(-8) M) the inside-out directed K+ gradient (delta psi = -86 mV, with a negative charge inside) stimulated the initial rate of the energy-dependent accumulation of Ca2+ transfer whereas the oppositely directed K+ gradient (delta psi = +72 mV, with a positive charge inside) had no effect on this process.	Valinomycin	19-30	carbonic anhydrase 2	Homo sapiens	200-203
1724618-3	1990	The cyclic peptide microcystin-LR (MLR) and the depsipeptides, valinomycin (VLM) and enniatin-B (ENB), bind to CaM and inhibit PDE activity.	Valinomycin	63-74	calmodulin 1	Homo sapiens	111-114
2142942-1	1990	Effects of valinomycin and nigericin on the ATP-driven transhydrogenase reaction catalyzed by reconstituted transhydrogenase-ATPase vesicles.	Valinomycin	11-22	dynein axonemal heavy chain 8	Homo sapiens	125-131
2158497-0	1990	The K(+)-ionophores nonactin and valinomycin interact differently with the protein of reconstituted cytochrome c oxidase.	Valinomycin	33-44	cytochrome c, somatic	Homo sapiens	100-112
2158497-1	1990	The K(+)-ionophores valinomycin and nonactin induce a qualitatively identical change of the visible spectrum of isolated oxidized cytochrome c oxidase (red shift), but the amplitude is half with nonactin.	Valinomycin	20-31	cytochrome c, somatic	Homo sapiens	130-142
2158497-2	1990	Valinomycin, in the presence or absence of a protonophore, stimulates the respiration of the reconstituted enzyme to a higher extent than nonactin and results in a higher Km for cytochrome c.	Valinomycin	0-11	cytochrome c, somatic	Homo sapiens	178-190
1522230-15	1992	Clamping voltage with K+/valinomycin; depolarizing membrane voltage by reducing extracellular chloride; or addition of NPPB prevented PTH-induced calcium uptake.	Valinomycin	25-36	parathyroid hormone	Mus musculus	134-137
1428520-1	1992	Valinomycin, cyclo-[(L-Val-D-Hyv-D-Val-L-Lac)3-], was crystallized from aqueous dioxane solvent as a monohydrate complex in which water molecules were found within the ion-binding cavity of the ionophore: monoclinic P2(1), a = 14.377 (3), b = 41.554 (14), c = 14.080 (3) A, beta = 118.27 (2) degrees, Z = 4.	Valinomycin	0-11	cyclin dependent kinase inhibitor 1A	Homo sapiens	216-221
1449075-4	1992	The ATPase reconstituted into proteoliposomes catalyzed an ATP-dependent Na+ accumulation that was stimulated to the same extent by dissipating the membrane potential with valinomycin or with the uncoupler carbonylcyanide-m-chloro phenylhydrazone.	Valinomycin	172-183	ATPase	Escherichia coli	4-10
1699552-8	1990	Valinomycin (K+ ionophore) inhibited Spd uptake by C 6, P 388, Balb/c 3T3 and SV40/3T3 but not by L 1210 and U 251 cells.	Valinomycin	0-11	complement component 6	Mus musculus	51-54
34659244-7	2021	Indeed, valinomycin-induced compulsory mitochondrial depolarization in neutrophils restored inflammasome-dependent cell death and ATP-induced NLRP3 desensitization in neutrophils.	Valinomycin	8-19	NLR family, pyrin domain containing 3	Mus musculus	142-147
2606911-4	1989	In addition, the degree of valinomycin-induced fluorescence change of DiS-C3(5)-probed membranes in the presence of various concentrations of KCl was reduced by treatment of the membranes with neuraminidase.	Valinomycin	27-38	neuraminidase 1	Homo sapiens	193-206
2606911-6	1989	The membrane potentials estimated from the null point of valinomycin-induced changes in the DiS-C3(5) fluorescence of the control and neuraminidase-treated membranes were -25 to -29.7 and -40 to -48.8 mV, respectively.	Valinomycin	57-68	neuraminidase 1	Homo sapiens	134-147
2526631-0	1989	Effects of valinomycin on calcium mobilization in vascular smooth muscle cells induced by angiotensin II.	Valinomycin	11-22	angiotensinogen	Homo sapiens	90-104
