PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21725212-0	2011	Quinacrine sensitizes hepatocellular carcinoma cells to TRAIL and chemotherapeutic agents.	Quinacrine	0-10	TNF superfamily member 10	Homo sapiens	56-61
21779761-0	2011	Mechanisms for Kir channel inhibition by quinacrine: acute pore block of Kir2.x channels and interference in PIP2 interaction with Kir2.x and Kir6.2 channels.	Quinacrine	41-51	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	15-18
21779761-0	2011	Mechanisms for Kir channel inhibition by quinacrine: acute pore block of Kir2.x channels and interference in PIP2 interaction with Kir2.x and Kir6.2 channels.	Quinacrine	41-51	potassium inwardly rectifying channel subfamily J member 11	Homo sapiens	142-148
21779761-3	2011	In this work, the effects of quinacrine were studied on cardiac Kir channels expressed in HEK 293 cells and on the inward rectifier potassium currents, I(K1) and I(KATP), in cardiac myocytes.	Quinacrine	29-39	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	64-67
21779761-4	2011	We found that quinacrine differentially inhibited Kir channels, Kir6.2 ~ Kir2.3 > Kir2.1.	Quinacrine	14-24	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	50-53
21779761-4	2011	We found that quinacrine differentially inhibited Kir channels, Kir6.2 ~ Kir2.3 > Kir2.1.	Quinacrine	14-24	potassium inwardly rectifying channel subfamily J member 11	Homo sapiens	64-70
21779761-4	2011	We found that quinacrine differentially inhibited Kir channels, Kir6.2 ~ Kir2.3 > Kir2.1.	Quinacrine	14-24	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	73-79
21779761-4	2011	We found that quinacrine differentially inhibited Kir channels, Kir6.2 ~ Kir2.3 > Kir2.1.	Quinacrine	14-24	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	85-91
21779761-6	2011	We presented evidence that quinacrine displays a double action towards strong inward rectifier Kir2.x channels, i.e., direct pore block and interference in phosphatidylinositol 4,5-bisphosphate, PIP(2)-Kir channel interaction.	Quinacrine	27-37	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	95-98
21779761-8	2011	The interference of the drug with the interaction of Kir2.x and Kir6.2/SUR2A channels and PIP(2) is suggested from four sources of evidence: (1) Slow onset of current block when quinacrine is applied from either the inside or the outside of the channel.	Quinacrine	178-188	potassium inwardly rectifying channel subfamily J member 11	Homo sapiens	64-70
21779761-9	2011	(2) Mutation of Kir2.3(I213L) and mutation of Kir6.2(C166S) increase their affinity for PIP(2) and lowers its sensitivity for quinacrine.	Quinacrine	126-136	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	16-22
21779761-9	2011	(2) Mutation of Kir2.3(I213L) and mutation of Kir6.2(C166S) increase their affinity for PIP(2) and lowers its sensitivity for quinacrine.	Quinacrine	126-136	potassium inwardly rectifying channel subfamily J member 11	Homo sapiens	46-52
21779761-10	2011	(3) Mutations of Kir2.1(L222I and K182Q) which decreased its affinity for PIP(2) increased its sensitivity for quinacrine.	Quinacrine	111-121	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	17-23
21725212-2	2011	We find that quinacrine stabilizes p53 and induces p53-dependent and independent cell death.	Quinacrine	13-23	tumor protein p53	Homo sapiens	35-38
21725212-2	2011	We find that quinacrine stabilizes p53 and induces p53-dependent and independent cell death.	Quinacrine	13-23	tumor protein p53	Homo sapiens	51-54
21725212-3	2011	Treatment by quinacrine alone at concentrations of 10-20 mM for 1-2 d cannot kill hepatocellular carcinoma cells, such as HepG2, Hep3B, Huh7, which are also resistant to TRAIL.	Quinacrine	13-23	MIR7-3 host gene	Homo sapiens	136-140
21725212-3	2011	Treatment by quinacrine alone at concentrations of 10-20 mM for 1-2 d cannot kill hepatocellular carcinoma cells, such as HepG2, Hep3B, Huh7, which are also resistant to TRAIL.	Quinacrine	13-23	TNF superfamily member 10	Homo sapiens	170-175
21725212-4	2011	However, quinacrine renders these cells sensitive to treatment by TRAIL.	Quinacrine	9-19	TNF superfamily member 10	Homo sapiens	66-71
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	33-43	TNF receptor superfamily member 10b	Homo sapiens	110-113
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	33-43	TNF superfamily member 10	Homo sapiens	149-154
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	33-43	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	218-223
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	190-200	TNF superfamily member 10	Homo sapiens	48-53
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	190-200	TNF receptor superfamily member 10b	Homo sapiens	110-113
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	190-200	TNF superfamily member 10	Homo sapiens	149-154
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	190-200	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	218-223
21725212-6	2011	While the synergistic effect of quinacrine with TRAIL appears to be in part independent of p53, knockdown of p53 in HepG2 cells by siRNA results in more cell death after treatment by quinacrine and TRAIL.	Quinacrine	183-193	tumor protein p53	Homo sapiens	109-112
21725212-7	2011	The mechanism by which quinacrine sensitizes hepatocellular carcinoma cells to TRAIL and chemotherapies, and the potential for clinical application currently are being further explored.	Quinacrine	23-33	TNF superfamily member 10	Homo sapiens	79-84
21725213-4	2011	We show that quinacrine synergizes with 5-fluorouracil and significantly enhances the cytotoxicity of sorafenib in a panel of 10 human colorectal cancer cell lines, including those with KRAS mutations protein gel blot analysis confirmed that quinacrine"s anticancer activity partially arises from its ability to stabilize p53 and lower anti-apoptotic protein levels.	Quinacrine	13-23	KRAS proto-oncogene, GTPase	Homo sapiens	186-190
21725213-4	2011	We show that quinacrine synergizes with 5-fluorouracil and significantly enhances the cytotoxicity of sorafenib in a panel of 10 human colorectal cancer cell lines, including those with KRAS mutations protein gel blot analysis confirmed that quinacrine"s anticancer activity partially arises from its ability to stabilize p53 and lower anti-apoptotic protein levels.	Quinacrine	13-23	tumor protein p53	Homo sapiens	322-325
21658925-5	2011	Pretreatment with the PLA(2) inhibitor mepacrine (500 mug; i.c.v.)	Quinacrine	39-48	phospholipase A2 group IB	Rattus norvegicus	22-28
21569639-3	2011	In particular, quinacrine"s role on the NF-kappaB, p53, and AKT pathways are summarized.	Quinacrine	15-25	tumor protein p53	Homo sapiens	51-54
21569639-3	2011	In particular, quinacrine"s role on the NF-kappaB, p53, and AKT pathways are summarized.	Quinacrine	15-25	AKT serine/threonine kinase 1	Homo sapiens	60-63
21518868-0	2011	FER tyrosine kinase (FER) overexpression mediates resistance to quinacrine through EGF-dependent activation of NF-kappaB.	Quinacrine	64-74	FER tyrosine kinase	Homo sapiens	0-3
21518868-0	2011	FER tyrosine kinase (FER) overexpression mediates resistance to quinacrine through EGF-dependent activation of NF-kappaB.	Quinacrine	64-74	FER tyrosine kinase	Homo sapiens	21-24
21518868-1	2011	Quinacrine, a drug with antimalarial and anticancer activities that inhibits NF-kappaB and activates p53, has progressed into phase II clinical trials in cancer.	Quinacrine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	77-86
21518868-1	2011	Quinacrine, a drug with antimalarial and anticancer activities that inhibits NF-kappaB and activates p53, has progressed into phase II clinical trials in cancer.	Quinacrine	0-10	tumor protein p53	Homo sapiens	101-104
21518868-2	2011	To further elucidate its mechanism of action and identify pathways of drug resistance, we used an unbiased method for validation-based insertional mutagenesis to isolate a quinacrine-resistant cell line in which an inserted CMV promoter drives overexpression of the FER tyrosine kinase (FER).	Quinacrine	172-182	FER tyrosine kinase	Homo sapiens	266-269
21518868-2	2011	To further elucidate its mechanism of action and identify pathways of drug resistance, we used an unbiased method for validation-based insertional mutagenesis to isolate a quinacrine-resistant cell line in which an inserted CMV promoter drives overexpression of the FER tyrosine kinase (FER).	Quinacrine	172-182	FER tyrosine kinase	Homo sapiens	287-290
21518868-3	2011	Overexpression of FER from a cDNA confers quinacrine resistance to several different types of cancer cell lines.	Quinacrine	42-52	FER tyrosine kinase	Homo sapiens	18-21
21518868-4	2011	We show that quinacrine kills cancer cells primarily by inhibiting the activation of NF-kappaB and that increased activation of NF-kappaB through FER overexpression mediates resistance.	Quinacrine	13-23	nuclear factor kappa B subunit 1	Homo sapiens	85-94
21518868-7	2011	We conclude that FER is on a pathway connecting EGFR to NF-kappaB activation and that this function is responsible for FER-dependent resistance to quinacrine.	Quinacrine	147-157	FER tyrosine kinase	Homo sapiens	17-20
21518868-7	2011	We conclude that FER is on a pathway connecting EGFR to NF-kappaB activation and that this function is responsible for FER-dependent resistance to quinacrine.	Quinacrine	147-157	epidermal growth factor receptor	Homo sapiens	48-52
21518868-7	2011	We conclude that FER is on a pathway connecting EGFR to NF-kappaB activation and that this function is responsible for FER-dependent resistance to quinacrine.	Quinacrine	147-157	FER tyrosine kinase	Homo sapiens	119-122
20417698-5	2010	Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H(2)O(2)-induced PLD activation but reversed H(2)O(2)-induced injury.	Quinacrine	63-73	phospholipase A2 group IB	Homo sapiens	75-91
21518517-1	2011	This work was aimed to investigate the effect of quinacrine on peripheral granulocytes and lymphocytes, interleukin 1 (IL-1) and interleukin 6 (IL-6) in peripheral blood serum of inflammatory reaction induced by microwave irradiation, and observe the protective effect of quinacrine against microwave irradiation injury.	Quinacrine	49-59	interleukin 6	Mus musculus	144-148
21518517-7	2011	The 2 concentrations of quinacrine (12.6 mg/kg, 50.4 mg/kg) could suppress level of IL-1beta in serum induced by microwave irradiation.	Quinacrine	24-34	interleukin 1 beta	Mus musculus	84-92
21518517-8	2011	The level of IL-6 in serum of mice was gradually increased after microwave irradiation with intensity of 50 mW/cm(2) for 7 days, but quinacrine administration could delay the rise of IL-6 level, specially within time of 2 days.	Quinacrine	133-143	interleukin 6	Mus musculus	13-17
21518517-8	2011	The level of IL-6 in serum of mice was gradually increased after microwave irradiation with intensity of 50 mW/cm(2) for 7 days, but quinacrine administration could delay the rise of IL-6 level, specially within time of 2 days.	Quinacrine	133-143	interleukin 6	Mus musculus	183-187
21518517-9	2011	It is concluded that the quinacrine administration can delay the increase of peripheral granulocytes and lymphocytes inducted by microwave irradiation, and may partially suppress the rise of IL-1beta and IL-6 in serum.	Quinacrine	25-35	interleukin 1 beta	Mus musculus	191-199
21518517-9	2011	It is concluded that the quinacrine administration can delay the increase of peripheral granulocytes and lymphocytes inducted by microwave irradiation, and may partially suppress the rise of IL-1beta and IL-6 in serum.	Quinacrine	25-35	interleukin 6	Mus musculus	204-208
20417698-5	2010	Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H(2)O(2)-induced PLD activation but reversed H(2)O(2)-induced injury.	Quinacrine	63-73	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	140-143
20118407-10	2010	The nonselective PLA(2) inhibitor quinacrine abolished the contractions triggered by both acetylcholine and A-23187, whereas the store-operated calcium channel inhibitor SKF-96365 prevented only the acetylcholine-induced contraction.	Quinacrine	34-44	phospholipase A2 group IB	Homo sapiens	17-23
20424169-0	2010	Inhibition of NF-kappaB signaling by quinacrine is cytotoxic to human colon carcinoma cell lines and is synergistic in combination with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or oxaliplatin.	Quinacrine	37-47	nuclear factor kappa B subunit 1	Homo sapiens	14-23
20424169-0	2010	Inhibition of NF-kappaB signaling by quinacrine is cytotoxic to human colon carcinoma cell lines and is synergistic in combination with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or oxaliplatin.	Quinacrine	37-47	TNF superfamily member 10	Homo sapiens	136-191
20424169-6	2010	We have demonstrated constitutive NF-kappaB activation in five of six human colon carcinoma cell lines; this activation is inhibited by quinacrine.	Quinacrine	136-146	nuclear factor kappa B subunit 1	Homo sapiens	34-43
20424169-7	2010	Quinacrine induced apoptosis in colon carcinomas and potentiated the cytotoxic activity of TRAIL in RKO and HT29 cells and that of L-OHP in HT29 cells.	Quinacrine	0-10	TNF superfamily member 10	Homo sapiens	91-96
20424169-9	2010	Importantly, 2 h of quinacrine pretreatment resulted in decreased expression of c-FLIP and Mcl-1, which were determined to be transcriptional targets of NF-kappaB.	Quinacrine	20-30	CASP8 and FADD like apoptosis regulator	Homo sapiens	80-86
20424169-9	2010	Importantly, 2 h of quinacrine pretreatment resulted in decreased expression of c-FLIP and Mcl-1, which were determined to be transcriptional targets of NF-kappaB.	Quinacrine	20-30	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	91-96
20424169-9	2010	Importantly, 2 h of quinacrine pretreatment resulted in decreased expression of c-FLIP and Mcl-1, which were determined to be transcriptional targets of NF-kappaB.	Quinacrine	20-30	nuclear factor kappa B subunit 1	Homo sapiens	153-162
20632941-6	2010	Quinacrine and diphenylene iodonium at 50 microM concentration prevented GC death induced by CN(-) or CN(-) + 0.1 mM Ca2+ but had no influence on respiration and photosynthetic O2 evolution in pea leaf slices.	Quinacrine	0-10	carbonic anhydrase 2	Homo sapiens	117-120
20407239-8	2010	Western blot analysis showed that quinacrine plus cisplatin significantly down-regulated cIAP-1 and up-regulated Bax and cleaved caspase-3 expression in Hela and SCC-VII cells compared with single-agent treatment.	Quinacrine	34-44	baculoviral IAP repeat containing 2	Homo sapiens	89-95
23555400-9	2010	The addition of phospholipase A2 (PLA2) inhibitor quinacrine abolished leukocyte activation by the bowel bag fluid.	Quinacrine	50-60	phospholipase A2 group IB	Homo sapiens	16-32
23555400-9	2010	The addition of phospholipase A2 (PLA2) inhibitor quinacrine abolished leukocyte activation by the bowel bag fluid.	Quinacrine	50-60	phospholipase A2 group IB	Homo sapiens	34-38
20407239-8	2010	Western blot analysis showed that quinacrine plus cisplatin significantly down-regulated cIAP-1 and up-regulated Bax and cleaved caspase-3 expression in Hela and SCC-VII cells compared with single-agent treatment.	Quinacrine	34-44	BCL2 associated X, apoptosis regulator	Homo sapiens	113-116
18754103-0	2009	Inhibition of rat hepatic CYP2E1 by quinacrine: molecular modeling investigation and effects on 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced mutagenicity.	Quinacrine	36-46	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	26-32
19542246-0	2009	Mepacrine inhibits subepithelial fibrosis by reducing the expression of arginase and TGF-beta1 in an extended subacute mouse model of allergic asthma.	Quinacrine	0-9	transforming growth factor, beta 1	Mus musculus	85-94
19542246-9	2009	These reductions by mepacrine were associated with a decrease in levels and expression of TGF-beta(1) and the reduction in activity, expression of arginase in lung cytosol, and immunolocalization in inflammatory cells present in perivascular and peribronchial regions.	Quinacrine	20-29	transforming growth factor, beta 1	Mus musculus	90-101
19542246-10	2009	These results suggest that mepacrine might reduce the development of subepithelial fibrosis by reducing the arginase and TGF-beta(1).	Quinacrine	27-36	transforming growth factor, beta 1	Mus musculus	121-132
19427915-8	2009	Heat treatment also resulted in decreased membrane fluidity and increased cPLA(2) activity as well as arachidonic acid level; these effects were reversed by QA pretreatment.	Quinacrine	157-159	phospholipase A2 group IVA	Rattus norvegicus	74-81
19427915-10	2009	These results suggest that QA protects striatum neurons against heat-induced neuronal necrosis, and also demonstrate that inhibition of cPLA(2) activity and stabilization of membranes may contribute to protective effect of quinacrine.	Quinacrine	223-233	phospholipase A2 group IVA	Rattus norvegicus	136-143
19901558-5	2009	We found that the anti-malaria drugs quinacrine (QC) and emetine prevented HSR in cancer cells, as judged by induction of hsp70 expression.	Quinacrine	37-47	heat shock protein 1B	Mus musculus	122-127
19956709-3	2009	As quinacrine is known to be a substrate for P-glycoprotein multi-drug resistance (MDR) transporters, we circumvented its poor BBB permeability by utilizing MDR(0/0) mice that are deficient in mdr1a and mdr1b genes.	Quinacrine	3-13	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	83-86
19956709-3	2009	As quinacrine is known to be a substrate for P-glycoprotein multi-drug resistance (MDR) transporters, we circumvented its poor BBB permeability by utilizing MDR(0/0) mice that are deficient in mdr1a and mdr1b genes.	Quinacrine	3-13	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	193-198