2719967-1	1989	Monoclonal antibodies raised against bilitranslocase, may display either inhibitory or enhancing activity on the electrogenic transport of sulfobromophthalein, evoked in rat liver plasma-membrane vesicles by the addition of valinomycin in the presence of K+.	Valinomycin	224-235	ceruloplasmin	Rattus norvegicus	37-52
2471518-1	1989	Valinomycin binds to soluble and reconstituted cytochrome c oxidase (COX) in a stoichiometric manner, as shown by a spectral shift of the oxidized gamma-band.	Valinomycin	0-11	cytochrome c oxidase subunit 8A	Homo sapiens	69-72
2471518-3	1989	Titration of the proton pumping activity of reconstituted COX with valinomycin reached a maximum of H+/e- - 0.73 after addition of 1 mole of valinomycin per mole of reconstituted COX.	Valinomycin	67-78	cytochrome c oxidase subunit 8A	Homo sapiens	58-61
2471518-3	1989	Titration of the proton pumping activity of reconstituted COX with valinomycin reached a maximum of H+/e- - 0.73 after addition of 1 mole of valinomycin per mole of reconstituted COX.	Valinomycin	67-78	cytochrome c oxidase subunit 8A	Homo sapiens	179-182
2471518-3	1989	Titration of the proton pumping activity of reconstituted COX with valinomycin reached a maximum of H+/e- - 0.73 after addition of 1 mole of valinomycin per mole of reconstituted COX.	Valinomycin	141-152	cytochrome c oxidase subunit 8A	Homo sapiens	58-61
2471518-3	1989	Titration of the proton pumping activity of reconstituted COX with valinomycin reached a maximum of H+/e- - 0.73 after addition of 1 mole of valinomycin per mole of reconstituted COX.	Valinomycin	141-152	cytochrome c oxidase subunit 8A	Homo sapiens	179-182
2471518-4	1989	It is concluded that K+-translocation in proton-pumping COX vesicles occurs via enzyme-bound valinomycin.	Valinomycin	93-104	cytochrome c oxidase subunit 8A	Homo sapiens	56-59
2619925-5	1989	Treatment with phospholipase A2 stimulated Ca2+ penetration into liposomes driven by a valinomycin-induced diffusion potential or a nigericin-induced H+ gradient.	Valinomycin	87-98	phospholipase A2 group IB	Homo sapiens	15-31
2526631-1	1989	The effect of the specific potassium (K+) ionophore valinomycin on increase in intracellular calcium concentration [( Ca2+]i) was studied in vascular smooth muscle cells (VSMC).	Valinomycin	52-63	carbonic anhydrase 2	Homo sapiens	118-121
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	carbonic anhydrase 2	Homo sapiens	82-85
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	angiotensinogen	Homo sapiens	108-122
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	angiotensinogen	Homo sapiens	124-127
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	carbonic anhydrase 2	Homo sapiens	149-152
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	carbonic anhydrase 2	Homo sapiens	149-152
2526631-2	1989	Valinomycin at more than 10(-9) M dose-dependently suppressed phasic increase in [Ca2+]i in VSMC induced by angiotensin II (AII) in both control and Ca2+-free solution, indicating that it suppressed the release of Ca2+ from intracellular Ca2+ stores.	Valinomycin	0-11	carbonic anhydrase 2	Homo sapiens	149-152
2526631-5	1989	These results indicate that decrease of intracellular K+ induced by valinomycin suppressed the release of Ca2+ from intracellular Ca2+ stores induced by IP3.	Valinomycin	68-79	carbonic anhydrase 2	Homo sapiens	106-109
2526631-5	1989	These results indicate that decrease of intracellular K+ induced by valinomycin suppressed the release of Ca2+ from intracellular Ca2+ stores induced by IP3.	Valinomycin	68-79	carbonic anhydrase 2	Homo sapiens	130-133
2839502-10	1988	In intact, ion-impermeable inside-out vesicles, in the presence of valinomycin, ATPase activity increased up to 175 mM K+.	Valinomycin	67-78	dynein axonemal heavy chain 8	Homo sapiens	80-86
2849819-3	1988	Being stored in the mitochondria, Cd2+ inhibits respiration and an energy dependent transport of penetrating cations (Cs+-valinomycin), and disturbs passive permeability of the inner mitochondrial membrane for monovalent cations and H+.	Valinomycin	122-133	Cd2 molecule	Rattus norvegicus	34-37
3128323-5	1988	After 2 h of incubation of the cells in the presence of ionophore and Ca2+, the released acrosin activity is related to the ionophores according to the sequence: A23187 greater than monensin greater than valinomycin greater than FCCP = without ionophore.	Valinomycin	204-215	acrosin	Homo sapiens	89-96
6327294-2	1984	This was demonstrated by assessing the inhibition of proteolytic processing of the precursor form of beta-lactamase caused by perturbation of the energized state of the membrane in cells treated with valinomycin.	Valinomycin	200-211	beta-lactamase	Escherichia coli	101-115
2439348-6	1987	Valinomycin decreased CsA"s effect on the membrane potential while the ionophore A-23187 and ionomycin caused depolarizations that were additive with CsA"s.	Valinomycin	0-11	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	22-25
3032620-4	1987	The results obtained show that, whilst ferrocytochrome c pulses of the aerobic oxidase vesicles at neutral pH and in the presence of saturating concentrations of valinomycin and K+ to ensure charge compensation produced H+/e- ratios around 1 (as has been shown previously), oxygen pulses of reduced anaerobic vesicles supplemented with cytochrome c, gave H+/e- ratios around 0.3.	Valinomycin	162-173	cytochrome c, somatic	Homo sapiens	44-56
3996489-4	1985	On the other hand, a potassium-specific ionophore, valinomycin, did not cause potentiation, but rather suppressed epo-dependent colony formation.	Valinomycin	51-62	erythropoietin	Mus musculus	114-117
3969678-3	1985	DBP and MEHP stimulated succinate state 4 respiration, impaired K+-valinomycin induced swelling with succinate, ascorbate, or ATP as the energy sources, and inhibited succinate state 3 respiration and succinate cytochrome c reductase activity.	Valinomycin	67-78	D-box binding PAR bZIP transcription factor	Rattus norvegicus	0-3
3969678-5	1985	MBP caused only slight stimulation of state 4 respiration and impairment of K+-valinomycin induced swelling with each of the 3 energy sources, however, of the 4 phthalate esters, it produced the greatest energy-independent swelling and led to the greatest release of soluble mitochondrial proteins.	Valinomycin	79-90	myelin basic protein	Rattus norvegicus	0-3
3443110-12	1987	Treatment with the K+ ionophores nonactin and valinomycin, which abolish mitochondrial membrane potential, inhibited synthesis of the mature forms of the P1 protein as well as a number of other mitochondrial proteins, as seen by two-dimensional gel electrophoresis of labeled polypeptides.	Valinomycin	46-57	60 kDa heat shock protein, mitochondrial	Cricetulus griseus	154-164
3667622-10	1987	Treatment with Cs+ plus valinomycin (as an alternative method of membrane depolarization) increases pHi much more effectively than it increases [Ca2+]i, and thus also partially supports this contention.	Valinomycin	24-35	glucose-6-phosphate isomerase	Homo sapiens	100-103
3107570-4	1987	Creation of a valinomycin-induced negative inside membrane potential combined with increased membrane permeability to Ca2+ (A23187), increased Ca2+-entry fivefold and more.	Valinomycin	14-25	carbonic anhydrase 2	Homo sapiens	118-121
3107570-4	1987	Creation of a valinomycin-induced negative inside membrane potential combined with increased membrane permeability to Ca2+ (A23187), increased Ca2+-entry fivefold and more.	Valinomycin	14-25	carbonic anhydrase 2	Homo sapiens	143-146
2437290-5	1987	Chlordecone also elevated [Ca++]i in synaptosomes in which mitochondrial Ca++ uptake had been abolished by valinomycin.	Valinomycin	107-118	carbonic anhydrase 1	Homo sapiens	27-33