19956709-3	2009	As quinacrine is known to be a substrate for P-glycoprotein multi-drug resistance (MDR) transporters, we circumvented its poor BBB permeability by utilizing MDR(0/0) mice that are deficient in mdr1a and mdr1b genes.	Quinacrine	3-13	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	203-208
19956709-5	2009	PrP(Sc) levels in the brains of prion-inoculated MDR(0/0) mice diminished upon the initiation of quinacrine treatment.	Quinacrine	97-107	prion protein	Mus musculus	0-3
19956709-5	2009	PrP(Sc) levels in the brains of prion-inoculated MDR(0/0) mice diminished upon the initiation of quinacrine treatment.	Quinacrine	97-107	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	49-52
19956709-8	2009	A similar phenomenon was observed in cultured differentiated prion-infected neuroblastoma cells: PrP(Sc) levels initially decreased after quinacrine treatment then rapidly recovered after 3 d of continuous treatment.	Quinacrine	138-148	prion protein	Mus musculus	97-100
19956709-9	2009	Biochemical characterization of PrP(Sc) that persisted in the brains of quinacrine-treated mice had a lower conformational stability and different immunoaffinities compared to that found in the brains of untreated controls.	Quinacrine	72-82	prion protein	Mus musculus	32-35
19956709-11	2009	From these data, we propose that quinacrine eliminates a specific subset of PrP(Sc) conformers, resulting in the survival of drug-resistant prion conformations.	Quinacrine	33-43	prion protein	Mus musculus	76-79
19393035-8	2009	Pre-treatment of cultures with 7-nitroindazole, apocyanin, and quinacrine, respective inhibitors of cNOS, NOX, and PLA2, all significantly diminished RONS production.	Quinacrine	63-73	nitric oxide synthase 3	Homo sapiens	100-104
19393035-8	2009	Pre-treatment of cultures with 7-nitroindazole, apocyanin, and quinacrine, respective inhibitors of cNOS, NOX, and PLA2, all significantly diminished RONS production.	Quinacrine	63-73	phospholipase A2 group IB	Homo sapiens	115-119
18754103-3	2009	The aim of the present study was to test the hypothesis that quinacrine inhibits hepatic CYP2E1.	Quinacrine	61-71	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	89-95
18754103-7	2009	Interestingly, treatment with quinacrine resulted in a significant decrease of CYP2E1 activity and expression.	Quinacrine	30-40	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	79-85
18754103-8	2009	To investigate any similarities in the inhibition of CYP2E1 by quinacrine and disulfiram, molecular modeling techniques were adopted and revealed that quinacrine molecule anchors inside the same binding pocket of the protein where disulfiram is also attached.	Quinacrine	63-73	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	53-59
18754103-8	2009	To investigate any similarities in the inhibition of CYP2E1 by quinacrine and disulfiram, molecular modeling techniques were adopted and revealed that quinacrine molecule anchors inside the same binding pocket of the protein where disulfiram is also attached.	Quinacrine	151-161	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	53-59
18754103-9	2009	Finally, as assessed by the sister chromatid exchanges (SCE) assay, quinacrine was demonstrated to reduce the mutagenic effects of the tobacco-specific N-nitrosamine 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which is known to be converted to active mutagen in the liver principally through CYP2E1.	Quinacrine	68-78	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	303-309
18754103-10	2009	We suggest that these antimutagenic effects of quinacrine could be possibly attributed, at least in part, to its ability to block the bioactivation of NNK, mainly by the inhibition of CYP2E1.	Quinacrine	47-57	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	184-190
18754103-11	2009	Our results, even preliminary, indicate that quinacrine as an inhibitor of CYP2E1 might be protective against chemically-induced toxicities such as NNK-induced mutagenicity.	Quinacrine	45-55	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	75-81
19237284-2	2009	Nuclear magnetic resonance spectroscopy confirmed that quinacrine binds to the hydrophobic groove that Bcl-xL uses for interacting with the BH3 domain of proapoptotic proteins.	Quinacrine	55-65	BCL2 like 1	Homo sapiens	103-109
19237284-0	2009	Deciphering the antitumoral activity of quinacrine: Binding to and inhibition of Bcl-xL.	Quinacrine	40-50	BCL2 like 1	Homo sapiens	81-87
19237284-1	2009	From the screening of a unique collection of 880 off-patent small organic molecules, we have found that quinacrine inhibits the interaction between a BH3 domain-derived peptide and the antiapoptotic protein Bcl-xL.	Quinacrine	104-114	BCL2 like 1	Homo sapiens	207-213
19287190-6	2009	Moreover, PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of PLA2, but not by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	53-62	BCL2 apoptosis regulator	Homo sapiens	21-26
19287190-6	2009	Moreover, PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of PLA2, but not by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	53-62	phospholipase A2 group IB	Homo sapiens	80-84
18592376-2	2009	Assessed with propidium iodide and lactate dehydrogenase (LDH) leakage, neurodamage from ethanol (6 days 100 mM ethanol with four withdrawal periods) was prevented by the PLA2 pan-inhibitor, mepacrine.	Quinacrine	191-200	phospholipase A2 group IB	Rattus norvegicus	171-175
19137016-3	2009	The small molecule 9-aminoacridine (9AA) and its derivative, the antimalaria drug quinacrine, have selective toxicity for tumor cells and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Quinacrine	82-92	tumor protein p53	Homo sapiens	213-216
19035307-5	2008	RESULTS: Putrescine and spermidine at 0.5 mg/l significantly stimulated cell growth, whereas mepacrine treatment confirmed the enhanced p21 expression previously reported by a recent study and growth inhibition.	Quinacrine	93-102	H3 histone pseudogene 16	Homo sapiens	136-139
18984060-8	2009	Mepacrine, a generic PLA(2) inhibitor and BEL, an inhibitor of Ca(2+)-independent PLA(2) (iPLA(2)) blocked apoptosis, while pBPB and AACOOPF(3), inhibitors of secretory and Ca(2+)-dependent PLA(2) respectively, had no significant effect.	Quinacrine	0-9	brain etomidate level	Mus musculus	21-45
18330854-3	2008	In this study we investigated the potential of a multimeric display of quinacrine derivatives, as compared to the monomer quinacrine, as a design principal for a novel class of inhibitors against Abeta fibril formation.	Quinacrine	71-81	amyloid beta precursor protein	Homo sapiens	196-201
18705753-6	2008	The caspase-9 and -3 activities in the MDR K562 and K562 cells were increased with the dose rise of quinacrine.	Quinacrine	100-110	caspase 9	Homo sapiens	4-20
18705753-8	2008	The enhanced anti-tumor effects of vincristine by quinacrine in the resistant/non-resistant K562 cells could be because of the direct injury and the potentiating apoptotic effect of vincristine via activating the initiator caspase-9 and subsequently the effector caspase-3, and the long circulatory effect of stealthy liposomes.	Quinacrine	50-60	caspase 9	Homo sapiens	223-232
18705753-8	2008	The enhanced anti-tumor effects of vincristine by quinacrine in the resistant/non-resistant K562 cells could be because of the direct injury and the potentiating apoptotic effect of vincristine via activating the initiator caspase-9 and subsequently the effector caspase-3, and the long circulatory effect of stealthy liposomes.	Quinacrine	50-60	caspase 3	Homo sapiens	263-272
18647832-4	2008	Qa inhibits PrP(Sc) formation in cultured cells.	Quinacrine	0-2	prion protein	Mus musculus	12-15
18647832-9	2008	Although the combination of GSI and Qa diminished PrP(Sc) in the brains of RML-infected mice, GSI toxicity prevented us from being able to assess the effect the GSI plus Qa combination on incubation times.	Quinacrine	36-38	prion protein	Mus musculus	50-53
18442795-3	2008	Mepacrine, a known antimalarial drug, has been shown to possess antioxidant, anti-inflammatory, platelet anti-aggregant, and PLA2 inhibitory activities.	Quinacrine	0-9	phospholipase A2, group IIA (platelets, synovial fluid)	Mus musculus	125-129
18442795-10	2008	Mepacrine effectively reduced the rise in IL-4, IL-5, IL-13, and OVA-specific IgE and restored IFN-gamma levels.	Quinacrine	0-9	interleukin 4	Mus musculus	42-46
18442795-10	2008	Mepacrine effectively reduced the rise in IL-4, IL-5, IL-13, and OVA-specific IgE and restored IFN-gamma levels.	Quinacrine	0-9	interleukin 5	Mus musculus	48-52
18442795-10	2008	Mepacrine effectively reduced the rise in IL-4, IL-5, IL-13, and OVA-specific IgE and restored IFN-gamma levels.	Quinacrine	0-9	interleukin 13	Mus musculus	54-59
18442795-10	2008	Mepacrine effectively reduced the rise in IL-4, IL-5, IL-13, and OVA-specific IgE and restored IFN-gamma levels.	Quinacrine	0-9	interferon gamma	Mus musculus	95-104
18442795-11	2008	Mepacrine also significantly prevented the increase of sPLA2 (secretory phospholipase A2) activity in BAL fluid supernatant and Cys-LT (cysteinyl leukotrienes) in lung tissue homogenates of asthmatic mice.	Quinacrine	0-9	phospholipase A2, group IIA (platelets, synovial fluid)	Mus musculus	55-60
18442795-11	2008	Mepacrine also significantly prevented the increase of sPLA2 (secretory phospholipase A2) activity in BAL fluid supernatant and Cys-LT (cysteinyl leukotrienes) in lung tissue homogenates of asthmatic mice.	Quinacrine	0-9	phospholipase A2, group IIA (platelets, synovial fluid)	Mus musculus	62-88
18442795-13	2008	These findings indicate that mepacrine reduces the asthmatic features in ovalbumin induced asthma by acting on PLA2-Cys-LT axis.	Quinacrine	29-38	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	73-82
18442795-13	2008	These findings indicate that mepacrine reduces the asthmatic features in ovalbumin induced asthma by acting on PLA2-Cys-LT axis.	Quinacrine	29-38	phospholipase A2, group IIA (platelets, synovial fluid)	Mus musculus	111-115
18375719-4	2008	The DAGL inhibitor RHC 802675 (1 microM) and the CYP and PLA(2) inhibitors quinacrine (5 microM) (EC(50): RHC 802675 2.8 +/- 0.4 mM vs. control 1.4 +/- 0.3 mM; quinacrine 4.8 +/- 0.4 mM vs. control 2.0 +/- 0.3 mM; n = 5) and arachidonyltrifluoromethyl ketone (AACOCF(3), 1 microM) reduced Ca(2+)-induced relaxation of mesenteric arteries.	Quinacrine	75-85	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	49-52
18190795-12	2008	Although PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), increased Bcl-2 expression by PA was not abrogated by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	52-61	BCL2 apoptosis regulator	Homo sapiens	20-25
18190795-12	2008	Although PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), increased Bcl-2 expression by PA was not abrogated by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	52-61	phospholipase A2 group IB	Homo sapiens	79-97
18190795-12	2008	Although PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), increased Bcl-2 expression by PA was not abrogated by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	52-61	phospholipase A2 group IB	Homo sapiens	99-105
18190795-12	2008	Although PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), increased Bcl-2 expression by PA was not abrogated by propranolol, an inhibitor of PA phospholyhydrolase (PAP).	Quinacrine	52-61	BCL2 apoptosis regulator	Homo sapiens	118-123
18330854-3	2008	In this study we investigated the potential of a multimeric display of quinacrine derivatives, as compared to the monomer quinacrine, as a design principal for a novel class of inhibitors against Abeta fibril formation.	Quinacrine	122-132	amyloid beta precursor protein	Homo sapiens	196-201
17989510-7	2007	Furthermore, mepacrine (a phospholipase A2 inhibitor) significantly attenuated the morphine-induced withdrawal syndrome in a manner that was different than that with a NOS inhibitor.	Quinacrine	13-22	phospholipase A2, group IB, pancreas	Mus musculus	26-42
18220957-4	2007	TLR7/9 antagonists, such as the anti-malaria drugs chloroquine, hydroxychloroquine and quinacrine, have been used since the 1950s to treat immune-mediated inflammatory disorders (IMID) such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Sjogren"s syndrome.	Quinacrine	87-97	toll like receptor 7	Homo sapiens	0-4
17944227-11	2007	Results from cells indicated that inhibition of cPLA2, reduction the release of active fatty acids such as AA, and possibly, stabilization of the cell membrane which was disturbed by hot treatment, may contribute to the mechanism underlying heat protection and heatstroke preventive effects of quinacrine.	Quinacrine	294-304	phospholipase A2 group IVA	Rattus norvegicus	48-53
18006756-0	2007	Deficient TP53 expression, function, and cisplatin sensitivity are restored by quinacrine in head and neck cancer.	Quinacrine	79-89	tumor protein p53	Homo sapiens	10-14
18006756-3	2007	The genotoxic drug doxorubicin and the anti-inflammatory and antimalarial drug quinacrine, previously identified as inducers of TP53, were used to examine the nature and potential reversibility of deficient TP53 expression and function.	Quinacrine	79-89	tumor protein p53	Homo sapiens	128-132
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	tumor protein p53	Homo sapiens	97-101
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	tumor protein p53	Homo sapiens	97-101
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	H3 histone pseudogene 16	Homo sapiens	168-171
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	tumor protein p53	Homo sapiens	97-101
18006756-8	2007	Quinacrine-induced TP53 reporter activity and growth suppression were attenuated by pifithrin-alpha and TP53 short hairpin RNA knockdown.	Quinacrine	0-10	tumor protein p53	Homo sapiens	19-23
18006756-8	2007	Quinacrine-induced TP53 reporter activity and growth suppression were attenuated by pifithrin-alpha and TP53 short hairpin RNA knockdown.	Quinacrine	0-10	tumor protein p53	Homo sapiens	104-108
18006756-10	2007	CONCLUSIONS: Deficient TP53 mRNA and protein expression underlies decreased function in a subset of HNSCC with wild-type TP53 and can be restored together with cisplatin sensitization by quinacrine.	Quinacrine	187-197	tumor protein p53	Homo sapiens	23-27
17628524-9	2007	However, mepacrine (PLA2 inhibitor) (1.1 and 2.2 micromol/animal, i.c.v.)	Quinacrine	9-18	phospholipase A2 group IB	Rattus norvegicus	20-24
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	B cell leukemia/lymphoma 2	Mus musculus	36-41
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	phospholipase A2, group IB, pancreas	Mus musculus	183-201
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	phospholipase A2, group IB, pancreas	Mus musculus	203-209
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	phospholipase A2, group IB, pancreas	Mus musculus	228-234
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	B cell leukemia/lymphoma 2	Mus musculus	288-293
17541981-6	2007	Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels.	Quinacrine	156-165	BCL2-like 1	Mus musculus	298-304
17553606-5	2007	The lethal effect and the increase in the incidence of rupture or PARP-immunoreactive cells induced by the coadministration of methamphetamine and morphine was significantly attenuated by pretreatment with mepacrine (phospholipase A(2) inhibitor) or fullerene (a radical scavenger), or by cooling from 30 to 90 min after drug administration.	Quinacrine	206-215	poly (ADP-ribose) polymerase family, member 1	Mus musculus	66-70
16581945-0	2006	Quinacrine is mainly metabolized to mono-desethyl quinacrine by CYP3A4/5 and its brain accumulation is limited by P-glycoprotein.	Quinacrine	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-70
17145133-0	2007	The effects of the glucocorticoid receptor antagonist RU486 and phospholipase A2 inhibitor quinacrine on acoustic injury of the mouse cochlea.	Quinacrine	91-101	phospholipase A2, group IB, pancreas	Mus musculus	64-80
17145133-4	2007	The purpose of the present study was to examine the effects of methylprednisolone, a glucocorticoid receptor inhibitor (RU486) and a phospholipase A2 inhibitor (quinacrine) on cochlear injury induced by acoustic overexposure.	Quinacrine	161-171	phospholipase A2, group IB, pancreas	Mus musculus	133-149
17975303-9	2007	H(2)O(2) increased the protein level of glucose transporter 1 (GLUT 1), which was blocked by PD 98059, SB 203580, SP 600125, mepacrine, or Bay11-7082.	Quinacrine	125-134	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	63-69
17634670-2	2007	Pretreatment with primaquine and quinacrine, which are phospholipase A2 inhibitors, significantly inhibited cortisol production activated by both low and high concentrations of ACTH.	Quinacrine	33-43	LOC104974671	Bos taurus	55-71
17253962-5	2007	We also demonstrate that hT2R14 is a receptor for aristolochic acid and report the first characterization of the ligand specificities of hT2R7, which is a broadly tuned receptor responding to strychnine, quinacrine, chloroquine and papaverine.	Quinacrine	204-214	taste 2 receptor member 14	Homo sapiens	25-31
17253962-5	2007	We also demonstrate that hT2R14 is a receptor for aristolochic acid and report the first characterization of the ligand specificities of hT2R7, which is a broadly tuned receptor responding to strychnine, quinacrine, chloroquine and papaverine.	Quinacrine	204-214	taste 2 receptor member 7	Homo sapiens	137-142