3029099-6	1987	Two compounds which selectively increase cellular permeability to K+, valinomycin, and nigericin, strongly inhibited tPA secretion, with IC50 values of approximately 50 nM.	Valinomycin	70-81	chromosome 20 open reading frame 181	Homo sapiens	117-120
3030328-3	1987	Both the activities of ATPase and the vesicular accumulation of H+ were stimulated by K+ in the presence of Mg2+, and enhanced by the K+-ionophore, valinomycin.	Valinomycin	148-159	dynein axonemal heavy chain 8	Homo sapiens	23-29
2873034-9	1986	In the presence of valinomycin and an outward-directed K gradient, there was increased quenching of acridine orange, indicating that the H+-ATPase is electrogenic.	Valinomycin	19-30	dynein axonemal heavy chain 8	Homo sapiens	137-146
2410909-2	1985	In the presence of valinomycin, the oxidation of cytochrome c is linked to proton ejection in the external medium, with an apparent stoichiometry (H+/e-) of 0.93 +/- 0.22, under conditions in which the enzyme is in the more active "pulsed" state (i.e., having undergone oxidation-reduction cycles).	Valinomycin	19-30	cytochrome c, somatic	Homo sapiens	49-61
2410570-2	1985	In the presence of valinomycin, proton pumping and cytochrome c oxidation by cytochrome oxidase are synchronous up to rate constants of approximately 9 sec-1.	Valinomycin	19-30	cytochrome c, somatic	Homo sapiens	51-63
6133682-11	1983	The ATPase was also activated by NH+4 in the presence of valinomycin.	Valinomycin	57-68	dynein axonemal heavy chain 8	Homo sapiens	4-10
6134723-8	1983	The purified ATPase, when reconstituted into soybean phospholipid vesicles, exhibits coupling, e.g. the ATPase activity can be stimulated at least 8-fold by valinomycin in the presence of potassium.	Valinomycin	157-168	ATPase	Enterococcus faecalis	13-19
6134723-8	1983	The purified ATPase, when reconstituted into soybean phospholipid vesicles, exhibits coupling, e.g. the ATPase activity can be stimulated at least 8-fold by valinomycin in the presence of potassium.	Valinomycin	157-168	ATPase	Enterococcus faecalis	104-110
6410583-1	1983	Activity of cholinesterase was higher in young erythrocytes when the cell populations of various age were studied; the enzymatic activity was increased after addition of valinomycine into a medium independently on the antibiotic concentration and the enzyme activation was more pronounced in the old population of erythrocytes.	Valinomycin	170-182	cholinesterase	Oryctolagus cuniculus	12-26
6829771-5	1983	In the presence of K+ and valinomycin, external SCN- inhibited ATP-dependent pH gradient formation by increasing the rate of proton efflux.	Valinomycin	26-37	sorcin	Homo sapiens	48-51
6319123-7	1983	Collapse of delta psi effected by valinomycin addition to turning-over b-c1 vesicles resulted in substantial oxidation of cytochrome b-566 and comparable reduction of cytochrome c1, with little oxidation of cytochrome b-562.	Valinomycin	34-45	mitochondrially encoded cytochrome b	Homo sapiens	122-134
6319123-7	1983	Collapse of delta psi effected by valinomycin addition to turning-over b-c1 vesicles resulted in substantial oxidation of cytochrome b-566 and comparable reduction of cytochrome c1, with little oxidation of cytochrome b-562.	Valinomycin	34-45	cytochrome c1	Homo sapiens	167-180
6415207-5	1983	Further, a cause-and-effect relationship between these two events is suggested by results that demonstrate that inhibition of anti-Fab--induced depolarization by valinomycin also inhibits the subsequent increase in mI-A antigen expression and "passive" (non-ligand-mediated) depolarization of murine B cells by K+ results in hyper-mI-A antigen expression.	Valinomycin	162-173	MIA SH3 domain containing	Mus musculus	215-219