16794572-10	2007	Quinacrine, [corrected] a PLA2 antagonist significantly blocked IL-1-induced [corrected] increase in PGE2 and corticosterone concentrations.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	26-30
16794572-10	2007	Quinacrine, [corrected] a PLA2 antagonist significantly blocked IL-1-induced [corrected] increase in PGE2 and corticosterone concentrations.	Quinacrine	0-10	interleukin 1 beta	Homo sapiens	64-68
17263456-5	2007	Quinacrine and 5,8,11,14-eicosatetraenoic trifluoromethyl ketone, both PLA2 inhibitors, significantly attenuated baicalein-induced hydroxyl radical formation.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	71-75
17065600-8	2007	In addition, pretreatment of ES cells with mepacrine decreased PRL/IGFBP1 expression and inhibited morphological change, whereas pretreatment with propranolol caused no changes, as compared to cAMP-treated cells, which suggests that PA induces decidualization through phospholipase A2 (PLA2G1B).	Quinacrine	43-52	prolactin	Homo sapiens	63-66
17065600-8	2007	In addition, pretreatment of ES cells with mepacrine decreased PRL/IGFBP1 expression and inhibited morphological change, whereas pretreatment with propranolol caused no changes, as compared to cAMP-treated cells, which suggests that PA induces decidualization through phospholipase A2 (PLA2G1B).	Quinacrine	43-52	insulin like growth factor binding protein 1	Homo sapiens	67-73
17065600-8	2007	In addition, pretreatment of ES cells with mepacrine decreased PRL/IGFBP1 expression and inhibited morphological change, whereas pretreatment with propranolol caused no changes, as compared to cAMP-treated cells, which suggests that PA induces decidualization through phospholipase A2 (PLA2G1B).	Quinacrine	43-52	phospholipase A2 group IB	Homo sapiens	268-284
17065600-8	2007	In addition, pretreatment of ES cells with mepacrine decreased PRL/IGFBP1 expression and inhibited morphological change, whereas pretreatment with propranolol caused no changes, as compared to cAMP-treated cells, which suggests that PA induces decidualization through phospholipase A2 (PLA2G1B).	Quinacrine	43-52	phospholipase A2 group IB	Homo sapiens	286-293
16581945-0	2006	Quinacrine is mainly metabolized to mono-desethyl quinacrine by CYP3A4/5 and its brain accumulation is limited by P-glycoprotein.	Quinacrine	0-10	phosphoglycolate phosphatase	Mus musculus	114-128
16330112-3	2006	NT and EGF enhanced [3H]-AA release, which was diminished by inhibitors of PLA2 (quinacrine), EGFR (AG1478) and MEK (U0126).	Quinacrine	81-91	phospholipase A2 group IB	Homo sapiens	75-79
16598196-5	2006	Inhibition of PLA(2) by mepacrine and methyl arachidonyl fluorophosphate, AT(2) receptor by PD123319, Src family kinases by, 1-(tert-butyl)-3-(4-chlorophenyl)-4-aminopyrazolo[3,4-d] pyrimidine (PP2) and c-Src by overexpression of a dominant-negative mutant of c-Src abrogated these effects.	Quinacrine	24-33	phospholipase A2	Oryctolagus cuniculus	14-20
16623930-4	2006	To determine the effect of add-on Quinacrine (Qn) treatment on serum BAFF levels and the effect of this treatment on SLE disease activity index (SLEDAI), antidsDNA and anticardiolipin (aCL) antibody levels, we treated 29 stable SLE patients, who were maintained on prednisolone and hydroxychloroquine and in some on azathioprine (AZT), with additional Qn (100 mg/d) with an aim to further reduce disease activity.	Quinacrine	46-48	TNF superfamily member 13b	Homo sapiens	69-73
16498630-4	2006	Both PLA2 and melittin, an activator of endogenous PLA2, induced spinal neuronal death in vitro, which was substantially reversed by mepacrine, a PLA2 inhibitor.	Quinacrine	133-142	phospholipase A2 group IB	Homo sapiens	5-9
16498630-4	2006	Both PLA2 and melittin, an activator of endogenous PLA2, induced spinal neuronal death in vitro, which was substantially reversed by mepacrine, a PLA2 inhibitor.	Quinacrine	133-142	phospholipase A2 group IB	Homo sapiens	51-55
16498630-4	2006	Both PLA2 and melittin, an activator of endogenous PLA2, induced spinal neuronal death in vitro, which was substantially reversed by mepacrine, a PLA2 inhibitor.	Quinacrine	133-142	phospholipase A2 group IB	Homo sapiens	51-55
16498630-7	2006	Importantly, the PLA2-induced demyelination was significantly reversed by mepacrine.	Quinacrine	74-83	phospholipase A2 group IB	Homo sapiens	17-21
16511916-0	2006	Quinacrine but not chloroquine inhibits PMA induced upregulation of matrix metalloproteinases in leukocytes: quinacrine acts at the transcriptional level through a PLA2-independent mechanism.	Quinacrine	109-119	phospholipase A2 group IB	Homo sapiens	164-168
16511916-7	2006	RESULTS: Quinacrine suppressed PMA induced MMP-1 release in mononuclear cells (MNC) in a dose- and time-dependent manner.	Quinacrine	9-19	matrix metallopeptidase 1	Homo sapiens	43-48
16511916-8	2006	RT-PCR showed that quinacrine downregulated induced as well as noninduced steady-state mRNA levels of MMP-1, MMP-2, and MMP-8, but had no effect on MMP-3.	Quinacrine	19-29	matrix metallopeptidase 1	Homo sapiens	102-107
16511916-8	2006	RT-PCR showed that quinacrine downregulated induced as well as noninduced steady-state mRNA levels of MMP-1, MMP-2, and MMP-8, but had no effect on MMP-3.	Quinacrine	19-29	matrix metallopeptidase 2	Homo sapiens	109-114
16511916-8	2006	RT-PCR showed that quinacrine downregulated induced as well as noninduced steady-state mRNA levels of MMP-1, MMP-2, and MMP-8, but had no effect on MMP-3.	Quinacrine	19-29	matrix metallopeptidase 8	Homo sapiens	120-125
16375935-4	2006	This response was abolished when cells were pre-incubated with the phospholipase A(2) (PLA(2)) inhibitor quinacrine or with the cyclooxygenase inhibitor indomethacin.	Quinacrine	105-115	phospholipase A2 group IB	Homo sapiens	67-85
16375935-4	2006	This response was abolished when cells were pre-incubated with the phospholipase A(2) (PLA(2)) inhibitor quinacrine or with the cyclooxygenase inhibitor indomethacin.	Quinacrine	105-115	phospholipase A2 group IB	Homo sapiens	87-93
16394696-8	2006	Protein kinase C and phospholipase A2 were inhibited by chelerythrine or quinacrine, respectively.	Quinacrine	73-83	phospholipase A2 group IB	Rattus norvegicus	21-37
16394696-13	2006	In contrast, chelerythrine (P < 0.05) and quinacrine (P < 0.05) resulted in a blockade of HO-1 induction.	Quinacrine	45-55	heme oxygenase 1	Rattus norvegicus	96-100
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Quinacrine	103-113	tumor protein p53	Homo sapiens	143-146
17546512-7	2006	Both Ang II-induced superoxide anion and LTC(4) generation were decreased in control cells by pertussis toxin and fluvastatin (Flu), whereas in each patient group, mepacrin, verapamil and Flu were effective, suggesting alterations in signal pathways, which may be attributed to isoprenylation.	Quinacrine	164-172	angiotensinogen	Homo sapiens	5-11
16339857-8	2005	Transport of daunorubicin was reduced by the P-gp inhibitors verapamil and quinacrine and also by the organic cation tetraethylammonium.	Quinacrine	75-85	Multi drug resistance 65	Drosophila melanogaster	45-49
16177561-8	2005	In addition, in vivo delivery of quinacrine and amsacrine induced p53 transcriptional activity in tumor xenografts.	Quinacrine	33-43	tumor protein p53	Homo sapiens	66-69
16287968-3	2005	Among the compounds isolated were derivatives of 9-aminoacridine (9AA), including the antimalaria drug quinacrine, which strongly induced p53 function in RCC and other types of cancer cells.	Quinacrine	103-113	tumor protein p53	Homo sapiens	138-141
16287968-5	2005	In contrast to agents that target IkappaB kinase 2, 9AA and quinacrine can effectively suppress both basal and inducible activities of NF-kappaB, representing inhibitors of a previously undescribed type that convert NF-kappaB from a transactivator into a transrepressor, leading to accumulation of inactive nuclear complexes with unphosphorylated Ser-536 in the p65/RelA subunit.	Quinacrine	60-70	nuclear factor kappa B subunit 1	Homo sapiens	135-144
16287968-5	2005	In contrast to agents that target IkappaB kinase 2, 9AA and quinacrine can effectively suppress both basal and inducible activities of NF-kappaB, representing inhibitors of a previously undescribed type that convert NF-kappaB from a transactivator into a transrepressor, leading to accumulation of inactive nuclear complexes with unphosphorylated Ser-536 in the p65/RelA subunit.	Quinacrine	60-70	nuclear factor kappa B subunit 1	Homo sapiens	216-225
16287968-5	2005	In contrast to agents that target IkappaB kinase 2, 9AA and quinacrine can effectively suppress both basal and inducible activities of NF-kappaB, representing inhibitors of a previously undescribed type that convert NF-kappaB from a transactivator into a transrepressor, leading to accumulation of inactive nuclear complexes with unphosphorylated Ser-536 in the p65/RelA subunit.	Quinacrine	60-70	RELA proto-oncogene, NF-kB subunit	Homo sapiens	362-365
16287968-5	2005	In contrast to agents that target IkappaB kinase 2, 9AA and quinacrine can effectively suppress both basal and inducible activities of NF-kappaB, representing inhibitors of a previously undescribed type that convert NF-kappaB from a transactivator into a transrepressor, leading to accumulation of inactive nuclear complexes with unphosphorylated Ser-536 in the p65/RelA subunit.	Quinacrine	60-70	RELA proto-oncogene, NF-kB subunit	Homo sapiens	366-370
16287968-8	2005	The results demonstrate, in principle, the possibility to kill cancer cells selectively through simultaneous inhibition of NF-kappaB and activation of p53 by a single small molecule and suggest anticancer applications for the well known antimalaria drug quinacrine.	Quinacrine	254-264	nuclear factor kappa B subunit 1	Homo sapiens	123-132
16287968-8	2005	The results demonstrate, in principle, the possibility to kill cancer cells selectively through simultaneous inhibition of NF-kappaB and activation of p53 by a single small molecule and suggest anticancer applications for the well known antimalaria drug quinacrine.	Quinacrine	254-264	tumor protein p53	Homo sapiens	151-154
15950537-7	2005	The presence of inhibitors of PLA2 (bromoenol lactone, aristolochic acid and quinacrine dihydrochloride) diminished the label in SM significantly during the 90-min labeling.	Quinacrine	77-103	phospholipase A2, group IB, pancreas	Mus musculus	30-34
15368540-9	2005	PLA2 inhibitors quinacrine and AACOCF3, and cyclooxygenase inhibitor indomethacin blocked the effect of PLAA peptide on PKC, indicating arachidonic acid and its metabolites were involved.	Quinacrine	16-26	phospholipase A2 group IB	Rattus norvegicus	0-4
15672687-0	2004	Toxicity of quinacrine can be reduced by co-administration of P-glycoprotein inhibitor in sporadic Creutzfeldt-Jakob disease.	Quinacrine	12-22	ATP binding cassette subfamily B member 1	Homo sapiens	62-76
15528199-8	2005	Treatment with quinacrine or pentosan polysulfate cleared the PrPSc from the ScGT1-1 cell cultures, and the increase in levels of monomeric SNAP-25 and synaptophysin was reversible.	Quinacrine	15-25	prion protein	Mus musculus	62-67
15528199-8	2005	Treatment with quinacrine or pentosan polysulfate cleared the PrPSc from the ScGT1-1 cell cultures, and the increase in levels of monomeric SNAP-25 and synaptophysin was reversible.	Quinacrine	15-25	synaptosomal-associated protein 25	Mus musculus	140-147
15528199-8	2005	Treatment with quinacrine or pentosan polysulfate cleared the PrPSc from the ScGT1-1 cell cultures, and the increase in levels of monomeric SNAP-25 and synaptophysin was reversible.	Quinacrine	15-25	synaptophysin	Mus musculus	152-165
15527871-6	2005	Quinacrine, a phospholipase A2 (PLA2) inhibitor, was employed to determine its protective effect on SAM-induced PD-like changes by the inhibition of lyso-PTC formation.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
15527871-6	2005	Quinacrine, a phospholipase A2 (PLA2) inhibitor, was employed to determine its protective effect on SAM-induced PD-like changes by the inhibition of lyso-PTC formation.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	32-36
15672687-5	2004	We disclosed the permeability of quinacrine can be enhanced by presence of p-glycoprotein inhibitor at blood-brain barrier in vitro.	Quinacrine	33-43	ATP binding cassette subfamily B member 1	Homo sapiens	75-89
15569390-2	2004	In a cell-based assay, quinacrine inhibits the conversion of normal host prion protein (PrPC) to PrPSc at a half-maximal concentration of 300 nM.	Quinacrine	23-33	prion protein	Mus musculus	97-102
15569390-4	2004	If quinacrine penetrates brain tissue in concentrations exceeding that demonstrated for in vitro inhibition of PrPSc, it may be useful in the treatment of prion disease.	Quinacrine	3-13	prion protein	Mus musculus	111-116
15569390-7	2004	RESULTS: Quinacrine was demonstrated to penetrate rapidly into brain tissue, achieving concentrations up to 1500 ng/g, which is several-fold greater than that demonstrated to inhibit formation of PrPSc in cell culture.	Quinacrine	9-19	prion protein	Mus musculus	196-201
15569390-11	2004	The relative importance of free quinacrine in these compartments upon the conversion of normal host prion protein (PrPC) to PrPSc will be critical toward its potential benefit.	Quinacrine	32-42	prion protein	Mus musculus	124-129
15345496-9	2004	Quinacrine, an inhibitor of PLA2, overruled the effect of the agonists on Na+ transport.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	28-32
15297306-4	2004	Immunofluorescence microscopy using 2 MRP4-specific antibodies revealed staining mainly in intracellular structures, which largely colocalized with the accumulation of mepacrine as marker for delta-granules and to a lower extent at the plasma membrane.	Quinacrine	168-177	ATP binding cassette subfamily C member 4	Homo sapiens	38-42
15319801-9	2004	However, bradykinin contractions were antagonized in a noncompetitive manner by quinacrine (10(-5) mM).	Quinacrine	80-90	kininogen 1	Homo sapiens	9-19
15307186-7	2004	Our results demonstrate direct binding of TLR9 to CpG-DNA and suggest that the therapeutic activity of chloroquine and quinacrine in autoimmune diseases may be due to its activity as a TLR9 antagonist and inhibitor of endosomal acidification.	Quinacrine	119-129	toll like receptor 9	Homo sapiens	42-46
15307186-7	2004	Our results demonstrate direct binding of TLR9 to CpG-DNA and suggest that the therapeutic activity of chloroquine and quinacrine in autoimmune diseases may be due to its activity as a TLR9 antagonist and inhibitor of endosomal acidification.	Quinacrine	119-129	toll like receptor 9	Homo sapiens	185-189
15371093-4	2004	Treatment with mepacrine, a phospholipase A2 inhibitor, attenuated the increases in serum and lung lavage ferritin concentrations, lung inflammation, and lung leak that occur in rats subjected to hemorrhage.	Quinacrine	15-24	phospholipase A2 group IB	Rattus norvegicus	28-44
15307186-6	2004	Furthermore, chloroquine and quinacrine, therapeutic agents for autoimmune diseases like rheumatoid arthritis and systemic lupus erythematosus, directly blocked TLR9-CpG-DNA interaction but not TLR2-Pam3Cys binding.	Quinacrine	29-39	toll like receptor 9	Homo sapiens	161-165
15349121-4	2004	RESULTS: A large cell infiltrate by macrophages, CD4(+), CD8(+), and natural killer cells was evident a few hours after quinacrine injection.	Quinacrine	120-130	Cd4 molecule	Rattus norvegicus	49-52
15082450-4	2004	Acidotropic fluorophores, such as quinacrine and LysoTrackers, clearly and selectively labeled renin granules.	Quinacrine	34-44	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	95-100
15082450-5	2004	Immunohistochemistry of mouse kidney with a specific renin antibody and quinacrine staining colocalized renin granules and quinacrine fluorescence.	Quinacrine	72-82	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	104-109
15082450-5	2004	Immunohistochemistry of mouse kidney with a specific renin antibody and quinacrine staining colocalized renin granules and quinacrine fluorescence.	Quinacrine	123-133	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	53-58
15046864-5	2004	Treatment of PrP(187R-GFP) cells with quinacrine or doxycycline, agents known to inhibit the replication of PrP-scrapie (PrP(Sc)) in experimental models, gave conflicting results; doxycycline reverted the mutant phenotype of PrP(187R-GFP) cells, whereas quinacrine had no effect.	Quinacrine	38-48	prion protein	Homo sapiens	13-16
15046864-5	2004	Treatment of PrP(187R-GFP) cells with quinacrine or doxycycline, agents known to inhibit the replication of PrP-scrapie (PrP(Sc)) in experimental models, gave conflicting results; doxycycline reverted the mutant phenotype of PrP(187R-GFP) cells, whereas quinacrine had no effect.	Quinacrine	38-48	prion protein	Homo sapiens	108-111
15046864-5	2004	Treatment of PrP(187R-GFP) cells with quinacrine or doxycycline, agents known to inhibit the replication of PrP-scrapie (PrP(Sc)) in experimental models, gave conflicting results; doxycycline reverted the mutant phenotype of PrP(187R-GFP) cells, whereas quinacrine had no effect.	Quinacrine	38-48	prion protein	Homo sapiens	108-111
15046864-5	2004	Treatment of PrP(187R-GFP) cells with quinacrine or doxycycline, agents known to inhibit the replication of PrP-scrapie (PrP(Sc)) in experimental models, gave conflicting results; doxycycline reverted the mutant phenotype of PrP(187R-GFP) cells, whereas quinacrine had no effect.	Quinacrine	38-48	prion protein	Homo sapiens	108-111
14644748-6	2004	ANG II-induced inhibition of alpha-MG uptake was blocked by genistein, herbimycin A [tyrosine kinase (TK) inhibitors], mepacrine, and AACOCF3 (phospholipase A2 inhibitors), suggesting the role of TK phosphorylation and arachidonic acid (AA).	Quinacrine	119-128	angiogenin	Oryctolagus cuniculus	0-3
15176436-8	2004	In the presence of P-glycoprotein (P-gp) inhibitor, cyclosporine or verapamil, the apical-to-basolateral transport of quinacrine increased.	Quinacrine	118-128	phosphoglycolate phosphatase	Mus musculus	19-33
15176436-8	2004	In the presence of P-glycoprotein (P-gp) inhibitor, cyclosporine or verapamil, the apical-to-basolateral transport of quinacrine increased.	Quinacrine	118-128	phosphoglycolate phosphatase	Mus musculus	35-39
15176436-15	2004	These findings suggest that quinacrine transport at the BBB is mediated by the efflux system (P-gp) and the influx system (organic cation transporter-like machinery).	Quinacrine	28-38	phosphoglycolate phosphatase	Mus musculus	94-98
15915714-2	2004	It was shown, that inhibitors of phospholipase A2 (quinacrine, 10-100 microM), cyclooxygenase (aspirin, 10-100 microM) and cyclo- and lipoxygenase (BW755c, 1-100 microM) lowered electrophoretic mobility (EPM) of erythrocytes by 20-30%.	Quinacrine	51-61	phospholipase A2 group IB	Homo sapiens	33-49
14709393-7	2004	When exocytosis events occurred, the microfluidic system detected the fluorescent signal of quinacrine, which was released from RBL-2H3 cells by using a photomultiplier tube (PMT) fitted onto a microscope.	Quinacrine	92-102	RB transcriptional corepressor like 2	Rattus norvegicus	128-133
12814911-3	2003	Exposure of the skinned EDL fibers to indomethacin (200 microM) (n = 7) and another PLA2 inhibitor quinacrine (200 microM) (n = 5) resulted in the return of large DIFRs after use-dependent rundown.	Quinacrine	99-109	phospholipase A2 group IB	Rattus norvegicus	84-88
14717925-7	2004	Inhibition of PLA2 by mepacrine and methyl arachidonyl fluorophosphonate ketone (AACOCF3) attenuated both arachidonic acid release and ERK 1/2 activation by cyclic stretch, supporting the importance of PLA2 as a mediator of mechanotransduction in renal proximal tubular cells.	Quinacrine	22-31	phospholipase A2	Oryctolagus cuniculus	14-18
14687699-3	2004	The following results indicate that the phospholipase A2 (PLA2)/COX/prostaglandin E (PGE2) pathway is implicated in this process: (1) The inhibitory effect of BK on Ang-(1-7)-stimulated enzyme is abolished in a dose-dependent manner by quinacrine (10(-9)-10(-6)M), a nonspecific PLA2 inhibitor, and by PACOCF3 (10(-7)M), an inhibitor of a Ca(2+)-independent PLA2.	Quinacrine	236-246	phospholipase A2 group IB	Homo sapiens	40-56
14687699-3	2004	The following results indicate that the phospholipase A2 (PLA2)/COX/prostaglandin E (PGE2) pathway is implicated in this process: (1) The inhibitory effect of BK on Ang-(1-7)-stimulated enzyme is abolished in a dose-dependent manner by quinacrine (10(-9)-10(-6)M), a nonspecific PLA2 inhibitor, and by PACOCF3 (10(-7)M), an inhibitor of a Ca(2+)-independent PLA2.	Quinacrine	236-246	phospholipase A2 group IB	Homo sapiens	58-62
15051151-6	2004	Experiments aimed at delineating the metabotropic pathway leading to K channel activation by histamine indicated the involvement of a pertussis toxin-insensitive G protein, and a quinacrine-sensitive cytosolic phospholipase A2.	Quinacrine	179-189	phospholipase A2 group IVA	Gallus gallus	200-226
12907422-12	2003	Pretreatment with the phospholipase A2 inhibitors mepacrine and 7,7-dimethyl-5,8-eicosadienoic acid, the lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate, nordihydroguaiaretic acid, and ebselen, or the hydroperoxide isomerase inhibitors miconazole and clotrimazole also blocked ACh-induced relaxations.	Quinacrine	50-59	phospholipase A2	Oryctolagus cuniculus	22-38
14583784-3	2003	The induction of proteasome activity and protein degradation by PIF was blocked by quinacrine, a nonspecific phospholipase A(2) (PLA(2)) inhibitor and trifluroacetyl AA, an inhibitor of cytosolic PLA(2).	Quinacrine	83-93	Pif	Mus musculus	64-67
14583784-3	2003	The induction of proteasome activity and protein degradation by PIF was blocked by quinacrine, a nonspecific phospholipase A(2) (PLA(2)) inhibitor and trifluroacetyl AA, an inhibitor of cytosolic PLA(2).	Quinacrine	83-93	phospholipase A2, group IB, pancreas	Mus musculus	109-127
14583784-3	2003	The induction of proteasome activity and protein degradation by PIF was blocked by quinacrine, a nonspecific phospholipase A(2) (PLA(2)) inhibitor and trifluroacetyl AA, an inhibitor of cytosolic PLA(2).	Quinacrine	83-93	phospholipase A2, group IB, pancreas	Mus musculus	129-135
14583784-3	2003	The induction of proteasome activity and protein degradation by PIF was blocked by quinacrine, a nonspecific phospholipase A(2) (PLA(2)) inhibitor and trifluroacetyl AA, an inhibitor of cytosolic PLA(2).	Quinacrine	83-93	phospholipase A2, group IB, pancreas	Mus musculus	196-202
14677173-0	2003	Mepacrine inhibits matrix metalloproteinases-1 (MMP-1) and MMP-9 activation in human fibroblast-like synoviocytes.	Quinacrine	0-9	matrix metallopeptidase 1	Homo sapiens	19-53
14677173-0	2003	Mepacrine inhibits matrix metalloproteinases-1 (MMP-1) and MMP-9 activation in human fibroblast-like synoviocytes.	Quinacrine	0-9	matrix metallopeptidase 9	Homo sapiens	59-64
14677173-8	2003	Mepacrine inhibited MMP-1 as well as MMP-9, but had no effect on MMP-3 at the mRNA level.	Quinacrine	0-9	matrix metallopeptidase 1	Homo sapiens	20-25
14677173-8	2003	Mepacrine inhibited MMP-1 as well as MMP-9, but had no effect on MMP-3 at the mRNA level.	Quinacrine	0-9	matrix metallopeptidase 9	Homo sapiens	37-42
14677173-9	2003	Possible mechanisms to explain these findings were investigated, and it was found that mepacrine had a strikingly different effect on c-Jun, as opposed to c-Fos activation.	Quinacrine	87-96	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	134-139
14677173-10	2003	While mepacrine treatment alone led to increased concentrations of c-Jun within the nuclear compartment, c-Fos translocation into the nucleus was blocked in synoviocytes treated with mepacrine and stimulated with PMA.	Quinacrine	6-15	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-72
14677173-10	2003	While mepacrine treatment alone led to increased concentrations of c-Jun within the nuclear compartment, c-Fos translocation into the nucleus was blocked in synoviocytes treated with mepacrine and stimulated with PMA.	Quinacrine	183-192	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-110
14681337-6	2004	Other classes of drugs that demonstrated inhibition of aldehyde oxidase included phenothiazines, tricyclic antidepressants, tricyclic atypical antipsychotic agents, and dihydropyridine calcium channel blockers, along with some other drugs, including loratadine, cyclobenzaprine, amodiaquine, maprotiline, ondansetron, propafenone, domperidone, quinacrine, ketoconazole, verapamil, tacrine, and salmeterol.	Quinacrine	344-354	aldehyde oxidase 1	Homo sapiens	55-71
14552885-5	2003	cPLA(2) levels and neuronal death were modulated by daily intraperitoneal injections of quinacrine, an inhibitor of phospholipase A(2) that can cross the blood brain barrier.	Quinacrine	88-98	phospholipase A2 group IVA	Homo sapiens	0-7
14552885-5	2003	cPLA(2) levels and neuronal death were modulated by daily intraperitoneal injections of quinacrine, an inhibitor of phospholipase A(2) that can cross the blood brain barrier.	Quinacrine	88-98	phospholipase A2 group IB	Homo sapiens	116-134
12813050-4	2003	This toxicity was inhibited by the PLA2 inhibitors aristolochic acid, quinacrine, and PTK.	Quinacrine	70-80	phospholipase A2 group IB	Homo sapiens	35-39
12808118-2	2003	The recent discovery of the inhibitory action of quinacrine on PrP(Sc) formation in scrapie-infected neuroblastoma (ScN2a) cells raised the possibility of a treatment for patients with prion disease.	Quinacrine	49-59	prion protein	Homo sapiens	63-66
12808118-2	2003	The recent discovery of the inhibitory action of quinacrine on PrP(Sc) formation in scrapie-infected neuroblastoma (ScN2a) cells raised the possibility of a treatment for patients with prion disease.	Quinacrine	49-59	sodium voltage-gated channel alpha subunit 2	Homo sapiens	116-121
12713826-6	2003	Preliminary data from molecular modeling investigations showed that the imidazole derivative 15 and the HMT inhibitor quinacrine possess identical binding areas.	Quinacrine	118-128	histamine N-methyltransferase	Rattus norvegicus	104-107
12675279-2	2003	Treatment with quinacrine, an inhibitor of phospholipase A2, abolished the relaxation by acetylcholine.	Quinacrine	15-25	phospholipase A2 group IB	Homo sapiens	43-59
12079427-4	2002	Crude venom induced a contraction in rat tracheal preparations through phospholipase A(2) (PLA(2)) activity, as shown by the complete and partial inhibition of contraction by PLA(2) inhibitors 4-bromophenacyl bromide and quinacrine.	Quinacrine	221-231	phospholipase A2 group IB	Rattus norvegicus	91-97
12582837-0	2003	Quinacrine abolishes increases in cytoplasmic phospholipase A2 mRNA levels in the rat hippocampus after kainate-induced neuronal injury.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	46-62
12582837-1	2003	The present investigation was carried out to study the possible effects of quinacrine in modulating cytoplasmic phospholipase A(2) (cPLA(2)) mRNA levels in rat hippocampus after kainate treatment.	Quinacrine	75-85	phospholipase A2 group IB	Rattus norvegicus	112-130
12582837-1	2003	The present investigation was carried out to study the possible effects of quinacrine in modulating cytoplasmic phospholipase A(2) (cPLA(2)) mRNA levels in rat hippocampus after kainate treatment.	Quinacrine	75-85	phospholipase A2 group IVA	Rattus norvegicus	132-139
12582837-4	2003	Rats that received once daily intraperitoneal injections of quinacrine (5 mg/kg) after the intracerebroventricular kainate injections showed almost complete attenuation of increased cPLA(2) expression, at both 3 and 7 days after kainate injection.	Quinacrine	60-70	phospholipase A2 group IVA	Rattus norvegicus	182-189
12582837-5	2003	These results show that in addition to its well-known effect of inhibition of PLA(2) activity, quinacrine could also inhibit cPLA(2) expression, and further supports a role for PLA(2) in kainate-induced neuronal injury.	Quinacrine	95-105	phospholipase A2 group IVA	Rattus norvegicus	125-132
12492473-7	2003	Quinacrine (phospholipase A2 inhibitor) and 1-O-octadecyl-2-O-methyl-rac-glycerol-3-phosphocholine (CoA-independent transacylase inhibitor) prevented all of these ceramide-elicited effects.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	12-28
14610335-3	2003	EGF-induced inhibition of Pi uptake was blocked by AG1478 (an EGF receptor antagonist), genistein or herbimycin A (tyrosine kinase inhibitors) and also blocked by mepacrine (a phospholipase A(2) (PLA(2)) inhibitor) and AACOCF(3 )(a cPLA(2) inhibitor).	Quinacrine	163-172	epidermal growth factor	Homo sapiens	0-3
14610335-3	2003	EGF-induced inhibition of Pi uptake was blocked by AG1478 (an EGF receptor antagonist), genistein or herbimycin A (tyrosine kinase inhibitors) and also blocked by mepacrine (a phospholipase A(2) (PLA(2)) inhibitor) and AACOCF(3 )(a cPLA(2) inhibitor).	Quinacrine	163-172	phospholipase A2 group IB	Homo sapiens	176-194
14610335-3	2003	EGF-induced inhibition of Pi uptake was blocked by AG1478 (an EGF receptor antagonist), genistein or herbimycin A (tyrosine kinase inhibitors) and also blocked by mepacrine (a phospholipase A(2) (PLA(2)) inhibitor) and AACOCF(3 )(a cPLA(2) inhibitor).	Quinacrine	163-172	phospholipase A2 group IIA	Homo sapiens	196-203
14574738-4	2003	Neutralization of stimulative irradiation effect on chemokinesis of polymorphonuclear leukocytes by quinacrine (the inhibitor of phospholipase A2) indicates for certain, that metabolism of eicosanoids takes immediate part in the cell response to ionizing radiation.	Quinacrine	100-110	phospholipase A2 group IB	Homo sapiens	129-145
12196138-6	2002	In an effort to develop therapeutics, the antimalarial drug quinacrine was identified as an inhibitor of PrP-res formation in scrapie-infected cell cultures.	Quinacrine	60-70	prion protein	Homo sapiens	105-108
12508297-8	2003	Quinacrine reduced the number of desmin-negative and albumin-positive cells by 88% (P < 0.05) and 84% (P < 0.05), indicating that it attenuated histopathologic changes that follow stretch injury of activated skeletal muscles.	Quinacrine	0-10	desmin	Rattus norvegicus	33-39
12849737-0	2003	Quinacrine attenuates increases in divalent metal transporter-1 and iron levels in the rat hippocampus, after kainate-induced neuronal injury.	Quinacrine	0-10	RoBo-1	Rattus norvegicus	35-63
12849737-1	2003	The present investigation was carried out to elucidate the effect of the antimalarial drug quinacrine on levels of expression of the non-heme iron transporter, divalent metal transporter-1 (DMT1) and iron, in the hippocampus of rats after kainate treatment.	Quinacrine	91-101	RoBo-1	Rattus norvegicus	160-188
12849737-1	2003	The present investigation was carried out to elucidate the effect of the antimalarial drug quinacrine on levels of expression of the non-heme iron transporter, divalent metal transporter-1 (DMT1) and iron, in the hippocampus of rats after kainate treatment.	Quinacrine	91-101	RoBo-1	Rattus norvegicus	190-194
12849737-4	2003	The increases in DMT1 and iron staining were significantly attenuated by quinacrine.	Quinacrine	73-83	RoBo-1	Rattus norvegicus	17-21
12849737-6	2003	injections of quinacrine (5 mg/kg) for 7 days or 2 weeks showed significantly lower levels of DMT1 immunoreactivity and iron staining, compared with rats injected with kainate and saline.	Quinacrine	14-24	RoBo-1	Rattus norvegicus	94-98
12070017-2	2002	Platelets of mice with the ashen mutation on the C3H/HeSnJ inbred strain background have greatly reduced amounts of dense granule components such as serotonin and adenine nucleotides though near-normal numbers of dense granules as enumerated by the dense granule-specific fluorescent dye mepacrine.	Quinacrine	288-297	RAB27A, member RAS oncogene family	Mus musculus	27-32
12082016-9	2002	Further exploration of antimalarial compounds identified the common medicinals chloroquine, quinacrine, and amodiaquine as Tp53-inducers.	Quinacrine	92-102	tumor protein p53	Homo sapiens	123-127
11891218-5	2002	On the other hand, quinacrine abolished the effects of UK14304, but not of AA, suggesting that AA released through PLA2 is responsible for MAPK activation by alpha(2B)-AR.	Quinacrine	19-29	adrenoceptor alpha 2B	Rattus norvegicus	158-170
11812648-6	2002	But the elevation of intracellular ROS was inhibited by mepacrine, a phospholipase A2 inhibitor.	Quinacrine	56-65	phospholipase A2 group IB	Homo sapiens	69-85
11641439-5	2001	PMA promoted the generation of PGE(2) in the medium of HASMC and caused activation of both extracellular signal-regulated kinase (ERK) and PKA through a process ablated by indomethacin, NS-398, quinacrine, and PD98059.	Quinacrine	194-204	mitogen-activated protein kinase 1	Homo sapiens	91-128
11858795-6	2002	In the presence of quinacrine, agonist-induced NO release became Mg2+ -independent and could not be attributed to an inhibition of phospholipase A2 activity.	Quinacrine	19-29	mucin 7, secreted	Homo sapiens	65-68
12462986-6	2002	On the other hand, quinacrine inhibited PLA2 activity, and we propose here that the anti-angiogenic effect occurs via inhibition of the enzyme PLA2.	Quinacrine	19-29	phospholipase A2, group V	Mus musculus	40-44
12462986-6	2002	On the other hand, quinacrine inhibited PLA2 activity, and we propose here that the anti-angiogenic effect occurs via inhibition of the enzyme PLA2.	Quinacrine	19-29	phospholipase A2, group V	Mus musculus	143-147
11786377-6	2002	Mepacrine and parabromophenacyl bromide (pBpB), two PLA(2) inhibitors, decreased the hormone-stimulated AA release to 85+/-9 and 70+/-24% respectively.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	52-58
11786377-8	2002	The inhibitory effect of mepacrine on the release of AA was evident in hCG-treated Leydig cells, but not in the melittin-treated cells.	Quinacrine	25-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
11755955-4	2001	This enhancement could be specifically prohibited by the alpha(2A)-adrenoceptor antagonist, atipamezole, the p38 mitogen-activated protein kinase (p38MAPK) inhibitor SB203580, and the cytosolic phospholipase A(2) (cPLA(2)) inhibitor, mepacrine.	Quinacrine	234-243	mitogen-activated protein kinase 14	Homo sapiens	109-145
11755955-4	2001	This enhancement could be specifically prohibited by the alpha(2A)-adrenoceptor antagonist, atipamezole, the p38 mitogen-activated protein kinase (p38MAPK) inhibitor SB203580, and the cytosolic phospholipase A(2) (cPLA(2)) inhibitor, mepacrine.	Quinacrine	234-243	mitogen-activated protein kinase 14	Homo sapiens	147-154
11755955-4	2001	This enhancement could be specifically prohibited by the alpha(2A)-adrenoceptor antagonist, atipamezole, the p38 mitogen-activated protein kinase (p38MAPK) inhibitor SB203580, and the cytosolic phospholipase A(2) (cPLA(2)) inhibitor, mepacrine.	Quinacrine	234-243	phospholipase A2 group IVA	Homo sapiens	184-221
11078959-7	2001	While NF-kappa B-DNA interactions are not effected, AP-1-DNA binding is blocked by quinacrine.	Quinacrine	83-93	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	52-56
11078959-8	2001	Such differential effects are presumably due to intercalation of quinacrine into the AP-1 consensus element.	Quinacrine	65-75	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-89