6415207-5	1983	Further, a cause-and-effect relationship between these two events is suggested by results that demonstrate that inhibition of anti-Fab--induced depolarization by valinomycin also inhibits the subsequent increase in mI-A antigen expression and "passive" (non-ligand-mediated) depolarization of murine B cells by K+ results in hyper-mI-A antigen expression.	Valinomycin	162-173	MIA SH3 domain containing	Mus musculus	331-335
6305365-4	1983	The rates of both cytochrome c oxidation and proton uptake were stimulated by addition of ionophores such as trifluoromethoxy carbonyl cyanide phenylhydrazone (FCCP), nigericin and valinomycin.	Valinomycin	181-192	cytochrome c, somatic	Homo sapiens	18-30
6829771-2	1983	The addition of SCN- to vesicles in the presence of KC1 and valinomycin reduced ATP-dependent proton accumulation in a dose-dependent manner.	Valinomycin	60-71	sorcin	Homo sapiens	16-19
6829771-3	1983	Inhibition was most pronounced in the presence of internal SCN-, which was obtained by preincubation of vesicles with SCN- or by the addition of K+-valinomycin, which facilitates entry of SCN-.	Valinomycin	148-159	sorcin	Homo sapiens	59-62
6815650-9	1982	Previous treatment of cells with the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenylhydrazone blocked TRH-induced 45Ca2+ efflux from mitochondria, while previous treatment with valinomycin, an agent that depleted both 45Ca2+ pools, blocked any additional effect of TRH on these pools.	Valinomycin	196-207	thyrotropin releasing hormone	Rattus norvegicus	121-124
6288084-0	1982	Differential effects of 2,4-dinitrophenol and valinomycin (+ K+) on uncoupler-stimulated ATPase of human tumor mitochondria.	Valinomycin	46-57	dynein axonemal heavy chain 8	Homo sapiens	89-95
7141069-4	1982	The addition of valinomycin (10(-11) to 10(-15) M) in the presence of ouabain and erythropoietin (Ep) did not alter the erythroid colony-forming stimulation which was characteristic of cultures in which only ouabain (10(-15) M) and Ep were added.	Valinomycin	16-27	erythropoietin	Mus musculus	82-96
7241088-0	1981	Ion transport mediated by the valinomycin analogue cyclo(L-Lac-L-Val-D-Pro-D-Val)3 in lipid bilayer membranes.	Valinomycin	30-41	lactase	Homo sapiens	59-62
7241088-1	1981	Cyclo(L-Lac-L-Val-D-Pro-D-Val)3 (PV-Lac) a structural analogue of the ion-carrier valinomycin, increases the cation permeability of lipid bilayer membranes by forming a 1:1 ion-carrier complex.	Valinomycin	82-93	lactase	Homo sapiens	8-11
7241088-1	1981	Cyclo(L-Lac-L-Val-D-Pro-D-Val)3 (PV-Lac) a structural analogue of the ion-carrier valinomycin, increases the cation permeability of lipid bilayer membranes by forming a 1:1 ion-carrier complex.	Valinomycin	82-93	lactase	Homo sapiens	36-39
7241088-13	1981	ks is much smaller for PV-Lac than for valinomycin and thus limits the efficiency with which the carrier is able to translocate cations across the membrane.	Valinomycin	39-50	lactase	Homo sapiens	26-29
7305997-6	1981	Valinomycin plus K+ accelerates cytochrome b566 oxidation and retards net oxidation of cytochrome b562.	Valinomycin	0-11	mitochondrially encoded cytochrome b	Homo sapiens	32-44
7305997-10	1981	Valinomycin or a pH increase in the medium promote reduction of cytochrome b562 and decrease net reduction of cytochrome b566.	Valinomycin	0-11	mitochondrially encoded cytochrome b	Homo sapiens	64-76
7305997-12	1981	Addition of valinomycin to mitochondria and submitochondrial particles in the respiring steady state causes, at pH values around neutrality, preferential oxidation of cytochrome b566 with respect to cytochrome b562.	Valinomycin	12-23	mitochondrially encoded cytochrome b	Homo sapiens	167-179
363170-0	1978	Valinomycin inhibition of insulin release and alteration of the electrical properties of pancreatic B cells.	Valinomycin	0-11	insulin	Homo sapiens	26-33