11078959-11	2001	Furthermore, the differential effects of quinacrine might be exploited to study and gain additional insight in the involvement of AP-1 and NF-kappa B in gene regulation.	Quinacrine	41-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	130-134
11078959-11	2001	Furthermore, the differential effects of quinacrine might be exploited to study and gain additional insight in the involvement of AP-1 and NF-kappa B in gene regulation.	Quinacrine	41-51	nuclear factor kappa B subunit 1	Homo sapiens	139-149
11641439-5	2001	PMA promoted the generation of PGE(2) in the medium of HASMC and caused activation of both extracellular signal-regulated kinase (ERK) and PKA through a process ablated by indomethacin, NS-398, quinacrine, and PD98059.	Quinacrine	194-204	mitogen-activated protein kinase 1	Homo sapiens	130-133
11550224-7	2001	PrP106-126 neurotoxicity was mediated through the 5-lipoxygenase (5-LOX) pathway, as shown by abrogation of neuronal death with the 5-LOX inhibitors quinacrine, nordihydroguaiaretic acid, and caffeic acid.	Quinacrine	149-159	arachidonate 5-lipoxygenase	Homo sapiens	132-137
11812506-5	2002	Consistent with our earlier work, pretreatment with the PLA(2) inhibitor quinacrine (25 mg/kg) blocked the development of cocaine and amphetamine sensitization.	Quinacrine	73-83	phospholipase A2 group IB	Rattus norvegicus	56-62
11774821-1	2001	OBJECTIVE: To explore the influence of quinacrine, which is an inhibitor of phospholipase A2, on gut-origin bacteria/endotoxin translocation in rats with gut ischemia/reperfusion injury.	Quinacrine	39-49	phospholipase A2 group IB	Rattus norvegicus	76-92
11551515-6	2001	The phospholipase A(2) (PLA(2)) inhibitor, mepacrine, completely inhibited the [14C]-AA response.	Quinacrine	43-52	phospholipase A2 group IB	Rattus norvegicus	4-22
11774821-5	2001	RESULTS: Plasma contents of endotoxin and TNF alpha were lowered in both quinacrine treatment groups (P < 0.01).	Quinacrine	73-83	tumor necrosis factor	Rattus norvegicus	42-51
11551515-6	2001	The phospholipase A(2) (PLA(2)) inhibitor, mepacrine, completely inhibited the [14C]-AA response.	Quinacrine	43-52	phospholipase A2 group IB	Rattus norvegicus	24-30
11147818-5	2001	The phospholipase A2 (PLA2) inhibitors, aristolochic acid (ARIST) and quinacrine (QUIN), decreased the release of 3H and inhibited PEUU biodegradation (>50%, P<0.05).	Quinacrine	70-80	phospholipase A2 group IB	Homo sapiens	4-20
11566133-4	2001	RESULTS: Two ternary structures of human HNMT have been determined: the Thr105 variant complexed with its substrate histamine and reaction product AdoHcy and the Ile105 variant complexed with an inhibitor (quinacrine) and AdoHcy.	Quinacrine	206-216	histamine N-methyltransferase	Homo sapiens	41-45
11566133-9	2001	The interactions between HNMT and quinacrine provide the first structural insights into a large group of pharmacologic HNMT inhibitors and their mechanisms of inhibition.	Quinacrine	34-44	histamine N-methyltransferase	Homo sapiens	25-29
11566133-9	2001	The interactions between HNMT and quinacrine provide the first structural insights into a large group of pharmacologic HNMT inhibitors and their mechanisms of inhibition.	Quinacrine	34-44	histamine N-methyltransferase	Homo sapiens	119-123
11455009-1	2001	Quinacrine has been shown to act as a noncompetitive inhibitor of the nicotinic acetylcholine receptor (nAChR).	Quinacrine	0-10	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	70-102
11455009-1	2001	Quinacrine has been shown to act as a noncompetitive inhibitor of the nicotinic acetylcholine receptor (nAChR).	Quinacrine	0-10	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	104-109
11455009-9	2001	Results from both single-channel and macroscopic current recordings indicate that quinacrine increases the rate of nAChR desensitization and stabilizes the desensitized state.	Quinacrine	82-92	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	115-120
11311405-6	2001	The effect of IL-1beta was completely abolished when we treated cells with inhibitor of mitogen-activated protein kinases (MAPKs) (PD98059) (25 microM), phospholipase A(2) inhibitor mepacrine (30 microM) and protein synthesis inhibitor cycloheximide (CHX) (10 microg/ml).	Quinacrine	182-191	interleukin 1 beta	Rattus norvegicus	14-22
11339632-0	2001	Quinacrine induces cytochrome c-dependent apoptotic signaling in human cervical carcinoma cells.	Quinacrine	0-10	cytochrome c, somatic	Homo sapiens	19-31
11339632-1	2001	Quinacrine (QU), a phospholipase-A2 (PLA-2) inhibitor has been used clinically as a chemotherapeutic adjuvant.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	19-35
11339632-1	2001	Quinacrine (QU), a phospholipase-A2 (PLA-2) inhibitor has been used clinically as a chemotherapeutic adjuvant.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	37-42
11278180-7	2001	The phospholipase A2 inhibitors quinacrine and p-bromophenacyl bromide added at 0.1 mM concentration each to either slices from controls or Et-DHA treated fetal brains, decreased TBARS production.	Quinacrine	32-42	phospholipase A2 group IB	Rattus norvegicus	4-20
11207202-5	2001	The fMLP-induced PGE2 output is inhibited by indomethacin, quinacrine, and U-73122, inhibitors of cyclooxygenase, phospholipase A2, and phospholipase C, respectively.	Quinacrine	59-69	formyl peptide receptor 1	Homo sapiens	4-8
11207202-5	2001	The fMLP-induced PGE2 output is inhibited by indomethacin, quinacrine, and U-73122, inhibitors of cyclooxygenase, phospholipase A2, and phospholipase C, respectively.	Quinacrine	59-69	phospholipase A2 group IB	Homo sapiens	114-130
11226716-2	2001	In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents.	Quinacrine	87-97	phospholipase A2 group IB	Rattus norvegicus	107-111
11226716-2	2001	In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents.	Quinacrine	99-102	phospholipase A2 group IB	Rattus norvegicus	107-111
11490349-4	2001	PLA(2) inhibition (quinacrine, 10 mg/kg, intravenously) was given before shock was induced.	Quinacrine	19-29	phospholipase A2 group IB	Rattus norvegicus	0-6
11323430-6	2001	Oncogenic Ha-Ras(V12)-induced SRE activation was significantly inhibited by either pretreatment with mepacrine, a phospholipase A(2) inhibitor, or cotransfection with the antisense oligonucleotide of cytosolic phospholipase A(2).	Quinacrine	101-110	phospholipase A2 group IVA	Rattus norvegicus	200-228
11450704-16	2001	Inhibition of phospholipase A2 with quinacrine blocked the 1alpha,25(OH)2D3-dependent effect.	Quinacrine	36-46	phospholipase A2 group IB	Homo sapiens	14-30
11147818-5	2001	The phospholipase A2 (PLA2) inhibitors, aristolochic acid (ARIST) and quinacrine (QUIN), decreased the release of 3H and inhibited PEUU biodegradation (>50%, P<0.05).	Quinacrine	70-80	phospholipase A2 group IB	Homo sapiens	22-26
11147818-5	2001	The phospholipase A2 (PLA2) inhibitors, aristolochic acid (ARIST) and quinacrine (QUIN), decreased the release of 3H and inhibited PEUU biodegradation (>50%, P<0.05).	Quinacrine	82-86	phospholipase A2 group IB	Homo sapiens	4-20
11147818-5	2001	The phospholipase A2 (PLA2) inhibitors, aristolochic acid (ARIST) and quinacrine (QUIN), decreased the release of 3H and inhibited PEUU biodegradation (>50%, P<0.05).	Quinacrine	82-86	phospholipase A2 group IB	Homo sapiens	22-26
10831384-1	2000	A multidrug-resistant strain of Plasmodium yoelii nigeriensis (MDR) showing a wide spectrum of resistance to chloroquine, amodiaquine, mepacrine, mefloquine, halofantrine, quinine, and quinidine was used in this study for in vivo evaluation of the blood schizontocidal activity of pyronaridine, a topoisomerase II inhibitor, in Swiss mice.	Quinacrine	135-144	malic enzyme complex, mitochondrial	Mus musculus	63-66
10916087-8	2000	Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA.	Quinacrine	15-24	Jun proto-oncogene, AP-1 transcription factor subunit	Canis lupus familiaris	79-84
10916087-8	2000	Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA.	Quinacrine	15-24	early growth response 1	Canis lupus familiaris	86-91
10916087-8	2000	Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA.	Quinacrine	15-24	MYC proto-oncogene, bHLH transcription factor	Canis lupus familiaris	97-102
10916087-8	2000	Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA.	Quinacrine	15-24	Jun proto-oncogene, AP-1 transcription factor subunit	Canis lupus familiaris	171-176
10916087-8	2000	Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA.	Quinacrine	15-24	early growth response 1	Canis lupus familiaris	181-186
10856708-5	2000	The two structurally different PLA(2) inhibitors showed differential effects on the PMA-induced superoxide generation: pBPB inhibited it but mepacrine did not.	Quinacrine	141-150	phospholipase A2, group IB, pancreas	Mus musculus	31-37
10862823-3	2000	The elevation of both catecholamines induced by melittin (10 microg/animal) was abolished by centrally administered mepacrine (an inhibitor of phospholipase A(2)), but not by neomycin (an inhibitor of phospholipase C).	Quinacrine	116-125	phospholipase A and acyltransferase 1	Rattus norvegicus	143-158
10850852-9	2000	Treatment with mepacrine decreased lung neutrophil accumulation, ultrastructural lung abnormalities, lung lavage phospholipid levels, lung tissue GGT levels, and blood oxygenation impairment in rats given IL-1 intratracheally, suggesting a possible relationship between these events.	Quinacrine	15-24	gamma-glutamyltransferase 1	Rattus norvegicus	146-149
10884509-0	2000	Mechanism of suppression of cardiac L-type Ca(2+) currents by the phospholipase A(2) inhibitor mepacrine.	Quinacrine	95-104	phospholipase A2 group IB	Rattus norvegicus	66-84
10884509-2	2000	Mepacrine, a phospholipase A(2) inhibitor, has been shown to protect the heart from ischemic injury.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-31
10884509-14	2000	While mepacrine is a phospholipase A(2) inhibitor and reduces cAMP production, its inhibitory effect on I(Ca,L) mainly results from a direct block of the channel.	Quinacrine	6-15	phospholipase A2 group IB	Rattus norvegicus	21-39
10844614-7	2000	Not only did exogenous AA inhibit Na+ uptake, but two PLA2 inhibitors (mepacrine and AACOCF3) blocked the Ang II-mediated inhibition of Na+ uptake.	Quinacrine	71-80	phospholipase A2	Oryctolagus cuniculus	54-58
10792296-10	2000	The comparative life spans and thrombin sensitivity of TO (high) and mepacrine-positive platelets suggest that TO (high) labels platelet dense granules.	Quinacrine	69-78	coagulation factor II	Mus musculus	31-39
10706438-3	2000	In this study, we have demonstrated a transient expression of serotonin transporter mRNA in quinacrine-positive Merkel cells between embryonic day 16 and postnatal day 5.	Quinacrine	92-102	solute carrier family 6 member 4	Rattus norvegicus	62-83
10725159-3	2000	By the use of the selective inhibitors menadione and quinacrine, it was shown that the enzyme responsible for the oxidation of HMI into HMOI was aldehyde oxidase (AO; aldehyde:oxygen oxidoreductase, EC 1.2.3.1).	Quinacrine	53-63	aldehyde oxidase 1	Sus scrofa	145-161
11193825-7	2000	In AVP cells that were prelabeled with quinacrine, PACAP and NA acted synergistically to induce a loss of quinacrine fluorescence, indicating secretion of neurosecretory granules in AVP neurons.	Quinacrine	39-49	adenylate cyclase activating polypeptide 1	Homo sapiens	51-56
11193825-7	2000	In AVP cells that were prelabeled with quinacrine, PACAP and NA acted synergistically to induce a loss of quinacrine fluorescence, indicating secretion of neurosecretory granules in AVP neurons.	Quinacrine	106-116	adenylate cyclase activating polypeptide 1	Homo sapiens	51-56
10449625-7	1999	PKA was inhibited by adding H8 to the cultures; similarly, PLA(2) was inhibited with quinacrine or activated with melittin, and PKC was inhibited with chelerythrine.	Quinacrine	85-95	phospholipase A2 group IB	Homo sapiens	59-65
10595650-5	1999	These effects were inhibited by preincubating EC either in the presence of mepacrine (to block phospholipase A2) or of pertussis toxin (to increase ADP-ribosylation of Gi proteins).	Quinacrine	75-84	phospholipase A2 group IB	Homo sapiens	95-111
10779028-5	2000	Statistically significant differences between adults and both term and preterm infants, at two concentrations of mepacrine, were observed after stimulation with thrombin.	Quinacrine	113-122	coagulation factor II, thrombin	Homo sapiens	161-169
10779028-6	2000	CONCLUSION: Persistent mepacrine staining of infant PDGs, when compared with those of adults, after thrombin stimulation implies defective infant PDG release.	Quinacrine	23-32	coagulation factor II, thrombin	Homo sapiens	100-108
11093031-5	2000	The increase was blocked by specific inhibitors (quinacrine and AACOCF3) of phospholipase A2 (PLA2) and was inhibited by down-regulation of PKCalpha, demostrating that this isoform is involved in arachidonic acid production.	Quinacrine	49-59	phospholipase A2 group IIA	Gallus gallus	76-92
11093031-5	2000	The increase was blocked by specific inhibitors (quinacrine and AACOCF3) of phospholipase A2 (PLA2) and was inhibited by down-regulation of PKCalpha, demostrating that this isoform is involved in arachidonic acid production.	Quinacrine	49-59	phospholipase A2 group IIA	Gallus gallus	94-98
10517818-17	1999	Co-administration of the phospholipase A2 inhibitor quinacrine virtually eliminated adenosine-induced vasodilatation, yet synergistic interaction between adenosine and pulse perfusion persisted, albeit at a reduced level.	Quinacrine	52-62	phospholipase A2 group IB	Canis lupus familiaris	25-41
10492524-6	1999	The stimulated release of AA was dependent on extracellular Ca2+ and was inhibited by mepacrine (50 microM), a non-specific PLA2 inhibitor.	Quinacrine	86-95	phospholipase A2 group IIA	Homo sapiens	124-128
10501019-9	1999	Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium.	Quinacrine	58-68	phospholipase A2 group IB	Homo sapiens	82-98
10455307-7	1999	Myricetin-induced contractions were almost abolished by the phospholipase A2 (PLA2) inhibitor, quinacrine (10 microM), the cyclo-oxygenase inhibitor, indomethacin (10 microM), the thromboxane synthase inhibitor, dazoxiben (100 microM), the putative thromboxane A2 (TXA2)/prostaglandin endoperoxide receptor antagonist, ifetroban (3 microM).	Quinacrine	95-105	phospholipase A2 group IB	Rattus norvegicus	78-82
10417403-8	1999	VLDL-induced PAI-1 secretion was completely prevented by U73122, a specific inhibitor of phosphatidylinositol-specific phospholipase C, by H7 or by PKC downregulation, and by mepacrine (all P<0.01 versus VLDL-treated cells).	Quinacrine	175-184	serpin family E member 1	Homo sapiens	13-18
10535708-5	1999	The phospholipase A2 inhibitor quinacrine considerably inhibited this TEA-sensitive current, while 4-bromophenacylbromide exerted no effect.	Quinacrine	31-41	phospholipase A2 group IB	Rattus norvegicus	4-20
10385423-10	1999	Similarly, the phospholipase A2 inhibitors quinacrine and 7-7"-DEA did not impair the effect of TRH on alpha-MSH secretion.	Quinacrine	43-53	phospholipase A2 group IB	Canis lupus familiaris	15-31
10364464-5	1999	Functional inhibitors of phospholipase A2 (PLA2), such as dexamethasone and quinacrine, do not mimick the effects of NSAID.	Quinacrine	76-86	phospholipase A2 group IB	Homo sapiens	25-41
10364464-5	1999	Functional inhibitors of phospholipase A2 (PLA2), such as dexamethasone and quinacrine, do not mimick the effects of NSAID.	Quinacrine	76-86	phospholipase A2 group IB	Homo sapiens	43-47
10329383-2	1999	Both AA release and cell spreading after attachment to a FN substrate were inhibited by the PLA2 inhibitor mepacrine.	Quinacrine	107-116	phospholipase A2, group V	Mus musculus	92-96
10329383-4	1999	Cells ectopically expressing full-length chicken beta1-integrins both released AA and spread fully on a substrate of anti-chicken beta1-integrin monoclonal antibody, and inhibition of PLA2 by mepacrine suppressed both spreading and AA release.	Quinacrine	192-201	phospholipase A2 group IIA	Gallus gallus	184-188
10435777-8	1999	The use of nonspecific intracellular PLA2 inhibitors (quinacrine, heparin, gangliosides, vitamin E) in animal model studies of neurological disorders in vivo has provided some useful information on tolerance, toxicity, and effectiveness of these compounds.	Quinacrine	54-64	phospholipase A2 group IIA	Homo sapiens	37-41
10431763-3	1999	Dose-response curves to noradrenaline-induced vasoconstriction were performed before and after continuous infusions of two different PAF-receptor antagonists (WEB 2086 and yangambin) and of the phospholipase A2 inhibitor mepacrine.	Quinacrine	221-230	phospholipase A2	Oryctolagus cuniculus	194-210
10330231-7	1999	Mepacrine, a PLA2 inhibitor, prevented HO-1 induction by cytokine, suggesting a role for arachidonate, the product of PLA2 hydrolysis of phospholipids, in HO-1 expression.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	13-17
10330231-7	1999	Mepacrine, a PLA2 inhibitor, prevented HO-1 induction by cytokine, suggesting a role for arachidonate, the product of PLA2 hydrolysis of phospholipids, in HO-1 expression.	Quinacrine	0-9	heme oxygenase 1	Homo sapiens	39-43
10330231-7	1999	Mepacrine, a PLA2 inhibitor, prevented HO-1 induction by cytokine, suggesting a role for arachidonate, the product of PLA2 hydrolysis of phospholipids, in HO-1 expression.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	118-122
10330231-7	1999	Mepacrine, a PLA2 inhibitor, prevented HO-1 induction by cytokine, suggesting a role for arachidonate, the product of PLA2 hydrolysis of phospholipids, in HO-1 expression.	Quinacrine	0-9	heme oxygenase 1	Homo sapiens	155-159
10103124-5	1999	Responses induced by NMDA, carbachol or both agonists on microdiscs were reduced by phospholipase A2 inhibitors, the most striking effects being observed with mepacrine.	Quinacrine	159-168	phospholipase A2, group IB, pancreas	Mus musculus	84-100
10229494-8	1999	This increase in FAME (45%) was inhibited by mepacrine (quinacrine) (10 microM), an inhibitor of PLA2.	Quinacrine	45-54	phospholipase A2 group IB	Rattus norvegicus	97-101
10229494-8	1999	This increase in FAME (45%) was inhibited by mepacrine (quinacrine) (10 microM), an inhibitor of PLA2.	Quinacrine	56-66	phospholipase A2 group IB	Rattus norvegicus	97-101
10501019-9	1999	Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium.	Quinacrine	58-68	phospholipase A2 group IB	Homo sapiens	100-104
10501019-9	1999	Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium.	Quinacrine	70-74	phospholipase A2 group IB	Homo sapiens	82-98
10501019-9	1999	Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium.	Quinacrine	70-74	phospholipase A2 group IB	Homo sapiens	100-104
10077051-4	1999	AMs were stimulated with PLA2 or SPL rat serum, with or without administration of the PLA2 inhibitor quinacrine.	Quinacrine	101-111	phospholipase A2 group IB	Rattus norvegicus	86-90
10077051-8	1999	PLA2 (50 ng/ml) induced significant amounts of NO production, inducible NO synthase mRNA expression, and cytotoxicity toward the human umbilical vein endothelial cells in normal rat AMs, and these activities were significantly inhibited by quinacrine.	Quinacrine	240-250	phospholipase A2 group IIA	Homo sapiens	0-4
10077051-8	1999	PLA2 (50 ng/ml) induced significant amounts of NO production, inducible NO synthase mRNA expression, and cytotoxicity toward the human umbilical vein endothelial cells in normal rat AMs, and these activities were significantly inhibited by quinacrine.	Quinacrine	240-250	nitric oxide synthase 2	Homo sapiens	62-83
10077051-11	1999	This lung injury was prevented by the administration of the PLA2 inhibitor quinacrine.	Quinacrine	75-85	phospholipase A2 group IB	Rattus norvegicus	60-64
10080140-8	1999	The damage produced by A23187 (12.5 microM) was inhibited by preincubation of cells with the PLA2 inhibitor, quinacrine (1-100 microM).	Quinacrine	109-119	phospholipase A2 group IB	Rattus norvegicus	93-97
10050016-21	1999	Blockade of phospholipase A2 by quinacrine (10 microM) inhibited RVD by 53 %.	Quinacrine	32-42	phospholipase A2, group IB, pancreas	Mus musculus	12-28
10403565-3	1999	Incubation of the cells with quinacrine resulted in dose-dependent decreases in steroid production and StAR protein.	Quinacrine	29-39	steroidogenic acute regulatory protein	Mus musculus	103-107
10403565-4	1999	Twenty micromolars quinacrine inhibited 92 and 91% of LH-induced progesterone and StAR protein, respectively, and 98 and 90% of Bt2cAMP-induced progesterone and StAR protein.	Quinacrine	19-29	steroidogenic acute regulatory protein	Mus musculus	82-86
10403565-4	1999	Twenty micromolars quinacrine inhibited 92 and 91% of LH-induced progesterone and StAR protein, respectively, and 98 and 90% of Bt2cAMP-induced progesterone and StAR protein.	Quinacrine	19-29	steroidogenic acute regulatory protein	Mus musculus	161-165
10403565-5	1999	Reversal of this inhibition was obtained by incubation of quinacrine-treated cells with various levels of AA, which resulted in a dose-dependent increase in both steroid and StAR protein levels.	Quinacrine	58-68	steroidogenic acute regulatory protein	Mus musculus	174-178
10024011-2	1999	Experiments were performed with either mepacrine (0.2 microM) or bovine serum albumin (BSA, 0.02%) which inhibits phospholipase A2 activity or binds endogenously released arachidonic acid, respectively.	Quinacrine	39-48	phospholipase A2 group IB	Rattus norvegicus	114-130
10075017-7	1999	Addition of the PI-PLC inhibitor, ET 18OCH3, or the PLA2 inhibitor (quinacrine) alone, resulted in secretion of latent TGF-beta and, in the case of ET 18OCH3, active TGF-beta.	Quinacrine	68-78	phospholipase A2, group IB, pancreas	Mus musculus	52-56
10075017-7	1999	Addition of the PI-PLC inhibitor, ET 18OCH3, or the PLA2 inhibitor (quinacrine) alone, resulted in secretion of latent TGF-beta and, in the case of ET 18OCH3, active TGF-beta.	Quinacrine	68-78	transforming growth factor, beta 1	Mus musculus	119-127
10075017-7	1999	Addition of the PI-PLC inhibitor, ET 18OCH3, or the PLA2 inhibitor (quinacrine) alone, resulted in secretion of latent TGF-beta and, in the case of ET 18OCH3, active TGF-beta.	Quinacrine	68-78	transforming growth factor, beta 1	Mus musculus	166-174
10749996-1	1999	Treatment of human natural killer (NK) cells with phospholipase A(2) (PLA(2)) inhibitors, mepacrine and 4-bromophenacyl bromide (BPB), diminished their ability to lyse K562 target cells by as much as 100%.	Quinacrine	90-99	phospholipase A2 group IB	Homo sapiens	50-68
10749996-1	1999	Treatment of human natural killer (NK) cells with phospholipase A(2) (PLA(2)) inhibitors, mepacrine and 4-bromophenacyl bromide (BPB), diminished their ability to lyse K562 target cells by as much as 100%.	Quinacrine	90-99	phospholipase A2 group IB	Homo sapiens	70-76
10749996-8	1999	Finally, the 15-lipoxygenase product, 15S-hydroperoxyeicosatetraenoic acid (15S-HPETE), is also able to reverse mepacrine-induced inhibition of NK cytotoxicity.	Quinacrine	112-121	arachidonate 15-lipoxygenase	Homo sapiens	13-28
9788508-7	1998	Two protein kinase inhibitors (H-7 and H-8) strongly repressed Ni2+ and Co2+ enhanced expression, as did the phospholipase A2 inhibitor quinacrine.	Quinacrine	136-146	phospholipase A2 group IB	Homo sapiens	109-125
10394109-9	1999	The PT saponin induced inhibition of alpha-MG uptake was blocked by mepacrine, a phospholipase A2 inhibitor.	Quinacrine	68-77	phospholipase A2	Oryctolagus cuniculus	81-97
9653146-4	1998	Inhibition of PLA2 by mepacrine diminished both AA release and MAPK phosphorylation, induced by Ang II.	Quinacrine	22-31	phospholipase A2 group IB	Homo sapiens	14-18
9868740-7	1998	Phospholipase A2 inhibitors, mepacrine and 4-bromophenacyl bromide, inhibited the increase in mitochondrial permeability, but did not inhibit hepatocyte death caused by CCl4.	Quinacrine	29-38	phospholipase A2 group IB	Rattus norvegicus	0-16
9826060-11	1998	Conversely, the phospholipase A2 inhibitor quinacrine (100 microM) blocked the release of arachidonic acid and PGE2 without affecting the NKA-stimulated formation of IP3.	Quinacrine	43-53	phospholipase A2 group IB	Homo sapiens	16-32
9724516-2	1998	Binding of quinacrine to phospholipids and porcine pancreatic phospholipase A2 (PLA2) was investigated using fluorescence resonance energy transfer, Langmuir films, assay for the enzymatic activity, and molecular modeling.	Quinacrine	11-21	phospholipase A2 group IB	Homo sapiens	62-78
9724516-2	1998	Binding of quinacrine to phospholipids and porcine pancreatic phospholipase A2 (PLA2) was investigated using fluorescence resonance energy transfer, Langmuir films, assay for the enzymatic activity, and molecular modeling.	Quinacrine	11-21	phospholipase A2 group IB	Homo sapiens	80-84
9724516-6	1998	Quinacrine also bound to eosin-labeled PLA2, and the addition of 4 mM CaCl2 reversed this interaction almost completely.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	39-43
9724516-8	1998	Studies on the influence of quinacrine on the activity of PLA2 toward pyrene-labeled phospholipid analogues revealed that the hydrolysis of phosphatidylcholine was progressively reduced as a function of increasing [quinacrine].	Quinacrine	28-38	phospholipase A2 group IB	Homo sapiens	58-62
9724516-8	1998	Studies on the influence of quinacrine on the activity of PLA2 toward pyrene-labeled phospholipid analogues revealed that the hydrolysis of phosphatidylcholine was progressively reduced as a function of increasing [quinacrine].	Quinacrine	215-225	phospholipase A2 group IB	Homo sapiens	58-62
9724516-12	1998	Our data suggest that the inhibition of PLA2 by quinacrine is due to its binding to the enzyme.	Quinacrine	48-58	phospholipase A2 group IB	Homo sapiens	40-44
9729536-4	1998	Incubation of neutrophils with the nonselective PLA2 inhibitor quinacrine (0 to 100 microM) reduced oxidase activity in both primed and unprimed cells.	Quinacrine	63-73	phospholipase A2 group IB	Homo sapiens	48-52
9653146-4	1998	Inhibition of PLA2 by mepacrine diminished both AA release and MAPK phosphorylation, induced by Ang II.	Quinacrine	22-31	angiotensinogen	Homo sapiens	96-102
9647745-3	1998	The SRE stimulation by PA was dramatically reduced by either pre-treatment with mepacrine, an inhibitor of phospholipase A2 (PLA2), or co-transfection with antisense cytosolic phospholipase A2 (cPLA2) oligonucleotide, whereas lysophosphatidic acid (LPA)-induced SRE activation was not affected.	Quinacrine	80-89	phospholipase A2 group IB	Rattus norvegicus	125-129
9612295-8	1998	We conclude that paraquat-induced phosphatidylserine oxidation and apoptosis occurred in the absence of PLA2 activation and that quinacrine protected phosphatidylserine and cell viability after paraquat in a PLA2-independent manner.	Quinacrine	129-139	phospholipase A2, group IB, pancreas	Mus musculus	208-212
9636164-4	1998	We observed that Ang II activated p21ras and that mepacrine, a phospholipase A2 inhibitor, blocked this effect.	Quinacrine	50-59	phospholipase A2 group IB	Homo sapiens	63-79
9593858-4	1998	This conclusion is supported by the findings that ET-1-induced AA release is inhibited by AACOCF3, quinacrine and manoalide, PLA2 inhibitors, but not by U-73122, a PLC inhibitor, or by RHC-80267, a diacylglycerol lipase inhibitor.	Quinacrine	99-109	endothelin 1	Homo sapiens	50-54
9612295-3	1998	We now report that the phospholipase A2 (PLA2) inhibitor quinacrine can attenuate phosphatidylserine oxidation and also block paraquat-induced apoptosis.	Quinacrine	57-67	phospholipase A2, group IB, pancreas	Mus musculus	23-39
9612295-3	1998	We now report that the phospholipase A2 (PLA2) inhibitor quinacrine can attenuate phosphatidylserine oxidation and also block paraquat-induced apoptosis.	Quinacrine	57-67	phospholipase A2, group IB, pancreas	Mus musculus	41-45
9607407-7	1998	Mepacrine (10microM), a phospholipase A2 (PLA2) inhibitor, reduced only the inhibitory effect of angiotensin II on Na+,K+-ATPase activity.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	24-40
9607407-7	1998	Mepacrine (10microM), a phospholipase A2 (PLA2) inhibitor, reduced only the inhibitory effect of angiotensin II on Na+,K+-ATPase activity.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	42-46
9607407-7	1998	Mepacrine (10microM), a phospholipase A2 (PLA2) inhibitor, reduced only the inhibitory effect of angiotensin II on Na+,K+-ATPase activity.	Quinacrine	0-9	angiotensinogen	Homo sapiens	97-111
9572294-4	1998	The potentiating effects of H2O2 were strongly inhibited in the presence of the PLA2 inhibitor mepacrine, suggesting that the site of action was within the signal responsive arachidonic acid cascade.	Quinacrine	95-104	phospholipase A2 group IB	Homo sapiens	80-84
9518732-15	1998	Extracellular administration of the phospholipase A2 inhibitors mepacrine and 4-bromophenacyl bromide significantly suppressed ICa.	Quinacrine	64-73	phospholipase A2 group IB	Homo sapiens	36-52
9565103-9	1998	E-selectin expression, induced by BS-I, was inhibited in the presence of genistein, a tyrosine kinase inhibitor, and by mepacrine, an inhibitor of phospholipase A2.	Quinacrine	120-129	selectin E	Homo sapiens	0-10
9565103-9	1998	E-selectin expression, induced by BS-I, was inhibited in the presence of genistein, a tyrosine kinase inhibitor, and by mepacrine, an inhibitor of phospholipase A2.	Quinacrine	120-129	phospholipase A2 group IB	Homo sapiens	147-163
9528967-12	1998	GH-induced Jak2 and Stat5 activation were not affected by D609 or mepacrine, both inhibitors of phospholipase C. However, in the presence of D609 and mepacrine, GH maintained prolonged Jak2 and Stat5 activation.	Quinacrine	150-159	Janus kinase 2	Rattus norvegicus	185-189
9528967-12	1998	GH-induced Jak2 and Stat5 activation were not affected by D609 or mepacrine, both inhibitors of phospholipase C. However, in the presence of D609 and mepacrine, GH maintained prolonged Jak2 and Stat5 activation.	Quinacrine	150-159	signal transducer and activator of transcription 5A	Rattus norvegicus	194-199
9650446-5	1998	High concentrations of the PLA2 inhibitors, 4-bromophenacyl lactone and quinacrine, resulted in a generalized decrease in cellular mRNA levels.	Quinacrine	72-82	phospholipase A2 group IB	Homo sapiens	27-31
9650446-6	1998	Our results, obtained in fibroblasts, suggest treatment with 4-bromophenacyl lactone or quinacrine, instead of inhibiting PLA2 activity specifically, results in a generalized depression of cellular mRNA levels.	Quinacrine	88-98	phospholipase A2 group IB	Homo sapiens	122-126
9482700-8	1998	The cytokine-induced increase in ECP release was inhibited by the phospholipase A2 (PLA2) inhibitor mepacrine, indicating an involvement of PLA2 in the enhanced response but not in baseline degranulation.	Quinacrine	100-109	ribonuclease A family member 3	Homo sapiens	33-36
9480923-6	1998	In a further study to analyse the downstream mediator of Rac in the ceramide-signalling pathway, we observed that either pretreatment with mepacrine, a potent and specific inhibitor of phospholipase A2, or co-transfection with antisense cytosolic phospholipase A2 (cPLA2) oligonucleotide repressed the C2-ceramide-induced SRE activation selectively, implying a critical role of cPLA2 in C2-ceramide-induced signalling to nucleus.	Quinacrine	139-148	Rac family small GTPase 1	Rattus norvegicus	57-60
9510087-10	1998	Quinacrine, and to a lesser extent chloroquine, has an inhibitory effect on the lipopolysaccharide- or zymosan-induced expression of interleukin 1beta and tumor necrosis factor alpha, both at the mRNA and protein levels.	Quinacrine	0-10	interleukin 1 beta	Mus musculus	133-182
9482700-8	1998	The cytokine-induced increase in ECP release was inhibited by the phospholipase A2 (PLA2) inhibitor mepacrine, indicating an involvement of PLA2 in the enhanced response but not in baseline degranulation.	Quinacrine	100-109	phospholipase A2 group IB	Homo sapiens	66-82
9482700-8	1998	The cytokine-induced increase in ECP release was inhibited by the phospholipase A2 (PLA2) inhibitor mepacrine, indicating an involvement of PLA2 in the enhanced response but not in baseline degranulation.	Quinacrine	100-109	phospholipase A2 group IB	Homo sapiens	84-88
9482700-8	1998	The cytokine-induced increase in ECP release was inhibited by the phospholipase A2 (PLA2) inhibitor mepacrine, indicating an involvement of PLA2 in the enhanced response but not in baseline degranulation.	Quinacrine	100-109	phospholipase A2 group IB	Homo sapiens	140-144
9570525-2	1998	We report that quinacrine, chloroquine, and structurally related compounds completely inhibit the antiapoptotic effect of CpG-ODN on WEHI 231 murine B lymphoma cells and inhibit CpG-ODN-induced secretion of IL-6 by WEHI 231.	Quinacrine	15-25	interleukin 6	Mus musculus	207-211
9871443-6	1998	In the present study, it will be shown that the co-application of NMDA and carbachol synergistically increases the release of [3H]-DA and that this effect is reduced by mepacrine or 4-bromophenacylbromide (10(-7) M), two inhibitors of PLA2.	Quinacrine	169-178	phospholipase A2 group IB	Homo sapiens	235-239
9400378-6	1997	ACh-induced CD increases resistant to L-NAME and indomethacin were reduced after the administration of intracoronary quinacrine, an inhibitor of phospholipase A2, or proadifen, an inhibitor of cytochrome P-450.	Quinacrine	117-127	phospholipase A2 group IB	Canis lupus familiaris	145-161
9718078-5	1998	A cis-unsaturated free fatty acid, oleic acid, significantly enhanced OAG-induced medium levels of erythropoietin in normoxic Hep3B cells, whereas a phospholipase A2 inhibitor, mepacrine, significantly decreased hypoxia-induced erythropoietin production in Hep3B cells.	Quinacrine	177-186	phospholipase A2 group IB	Homo sapiens	149-165
9358529-8	1997	In common with a role for PLA2 and the subsequent release of arachidonic acid (AA), we have demonstrated dose-dependent inhibition of PDE-induced superoxide release by the PLA2 inhibitor mepacrine, as well as activation and priming of the fMLP-induced superoxide generation by AA.	Quinacrine	187-196	phospholipase A2 group IB	Homo sapiens	26-30
9346971-4	1997	cys4 mutants display the pH-dependent growth phenotypes characteristic of vma mutants and are unable to accumulate quinacrine in the vacuole, indicating loss of vacuolar acidification in vivo.	Quinacrine	115-125	cystathionine beta-synthase CYS4	Saccharomyces cerevisiae S288C	0-4
9342723-11	1997	Other studies with quinacrine indicated that only a small pool of PE is degraded by SPM-bound Ca(2+)-independent phospholipase A2 (PLA2).	Quinacrine	19-29	phospholipase A2 group IB	Homo sapiens	113-129
9362333-2	1997	Prior studies in a PT-like model (LLC-PKcl4 cells expressing rabbit AT1R) (LLC-PK-AT1R cells) determined that quinacrine, a nonspecific phospholipase A2 (PLA2) inhibitor, and the haloenol lactone suicide substrate (HELSS), a Ca2+-independent PLA2 inhibitor, attenuated apical (AP) AT1R recycling.	Quinacrine	110-120	phospholipase A2	Oryctolagus cuniculus	154-158