6896674-4	1982	As with MGBG and 4,4"-diacetyldiphenylurea-bis(guanylhydrazone), the potassium cationophore, valinomycin, increased the sensitivity of mitochondrial respiration to DBI.	Valinomycin	93-104	diazepam binding inhibitor	Rattus norvegicus	164-167
40970-2	1979	In the presence of valinomycin, 2 K+ ions were taken up by the vesicles per electron transferred from cytochrome c to oxygen.	Valinomycin	19-30	cytochrome c, somatic	Homo sapiens	102-114
207320-10	1978	The Km for cytochrome c in 67 mM, pH 7.4, phosphate buffer with ascorbate as substrate, was 9 micrometer in both absence and presence of valinomycin and FCCP.	Valinomycin	137-148	cytochrome c, somatic	Homo sapiens	11-23
656407-7	1978	Azide acts non-competitively towards cytochrome c when the latter is oxidized by cytochrome aa3-containing proteoliposomes both in the energized and deenergized (plus p-trifluoromethoxy carbonyl cyanide phenylhydrazone and valinomycin) conditions.	Valinomycin	223-234	cytochrome c, somatic	Homo sapiens	37-49
270668-7	1977	X537A, monensin A, and nigericin (all 5 muM) stimulate both prostaglandin output and K(+) efflux from renal medulla, while 5 muM valinomycin or A204 has no effect on either.	Valinomycin	129-140	latexin	Homo sapiens	125-128
134035-15	1976	This suggests that calcium-induced ATPase uniquely required the transition for activity, in contrast to the ATPase induced by uncoupler or valinomycin.	Valinomycin	139-150	dynein axonemal heavy chain 8	Homo sapiens	108-114
4334132-2	1971	Inhibition of prostaglandin, theophylline and cyclic amp stimulated growth hormone release by valinomycin in vitro.	Valinomycin	94-105	growth hormone 1	Homo sapiens	68-82
1247533-0	1976	Conformational studies of peptide cyclo-(D-Val-L-Pro-L-Val-D-Pro]3, a cation-binding analogue of valinomycin.	Valinomycin	97-108	pyrroline-5-carboxylate reductase 1	Homo sapiens	61-66
1257579-0	1976	Valinomycin inhibition of the inward slow current of cardiac muscle.	Valinomycin	0-11	myosin, heavy chain 7B, cardiac muscle, beta	Gallus gallus	53-67
48337-3	1975	Laser Raman spectroscopy has been used to probe specific molecular interactions inside two models of transport membrane proteins, valinomycin and gramicidin A. Conformational changes of these molecules, as well as specific interactions with ions, can be detected and may help elucidate how membrane transport proteins such as Na+ minus K+ ATPase and rhodopsin function.	Valinomycin	130-141	rhodopsin	Homo sapiens	350-359
4309957-0	1969	The effect of valinomycin on the toad bladder: antagonism to vasopressin and aldosterone.	Valinomycin	14-25	arginine vasopressin	Homo sapiens	61-72
24173131-6	1971	The increase in lactate production caused by valinomycin is accompanied by a correspondingly greater fall in pHe and pHi.	Valinomycin	45-56	glucose-6-phosphate isomerase 1	Mus musculus	117-120
33305795-10	2021	Direct assessment by whole-cell current-clamp confirmed that Vm in valinomycin-exposed cells was determined primarily by K+ equilibrium potential (EK) and was rapidly "reset" upon manipulation of [K+]o. Pre-treatment of sperm with valinomycin ([K+]o = 5.4 mM) had no effect on the P4-induced [Ca2+] transient (P = 0.95; eight experiments), but application of valinomycin to P4-pretreated sperm suppressed activity in 82% of oscillating cells (n = 257; P = 5 x 10-55 compared to control) and significantly reduced both the amplitude and frequency of persisting oscillations (P = 0.0001).	Valinomycin	67-78	choline kinase alpha	Homo sapiens	147-149
33305795-10	2021	Direct assessment by whole-cell current-clamp confirmed that Vm in valinomycin-exposed cells was determined primarily by K+ equilibrium potential (EK) and was rapidly "reset" upon manipulation of [K+]o. Pre-treatment of sperm with valinomycin ([K+]o = 5.4 mM) had no effect on the P4-induced [Ca2+] transient (P = 0.95; eight experiments), but application of valinomycin to P4-pretreated sperm suppressed activity in 82% of oscillating cells (n = 257; P = 5 x 10-55 compared to control) and significantly reduced both the amplitude and frequency of persisting oscillations (P = 0.0001).	Valinomycin	231-242	choline kinase alpha	Homo sapiens	147-149