9362333-2	1997	Prior studies in a PT-like model (LLC-PKcl4 cells expressing rabbit AT1R) (LLC-PK-AT1R cells) determined that quinacrine, a nonspecific phospholipase A2 (PLA2) inhibitor, and the haloenol lactone suicide substrate (HELSS), a Ca2+-independent PLA2 inhibitor, attenuated apical (AP) AT1R recycling.	Quinacrine	110-120	phospholipase A2	Oryctolagus cuniculus	242-246
9312202-10	1997	Quinacrine (a PA2 inhibitor) alone had no effect on matrix vesicle PKC, but in cultures treated for 12 hours with quinacrine and 24,25-(OH)2D3, a synergistic increase in matrix vesicle PKC was observed.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-17
9312202-10	1997	Quinacrine (a PA2 inhibitor) alone had no effect on matrix vesicle PKC, but in cultures treated for 12 hours with quinacrine and 24,25-(OH)2D3, a synergistic increase in matrix vesicle PKC was observed.	Quinacrine	114-124	protein kinase C, gamma	Rattus norvegicus	185-188
9312202-11	1997	Quinacrine caused a time-dependent decrease in matrix vesicle PKC and a dose- and time-dependent increase in plasma membrane PKC when incubated directly with the membranes, supporting the hypothesis that PA2 plays a role in the nongenomic regulation of PKC by 24,25-(OH)2D3.	Quinacrine	0-10	protein kinase C, gamma	Rattus norvegicus	62-65
9312202-11	1997	Quinacrine caused a time-dependent decrease in matrix vesicle PKC and a dose- and time-dependent increase in plasma membrane PKC when incubated directly with the membranes, supporting the hypothesis that PA2 plays a role in the nongenomic regulation of PKC by 24,25-(OH)2D3.	Quinacrine	0-10	protein kinase C, gamma	Rattus norvegicus	125-128
9312202-11	1997	Quinacrine caused a time-dependent decrease in matrix vesicle PKC and a dose- and time-dependent increase in plasma membrane PKC when incubated directly with the membranes, supporting the hypothesis that PA2 plays a role in the nongenomic regulation of PKC by 24,25-(OH)2D3.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	204-207
9312202-11	1997	Quinacrine caused a time-dependent decrease in matrix vesicle PKC and a dose- and time-dependent increase in plasma membrane PKC when incubated directly with the membranes, supporting the hypothesis that PA2 plays a role in the nongenomic regulation of PKC by 24,25-(OH)2D3.	Quinacrine	0-10	protein kinase C, gamma	Rattus norvegicus	125-128
9231737-5	1997	Pretreatment of cell cultures with the PLA2 inhibitors quinacrine and aristolochic acid resulted in a dose-dependent inhibition of melittin-stimulated PKC isozyme translocation as did the inhibitor of lipoxygenase, nordihydroguaiaretic acid, whereas the cyclooxygenase inhibitor indomethacin had no effect.	Quinacrine	55-65	phospholipase A2 group IB	Rattus norvegicus	39-43
9268696-1	1997	In HaCaT keratinocytes bradykinin-triggered actin reorganization was inhibited by quinacrine, a phospholipase A2 inhibitor, and restored by addition of arachidonic acid.	Quinacrine	82-92	kininogen 1	Homo sapiens	23-33
9268696-1	1997	In HaCaT keratinocytes bradykinin-triggered actin reorganization was inhibited by quinacrine, a phospholipase A2 inhibitor, and restored by addition of arachidonic acid.	Quinacrine	82-92	phospholipase A2 group IB	Homo sapiens	96-112
9283705-12	1997	Moreover, various PLA2 inhibitors (e.g. mepacrine and dexamethasone) prevented both the early alpha, beta-meATP-induced [3H]-AA release and/or the associated long-term morphological changes, without affecting the astrocytic elongation induced by bFGF.	Quinacrine	40-49	phospholipase A2 group IB	Rattus norvegicus	18-22
9283705-12	1997	Moreover, various PLA2 inhibitors (e.g. mepacrine and dexamethasone) prevented both the early alpha, beta-meATP-induced [3H]-AA release and/or the associated long-term morphological changes, without affecting the astrocytic elongation induced by bFGF.	Quinacrine	40-49	fibroblast growth factor 2	Rattus norvegicus	246-250
9231737-5	1997	Pretreatment of cell cultures with the PLA2 inhibitors quinacrine and aristolochic acid resulted in a dose-dependent inhibition of melittin-stimulated PKC isozyme translocation as did the inhibitor of lipoxygenase, nordihydroguaiaretic acid, whereas the cyclooxygenase inhibitor indomethacin had no effect.	Quinacrine	55-65	protein kinase C, alpha	Rattus norvegicus	151-154
9234831-8	1997	The EDHF-mediated dilations initiated by ACh and histamine, as well as K(ATP) activation by cromakalim, were blocked by mepacrine, a nonselective phospholipase A2 inhibitor.	Quinacrine	120-129	phospholipase A2 group IB	Rattus norvegicus	146-162
9237867-5	1997	This conclusion is supported by the following findings: (1) ET-1-evoked AA release was inhibited by the PLA2 inhibitors dexamethasone, mepacrine and manoalide in a concentration-dependent manner.	Quinacrine	135-144	endothelin 1	Homo sapiens	60-64
9249592-2	1997	Gent (10(-5) M) induced a time-dependent mesangial planar cell surface area reduction that was significantly inhibited by the PLA2 inhibitors aristolochic acid (AA) and quinacrine, by the platelet-activating factor (PAF) blocker BN-52021 (BN), and by verapamil.	Quinacrine	169-179	phospholipase A2 group IB	Rattus norvegicus	126-130
9237867-5	1997	This conclusion is supported by the following findings: (1) ET-1-evoked AA release was inhibited by the PLA2 inhibitors dexamethasone, mepacrine and manoalide in a concentration-dependent manner.	Quinacrine	135-144	phospholipase A2 group IB	Homo sapiens	104-108
9223659-4	1997	Quinacrine, a PLA2 inhibitor, suppressed the thrombin-induced AA release.	Quinacrine	0-10	phospholipase A2, group V	Mus musculus	14-18
9177247-4	1997	The cortical induction was reduced by MK-801, an N-methyl-D-aspartic acid-receptor antagonist, and by dexamethasone and quinacrine, phospholipase A2 (PLA2) inhibiting compounds.	Quinacrine	120-130	phospholipase A2 group IB	Rattus norvegicus	132-148
9177247-4	1997	The cortical induction was reduced by MK-801, an N-methyl-D-aspartic acid-receptor antagonist, and by dexamethasone and quinacrine, phospholipase A2 (PLA2) inhibiting compounds.	Quinacrine	120-130	phospholipase A2 group IB	Rattus norvegicus	150-154
9223659-4	1997	Quinacrine, a PLA2 inhibitor, suppressed the thrombin-induced AA release.	Quinacrine	0-10	coagulation factor II	Mus musculus	45-53
9223659-5	1997	In addition, quinacrine also suppressed the thrombin-induced prostaglandin E2 synthesis in these cells.	Quinacrine	13-23	coagulation factor II	Mus musculus	44-52
9160464-4	1997	Additional pharmacologic studies showed that phospholipase A2 and nitric oxide are involved in the mechanisms that produce the mechanical and thermal hyperalgesia, respectively, N omega-nitro-L-arginine methyl ester and mepacrine are relatively selective inhibitors of nitric oxide synthase and phospholipase A2, respectively.	Quinacrine	220-229	phospholipase A2 group IB	Rattus norvegicus	45-61
9263201-4	1997	These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2.	Quinacrine	122-132	phospholipase A2 group IB	Rattus norvegicus	87-103
9154867-1	1997	We hypothesized that phospholipase A2 (PLA2) metabolites contribute to the acute, neutrophil-dependent, edematous lung leak that develops after administration of interleukin-1 (IL-1) intratracheally to rats and tested this premise by using mepacrine to inhibit PLA2 activity in vivo.	Quinacrine	240-249	phospholipase A2 group IB	Rattus norvegicus	21-37
9154867-1	1997	We hypothesized that phospholipase A2 (PLA2) metabolites contribute to the acute, neutrophil-dependent, edematous lung leak that develops after administration of interleukin-1 (IL-1) intratracheally to rats and tested this premise by using mepacrine to inhibit PLA2 activity in vivo.	Quinacrine	240-249	phospholipase A2 group IB	Rattus norvegicus	39-43
9154867-1	1997	We hypothesized that phospholipase A2 (PLA2) metabolites contribute to the acute, neutrophil-dependent, edematous lung leak that develops after administration of interleukin-1 (IL-1) intratracheally to rats and tested this premise by using mepacrine to inhibit PLA2 activity in vivo.	Quinacrine	240-249	interleukin 1 alpha	Homo sapiens	177-181
9154867-4	1997	Mepacrine treatment also decreased lung neutrophil accumulation, but not lung lavage cytokine-induced neutrophil chemoattractant (CINC) levels, in rats given IL-1 intratracheally.	Quinacrine	0-9	interleukin 1 alpha	Homo sapiens	158-162
9154867-5	1997	In parallel experiments, mepacrine treatment reduced the adhesion of human neutrophils to IL-1-treated human umbilical vein endothelial cells in vitro.	Quinacrine	25-34	interleukin 1 alpha	Homo sapiens	90-94
9263201-4	1997	These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2.	Quinacrine	122-132	phospholipase A2 group IB	Rattus norvegicus	105-109
9263201-4	1997	These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2.	Quinacrine	122-132	phospholipase A2 group IB	Rattus norvegicus	189-193
9109393-4	1997	Either transfection of a dominant negative Rac mutant, RacN17, plasmid or pretreatment of mepacrine, a potent inhibitor of PLA2, blocked H2O2-induced SRE activation dramatically.	Quinacrine	90-99	phospholipase A2 group IB	Rattus norvegicus	123-127
9142863-10	1997	PLA2 inhibitors arachidonyl trifluoromethyl ketone (AACOCF3), parabromophenacyl bromide (pBPB), and quinacrine all abolished Ca/CaM inhibition of the Na-K-ATPase.	Quinacrine	100-110	phospholipase A2 group IB	Homo sapiens	0-4
9142863-10	1997	PLA2 inhibitors arachidonyl trifluoromethyl ketone (AACOCF3), parabromophenacyl bromide (pBPB), and quinacrine all abolished Ca/CaM inhibition of the Na-K-ATPase.	Quinacrine	100-110	calmodulin 3	Homo sapiens	128-131
9094163-3	1997	From enzymatic assays, PLA2 and diacylglycerol (DAG) lipase were activated by Cch and respectively inhibited by the PLA2 inhibitors, mepacrine and aristolochic acid, and by the DAG lipase inhibitor, RHC 80267.	Quinacrine	133-142	phospholipase A2 group IB	Rattus norvegicus	23-27
9106458-0	1997	The phospholipase A2 inhibitor, quinacrine, reduces infarct size in rats after transient middle cerebral artery occlusion.	Quinacrine	32-42	phospholipase A2 group IB	Rattus norvegicus	4-20
9106458-2	1997	The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was administered upon reperfusion to rats that underwent 2 h of middle cerebral artery occlusion (MCAO) via the intraluminal filament method.	Quinacrine	39-49	phospholipase A2 group IB	Rattus norvegicus	4-20
9106458-2	1997	The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was administered upon reperfusion to rats that underwent 2 h of middle cerebral artery occlusion (MCAO) via the intraluminal filament method.	Quinacrine	39-49	phospholipase A2 group IB	Rattus norvegicus	22-26
9099806-5	1997	Quinacrine, which predominantly blocks the activity of PLA2 in neurons, had no affect on either the light response or the IPSP, but did block increases in excitability (i.e. increased input resistance and elicited spike rate) of the B cell that results from pairings of light and presynaptic vestibular stimulation (i.e., in vitro associative conditioning).	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	55-59
9001889-1	1996	The phospholipase A2 inhibitors mepacrine, ONO-RS-082, and AACOCF3 completely inhibited prostaglandin E2 production induced by endothelin 1 in cultured rat mesangial cells, suggesting that phospholipase A2 is a critical enzyme in this process.	Quinacrine	32-41	phospholipase A2 group IB	Rattus norvegicus	4-20
9033286-9	1997	Extracellular Ca2+ chelation (EGTA) and PLA2 inhibitor therapy (aristolochic acid, dibucaine, or mepacrine) each conferred significant protective effects.	Quinacrine	97-106	phospholipase A2 group IB	Homo sapiens	40-44
9062648-1	1997	Mepacrine (quinacrine) has in a number of studies been shown to protect the heart from ischemic injury, a protection commonly claimed to be due to inhibition of phospholipase A2.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	161-177
9062648-1	1997	Mepacrine (quinacrine) has in a number of studies been shown to protect the heart from ischemic injury, a protection commonly claimed to be due to inhibition of phospholipase A2.	Quinacrine	11-21	phospholipase A2 group IB	Rattus norvegicus	161-177
9081684-8	1997	Quinacrine, a phospholipase A2 inhibitor, suppressed ATP-induced arachidonic acid release.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
9031747-6	1997	The phospholipase A2 inhibitor quinacrine (30 microM) nearly completely eliminated ACh-induced hyperpolarization.	Quinacrine	31-41	phospholipase A2 group IB	Rattus norvegicus	4-20
9144302-0	1997	Effect of quinacrine, a phospholipase A2 inhibitor on stress and chemically induced gastroduodenal ulcers.	Quinacrine	10-20	phospholipase A2 group IB	Rattus norvegicus	24-40
9144302-1	1997	Quinacrine, a phospholipase A2 inhibitor, has been studied for its ability to inhibit gastric secretion and to protect the gastric and duodenal mucosa against chemically and stress-induced ulcers.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
9215814-9	1997	Release of esterified fatty acids, which was partly inhibited by the phospholipase A2 inhibitor, mepacrine, was stimulated by increasing periods of ischemia while the incorporation of free fatty acids into phospholipids was inhibited.	Quinacrine	97-106	phospholipase A2	Oryctolagus cuniculus	69-85
9201246-9	1997	The antioxidants N-acetylcysteine, nordihydroguaiaretic acid and mepacrine dose-dependently inhibited gamma-irradiation-mediated TNF alpha production.	Quinacrine	65-74	tumor necrosis factor	Homo sapiens	129-138
9062867-6	1997	The detected enzyme activities were sensitive to specific inhibitors of HDC (alpha-fluoromethylhistidine and alpha-hydrazinohistidine) and HMT (quinacrine and metoprine); inhibitors of aromatic amino acid decarboxylase alpha-methyl-DOPA and NSD-1015 were inactive on HDC.	Quinacrine	144-154	histidine decarboxylase	Gallus gallus	72-75
9062867-6	1997	The detected enzyme activities were sensitive to specific inhibitors of HDC (alpha-fluoromethylhistidine and alpha-hydrazinohistidine) and HMT (quinacrine and metoprine); inhibitors of aromatic amino acid decarboxylase alpha-methyl-DOPA and NSD-1015 were inactive on HDC.	Quinacrine	144-154	histidine decarboxylase	Gallus gallus	267-270
8997299-7	1996	FMLP-induced impairment was normalized by the phospholipase A2 inhibitor quinacrine, the cyclooxygenase inhibitor indomethacin, and the antagonists of the prostaglandin H2 and/or thromboxane A2 receptor, ONO-3708 and S-1452, respectively.	Quinacrine	73-83	phospholipase A2 group IB	Rattus norvegicus	46-62
8913880-7	1996	Quinacrine (300 microM), a blocker of PLA2, completely inhibited bradykinin-induced arachidonic acid release.	Quinacrine	0-10	kininogen 1	Bos taurus	65-75
8941925-5	1996	In addition, AP AT1R recycling was selectively inhibited by quinacrine, a non-specific inhibitor of phospholipase A2 (PLA2) activity and HELSS, a mechanism-based inhibitor of calcium-independent PLA2 activity.	Quinacrine	60-70	phospholipase A2	Oryctolagus cuniculus	100-116
8941925-5	1996	In addition, AP AT1R recycling was selectively inhibited by quinacrine, a non-specific inhibitor of phospholipase A2 (PLA2) activity and HELSS, a mechanism-based inhibitor of calcium-independent PLA2 activity.	Quinacrine	60-70	phospholipase A2	Oryctolagus cuniculus	118-122
8954136-5	1996	Quinacrine, an inhibitor of phospholipase A2 activity, prevented Ca2+ release and p-hydroxymercuribenzoic acid, an inhibitor of lysophospholipid reesterification, induced a fast release of Ca2+ from isolated mitochondria.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	28-44
8954136-5	1996	Quinacrine, an inhibitor of phospholipase A2 activity, prevented Ca2+ release and p-hydroxymercuribenzoic acid, an inhibitor of lysophospholipid reesterification, induced a fast release of Ca2+ from isolated mitochondria.	Quinacrine	0-10	carbonic anhydrase 2	Rattus norvegicus	65-68
8954136-5	1996	Quinacrine, an inhibitor of phospholipase A2 activity, prevented Ca2+ release and p-hydroxymercuribenzoic acid, an inhibitor of lysophospholipid reesterification, induced a fast release of Ca2+ from isolated mitochondria.	Quinacrine	0-10	carbonic anhydrase 2	Rattus norvegicus	189-192
8983209-8	1996	Pretreatment of the cultures with quinacrine, an inhibitor of phospholipase A2, reduced the stress-induced CYPIA1 activity.	Quinacrine	34-44	phospholipase A2 group IB	Homo sapiens	62-78
8983209-8	1996	Pretreatment of the cultures with quinacrine, an inhibitor of phospholipase A2, reduced the stress-induced CYPIA1 activity.	Quinacrine	34-44	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	107-113
9001889-1	1996	The phospholipase A2 inhibitors mepacrine, ONO-RS-082, and AACOCF3 completely inhibited prostaglandin E2 production induced by endothelin 1 in cultured rat mesangial cells, suggesting that phospholipase A2 is a critical enzyme in this process.	Quinacrine	32-41	endothelin 1	Rattus norvegicus	127-139
8886479-6	1996	Dopamine (10 microM)-induced inhibition of Na+,K(+)-ATPase activity in WKY rats was significantly blocked by mepacrine (10 microM), a PLA2 inhibitor, suggesting the involvement of PLA2 in dopamine-mediated inhibition of Na+,K(+)-ATPase.	Quinacrine	109-118	phospholipase A2 group IB	Rattus norvegicus	134-138
8937434-4	1996	(2) SP-stimulated cAMP formation was inhibited by quinacrine, a non-specific phospholipase A2 inhibitor (IC50 = 9.5 microM), and by indomethacin (Indo), a cyclooxygenase inhibitor (IC50 = 3.5 nM), in a concentration-dependent manner, suggesting that SP induces cAMP accumulation via an Indo-sensitive pathway.	Quinacrine	50-60	phospholipase A2 group IB	Canis lupus familiaris	77-93