33305795-10	2021	Direct assessment by whole-cell current-clamp confirmed that Vm in valinomycin-exposed cells was determined primarily by K+ equilibrium potential (EK) and was rapidly "reset" upon manipulation of [K+]o. Pre-treatment of sperm with valinomycin ([K+]o = 5.4 mM) had no effect on the P4-induced [Ca2+] transient (P = 0.95; eight experiments), but application of valinomycin to P4-pretreated sperm suppressed activity in 82% of oscillating cells (n = 257; P = 5 x 10-55 compared to control) and significantly reduced both the amplitude and frequency of persisting oscillations (P = 0.0001).	Valinomycin	231-242	choline kinase alpha	Homo sapiens	147-149
33305795-12	2021	When valinomycin was applied in saline with elevated [K+], the inhibitory effect of valinomycin was reduced and was dependent on EK (P = 10-25).	Valinomycin	5-16	choline kinase alpha	Homo sapiens	129-131
33305795-12	2021	When valinomycin was applied in saline with elevated [K+], the inhibitory effect of valinomycin was reduced and was dependent on EK (P = 10-25).	Valinomycin	84-95	choline kinase alpha	Homo sapiens	129-131
33305795-13	2021	Amplitude and frequency of [Ca2+]i oscillations that persisted in the presence of valinomycin showed similar sensitivity to EK (P < 0.01).	Valinomycin	82-93	choline kinase alpha	Homo sapiens	124-126
32905804-3	2020	Valinomycin is a respiratory chain inhibitor that activates mitophagy via the PINK1/Parkin signaling pathway.	Valinomycin	0-11	PTEN induced putative kinase 1	Mus musculus	78-83
32905804-4	2020	However, the mechanism underlying the association between mitophagy and valinomycin in Abeta formation has not been explored.	Valinomycin	72-83	amyloid beta (A4) precursor protein	Mus musculus	87-92
32905804-6	2020	Our results prove that valinomycin induced a time-dependent increase in the mitophagy activation of N2a/APP695swe cells as indicated by increased levels of PINK1, Parkin, and LC3II as well as increased the colocalization of Parkin-Tom20 and fewer mitochondria (indicated by decreased Tom20 levels).	Valinomycin	23-34	PTEN induced putative kinase 1	Mus musculus	156-161
32905804-6	2020	Our results prove that valinomycin induced a time-dependent increase in the mitophagy activation of N2a/APP695swe cells as indicated by increased levels of PINK1, Parkin, and LC3II as well as increased the colocalization of Parkin-Tom20 and fewer mitochondria (indicated by decreased Tom20 levels).	Valinomycin	23-34	translocase of outer mitochondrial membrane 20	Mus musculus	231-236
32905804-6	2020	Our results prove that valinomycin induced a time-dependent increase in the mitophagy activation of N2a/APP695swe cells as indicated by increased levels of PINK1, Parkin, and LC3II as well as increased the colocalization of Parkin-Tom20 and fewer mitochondria (indicated by decreased Tom20 levels).	Valinomycin	23-34	translocase of outer mitochondrial membrane 20	Mus musculus	284-289
32905804-9	2020	Our findings suggest that the elimination of impaired mitochondria via valinomycin-induced mitophagy ameliorates AD by decreasing Abeta and improving ATP levels.	Valinomycin	71-82	amyloid beta (A4) precursor protein	Mus musculus	130-135
31840043-4	2019	Dissipation of the mitochondrial membrane potential with ionophores, such as CCCP and valinomycin, causes the accumulation of PINK1 on the outer mitochondrial membrane, a marked increase of pS65-ubiquitin and the recruitment of Parkin, which targets dysfunctional mitochondria for degradation by autophagy.	Valinomycin	86-97	PTEN induced kinase 1	Rattus norvegicus	126-131