8886479-6	1996	Dopamine (10 microM)-induced inhibition of Na+,K(+)-ATPase activity in WKY rats was significantly blocked by mepacrine (10 microM), a PLA2 inhibitor, suggesting the involvement of PLA2 in dopamine-mediated inhibition of Na+,K(+)-ATPase.	Quinacrine	109-118	phospholipase A2 group IB	Rattus norvegicus	180-184
8917368-3	1996	In vitro data, obtained by a polarographic technique, indicate that primaquine and, in particular, mepacrine increase EAT-cell oxygen consumption, while in vivo data, obtained in mice injected with an inoculum of about 1 x 10(6) tumour cells per mouse, show that both drugs, but notably mepacrine, accelerate tumour growth, as monitored by Cox"s statistical method for body weight, and lead to earlier death.	Quinacrine	99-108	cytochrome c oxidase subunit 4I1	Mus musculus	340-343
9247325-7	1997	Moreover, a PLA2 inhibitor quinacrine inhibited the stimulatory action of ET-1 on T production and suppressed basal and ET-1-induced PGE2 release whilst a lipoxygenase blocker NDGA did not modify T response to the peptide.	Quinacrine	27-37	phospholipase A2 group IB	Rattus norvegicus	12-16
9247325-7	1997	Moreover, a PLA2 inhibitor quinacrine inhibited the stimulatory action of ET-1 on T production and suppressed basal and ET-1-induced PGE2 release whilst a lipoxygenase blocker NDGA did not modify T response to the peptide.	Quinacrine	27-37	endothelin 1	Rattus norvegicus	74-78
9247325-7	1997	Moreover, a PLA2 inhibitor quinacrine inhibited the stimulatory action of ET-1 on T production and suppressed basal and ET-1-induced PGE2 release whilst a lipoxygenase blocker NDGA did not modify T response to the peptide.	Quinacrine	27-37	endothelin 1	Rattus norvegicus	120-124
8836147-6	1996	The presence of quinacrine, an antagonist of PLA2, during the membrane pretreatment inhibited their fusogenic activity, suggesting the importance of activation of PLA2.	Quinacrine	16-26	phospholipase A2 group IB	Rattus norvegicus	45-49
8836147-6	1996	The presence of quinacrine, an antagonist of PLA2, during the membrane pretreatment inhibited their fusogenic activity, suggesting the importance of activation of PLA2.	Quinacrine	16-26	phospholipase A2 group IB	Rattus norvegicus	163-167
8660827-2	1996	The A-LAK-mediated cytotoxicity against YAC-1 target cells was strongly inhibited by two inhibitors of sPLA2, p-BPB and mepacrine, suggesting the involvement of this enzyme in the lytic mechanism of A-LAK.	Quinacrine	120-129	alpha-kinase 1	Mus musculus	6-9
8943700-8	1996	The kinetics of the time dependent docosahexaenoic acid release and the effects of quinacrine suggest that this release is mediated in part by activation of phospholipase A2.	Quinacrine	83-93	phospholipase A2 group IB	Rattus norvegicus	157-173
8781605-3	1996	Several recent reports have shown that quinacrine, besides being a potent inhibitor of PLA2, suppresses the generation of ODFR.	Quinacrine	39-49	phospholipase A2 group IB	Rattus norvegicus	87-91
21153096-4	1996	From enzymatic assays, phospholipase A(2) and diacylglycerol lipase were activated by carbamylcholine and these activations were inhibited by the phospholipase A(2) inhibitors, mepacrine and aristolochic acid, and by the diacylglycerol lipase inhibitor RHC 80267.	Quinacrine	177-186	phospholipase A2 group IB	Rattus norvegicus	23-67
8768715-5	1996	The PMA-induced generation of these three PLD products was inhibited by mepacrine which, in parallel, significantly blocked PMA-induced desensitization of [3H]LTB4 binding, which suggested that elevation of one or more of these products played a role in desensitization.	Quinacrine	72-81	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	42-45
8768715-7	1996	The reduction of PMA-induced LTB4 receptor desensitization by mepacrine could be overcome to various degrees by adding back PLD-derived lipids such as arachidonic acid.	Quinacrine	62-71	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	124-127
8858301-12	1996	Inhibition of PAF biosynthesis by pretreatment of the animals with the phospholipase A2 inhibitor mepacrine (5 mg kg-1, i.v.)	Quinacrine	98-107	phospholipase A2	Oryctolagus cuniculus	71-87
8660827-2	1996	The A-LAK-mediated cytotoxicity against YAC-1 target cells was strongly inhibited by two inhibitors of sPLA2, p-BPB and mepacrine, suggesting the involvement of this enzyme in the lytic mechanism of A-LAK.	Quinacrine	120-129	ADP-ribosyltransferase 1	Mus musculus	40-45
8660827-2	1996	The A-LAK-mediated cytotoxicity against YAC-1 target cells was strongly inhibited by two inhibitors of sPLA2, p-BPB and mepacrine, suggesting the involvement of this enzyme in the lytic mechanism of A-LAK.	Quinacrine	120-129	alpha-kinase 1	Mus musculus	201-204
8621160-8	1996	Moreover, a commonly used phospholipase A2 (PLA2) inhibitor, quinacrine, decreased HGF-induced [3H]AA release and [3H]thymidine incorporation.	Quinacrine	61-71	phospholipase A2 group IB	Rattus norvegicus	26-42
8832056-13	1996	Mepacrine (500 microM), a non-specific PLA2 inhibitor, strikingly reduced PAF release.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	39-43
8832056-13	1996	Mepacrine (500 microM), a non-specific PLA2 inhibitor, strikingly reduced PAF release.	Quinacrine	0-9	PCNA clamp associated factor	Homo sapiens	74-77
8832056-16	1996	Mepacrine also suppressed [3H]-acetate incorporation into [3H]-PAF.	Quinacrine	0-9	PCNA clamp associated factor	Homo sapiens	63-66
8621160-8	1996	Moreover, a commonly used phospholipase A2 (PLA2) inhibitor, quinacrine, decreased HGF-induced [3H]AA release and [3H]thymidine incorporation.	Quinacrine	61-71	phospholipase A2 group IB	Rattus norvegicus	44-48
8621160-8	1996	Moreover, a commonly used phospholipase A2 (PLA2) inhibitor, quinacrine, decreased HGF-induced [3H]AA release and [3H]thymidine incorporation.	Quinacrine	61-71	hepatocyte growth factor	Rattus norvegicus	83-86
8583418-23	1995	The channels could be activated by GTP gamma S or by NaF in the presence of the phospholipase A2 inhibitor quinacrine, indicating that this enzyme is not involved in channel regulation.	Quinacrine	107-117	LOC104974671	Bos taurus	80-96
8616070-4	1996	In addition, inhibition of PLA2 by mepacrine (0-100 micromol/l) did not concomitantly inhibit FMLP-stimulated superoxide production.	Quinacrine	35-44	phospholipase A2 group IB	Homo sapiens	27-31
8616070-6	1996	In cells preincubated with GM-CSF, time- and dose-dependent priming of FMLP-stimulated PLA2 responses were observed and inhibition of PLA2 by mepacrine was accompanied by the inhibition of FMLP-stimulated superoxide production down to the level of unprimed cells.	Quinacrine	142-151	colony stimulating factor 2	Homo sapiens	27-33
8616070-6	1996	In cells preincubated with GM-CSF, time- and dose-dependent priming of FMLP-stimulated PLA2 responses were observed and inhibition of PLA2 by mepacrine was accompanied by the inhibition of FMLP-stimulated superoxide production down to the level of unprimed cells.	Quinacrine	142-151	formyl peptide receptor 1	Homo sapiens	71-75
8616070-6	1996	In cells preincubated with GM-CSF, time- and dose-dependent priming of FMLP-stimulated PLA2 responses were observed and inhibition of PLA2 by mepacrine was accompanied by the inhibition of FMLP-stimulated superoxide production down to the level of unprimed cells.	Quinacrine	142-151	phospholipase A2 group IB	Homo sapiens	134-138
8616070-6	1996	In cells preincubated with GM-CSF, time- and dose-dependent priming of FMLP-stimulated PLA2 responses were observed and inhibition of PLA2 by mepacrine was accompanied by the inhibition of FMLP-stimulated superoxide production down to the level of unprimed cells.	Quinacrine	142-151	formyl peptide receptor 1	Homo sapiens	189-193
8616070-8	1996	These data suggest that a mepacrine-sensitive PLA2 may have a role in the GM-CSF mediated priming of superoxide production.	Quinacrine	26-35	phospholipase A2 group IB	Homo sapiens	46-50
8616070-8	1996	These data suggest that a mepacrine-sensitive PLA2 may have a role in the GM-CSF mediated priming of superoxide production.	Quinacrine	26-35	colony stimulating factor 2	Homo sapiens	74-80
8740942-8	1996	The increased arachidonic acid cascade was sensitive to phospholipase A2 inhibiting Mepacrin treatment.	Quinacrine	84-92	phospholipase A2 group IB	Homo sapiens	56-72
8569417-0	1996	Cerebroprotective action of the phospholipase inhibitor quinacrine in the ischemia/reperfused gerbil hippocampus.	Quinacrine	56-66	LY6/PLAUR domain containing 8	Homo sapiens	32-55
8569417-1	1996	The phospholipase inhibitor quinacrine (mepacrine; 5 mg/kg, i.p.)	Quinacrine	28-38	LY6/PLAUR domain containing 8	Homo sapiens	4-27
8569417-3	1996	Quinacrine significantly reduced stroke injury assessed by locomotor activity monitoring and by histopathological measurement of hippocampal CA1 pyramidal cell loss.	Quinacrine	0-10	carbonic anhydrase 1	Homo sapiens	141-144
8747522-7	1996	The phospholipase A2 inhibitor mepacrine specifically eliminated the effect of plasmin stimulation on PAI activity.	Quinacrine	31-40	phospholipase A2 group IB	Homo sapiens	4-20
8747522-7	1996	The phospholipase A2 inhibitor mepacrine specifically eliminated the effect of plasmin stimulation on PAI activity.	Quinacrine	31-40	plasminogen	Homo sapiens	79-86
8747522-7	1996	The phospholipase A2 inhibitor mepacrine specifically eliminated the effect of plasmin stimulation on PAI activity.	Quinacrine	31-40	serpin family E member 1	Homo sapiens	102-105
8565149-4	1995	Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.	Quinacrine	68-77	kininogen 1	Homo sapiens	34-44
8565149-4	1995	Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.	Quinacrine	68-77	phospholipase A2 group IB	Homo sapiens	92-108
8786557-3	1996	In this study, we have investigated whether PLA2 inhibition, by quinacrine, has any effects on stimulant-induced behavioral sensitization.	Quinacrine	64-74	phospholipase A2 group IB	Rattus norvegicus	44-48
8866867-7	1996	Quinacrine (10-50 microM), an inhibitor of phospholipase A2, selectively inhibited the sensitization to 5-HT, but did not alter the sensitization to either phenylephrine or GTP.	Quinacrine	0-10	phospholipase A2	Oryctolagus cuniculus	43-59
8779929-6	1996	The PLA2 inhibitors quinacrine (1 microM), aristolochic acid (250 microM), and octadecylbenzoylacrylic acid (7 microM) inhibited BK channels by 61 +/- 6, 47 +/- 2, and 30 +/- 9%, respectively, and in a manner indistinguishable from general anesthetics inhibition.	Quinacrine	20-30	phospholipase A2 group IB	Rattus norvegicus	4-8
8603837-10	1996	Quinacrine, a phospholipase A2 inhibitor, inhibited ET-1-induced cAMP accumulation in a dose-dependent manner (IC50s for bovine and cat were 22 and 19 microM, respectively).	Quinacrine	0-10	LOC104974671	Bos taurus	14-30
8603837-10	1996	Quinacrine, a phospholipase A2 inhibitor, inhibited ET-1-induced cAMP accumulation in a dose-dependent manner (IC50s for bovine and cat were 22 and 19 microM, respectively).	Quinacrine	0-10	endothelin 1	Bos taurus	52-56
8838452-8	1996	A phospholipase A2 inhibitor (mepacrine) inhibited the EGF-induced contraction but a diacylglycerol-lipase inhibitor, 1,6-di-(O-(carbamoyl)cyclohexanone oxime)hexane (U-57908) and a phospholipase D inhibitor (wortmannin) did not affect it.	Quinacrine	30-39	pro-epidermal growth factor	Cavia porcellus	55-58
7595485-9	1995	Pretreatment of cells with either chelerythrine (1 microM, protein kinase C inhibitor) or quinacrine (5 microM, phospholipase A2 inhibitor) before addition of glutamate also blocked oxidation of DCF.	Quinacrine	90-100	phospholipase A2 group IB	Homo sapiens	112-128
8608187-3	1995	Brief exposure (60 min) of cells to the phospholipase A2 inhibitors, mepacrine (500 mumol/l) and heparin (1 g/l), reduced the number of colonies formed in the control group and completely abolished the increase in the number of colonies formed after treatment of the cells with phorbol ester.	Quinacrine	69-78	phospholipase A2, group IB, pancreas	Mus musculus	40-56
7575634-3	1995	Hydrogen peroxide-stimulated release of arachidonic acid was blocked with the phospholipase A2 inhibitor quinacrine.	Quinacrine	105-115	LOC104974671	Bos taurus	78-94
7573482-7	1995	Mepacrine (5 x 10(-5) M) had no direct effect on PCT transport but blocked the stimulatory effect of EGF on JPhos.	Quinacrine	0-9	pro-epidermal growth factor	Oryctolagus cuniculus	101-104
7654391-3	1995	The lipoxygenase inhibitors, nordihydroguaiaretic acid and diethylcarbamazine, and phospholipase A2 inhibitors, mepacrine and dibucaine, blocked the release of NCA in response to ETX, OZ, calcium ionophore A23187 (A23187), and phorbol myristate acetate (PMA).	Quinacrine	112-121	phospholipase A2 group IB	Homo sapiens	83-99
7565637-6	1995	Evidence in support of this includes (i) inhibition by mepacrine, a phospholipase A2 inhibitor, of [3H]2DG uptake evoked by TNF-alpha and IL-1 alpha, and (ii) stimulation of [3H]arachidonic acid release by TNF-alpha and IL-1 alpha.	Quinacrine	55-64	phospholipase A2, group IB, pancreas	Mus musculus	68-84
7565637-6	1995	Evidence in support of this includes (i) inhibition by mepacrine, a phospholipase A2 inhibitor, of [3H]2DG uptake evoked by TNF-alpha and IL-1 alpha, and (ii) stimulation of [3H]arachidonic acid release by TNF-alpha and IL-1 alpha.	Quinacrine	55-64	tumor necrosis factor	Mus musculus	124-133
7565637-6	1995	Evidence in support of this includes (i) inhibition by mepacrine, a phospholipase A2 inhibitor, of [3H]2DG uptake evoked by TNF-alpha and IL-1 alpha, and (ii) stimulation of [3H]arachidonic acid release by TNF-alpha and IL-1 alpha.	Quinacrine	55-64	interleukin 1 alpha	Mus musculus	138-148
7565637-6	1995	Evidence in support of this includes (i) inhibition by mepacrine, a phospholipase A2 inhibitor, of [3H]2DG uptake evoked by TNF-alpha and IL-1 alpha, and (ii) stimulation of [3H]arachidonic acid release by TNF-alpha and IL-1 alpha.	Quinacrine	55-64	tumor necrosis factor	Mus musculus	206-215
7565637-6	1995	Evidence in support of this includes (i) inhibition by mepacrine, a phospholipase A2 inhibitor, of [3H]2DG uptake evoked by TNF-alpha and IL-1 alpha, and (ii) stimulation of [3H]arachidonic acid release by TNF-alpha and IL-1 alpha.	Quinacrine	55-64	interleukin 1 alpha	Mus musculus	220-230
7646440-3	1995	PMA increased particulate phospholipase A2 (PLA2) activity, lysophosphatidylcholine formation and arachidonic acid release from bone marrow cells; these effects were abolished when cells were pretreated with the putative PLA2 inhibitors heparin and mepacrine.	Quinacrine	249-258	phospholipase A2, group IB, pancreas	Mus musculus	221-225
8640337-18	1995	The phospholipase A2 inhibitor, quinacrine (up to 100 microM) also blocked the effect of acetylcholine on the outflow of 3H-prostaglandins, but this was not followed by a compensatory increase in the outflow of [3H]-arachidonic acid.	Quinacrine	32-42	phospholipase A2 group IB	Rattus norvegicus	4-20
8608187-10	1995	The results indicate that phospholipase A2 activation is involved in the phorbol ester-mediated increase in colony formation, since, of the different agents applied, only staurosporine, an inhibitor of protein kinase C, and mepacrine and heparin, putative inhibitors of phospholipase A2, were capable of abolishing phorbol ester-mediated effects.	Quinacrine	224-233	phospholipase A2, group IB, pancreas	Mus musculus	26-42
8537304-6	1995	The stimulatory effect of mastoparan was little affected in cells that had been treated with pertussis toxin, but it was strongly suppressed in the presence of quinacrine, an inhibitor of phospholipase A2.	Quinacrine	160-170	phospholipase A2 group IB	Rattus norvegicus	188-204
8588070-6	1995	Coapplication of quinacrine (10 microM) and bromophenacyl bromide (100 microM), inhibitors of phospholipase A2 (PLA2), prevented the IL-1 alpha-induced increases in PGF2 alpha production.	Quinacrine	17-27	phospholipase A2 group IB	Homo sapiens	94-110
8588070-6	1995	Coapplication of quinacrine (10 microM) and bromophenacyl bromide (100 microM), inhibitors of phospholipase A2 (PLA2), prevented the IL-1 alpha-induced increases in PGF2 alpha production.	Quinacrine	17-27	phospholipase A2 group IB	Homo sapiens	112-116
8588070-6	1995	Coapplication of quinacrine (10 microM) and bromophenacyl bromide (100 microM), inhibitors of phospholipase A2 (PLA2), prevented the IL-1 alpha-induced increases in PGF2 alpha production.	Quinacrine	17-27	interleukin 1 alpha	Homo sapiens	133-143
7540278-9	1995	Moreover, PLA2-inhibitors, quinacrine and dexamethasone, partially inhibited cytotoxicity induced by either TNF or anti-Fas.	Quinacrine	27-37	phospholipase A2 group IB	Homo sapiens	10-14
7540278-9	1995	Moreover, PLA2-inhibitors, quinacrine and dexamethasone, partially inhibited cytotoxicity induced by either TNF or anti-Fas.	Quinacrine	27-37	tumor necrosis factor	Homo sapiens	108-111
7582109-6	1995	Administration of mepacrine reduced cytotoxicity caused by gp120.	Quinacrine	18-27	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	59-64
8529043-6	1995	Mepacrine, a PLA2 inhibitor, reversed the pump effect of all agents, and arachidonic acid (AA) produced a dose-dependent pump inhibition, in all three nephron segments.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-17
7759504-6	1995	Similarly, when the GH-induced liberation of [3H]AA was blocked by the PLA2 inhibitor mepacrine or the Ca2+ channel blocker verapamil, GH-induced accumulation of P4502C12 mRNA was absent.	Quinacrine	86-95	gonadotropin releasing hormone receptor	Rattus norvegicus	20-22
7759504-6	1995	Similarly, when the GH-induced liberation of [3H]AA was blocked by the PLA2 inhibitor mepacrine or the Ca2+ channel blocker verapamil, GH-induced accumulation of P4502C12 mRNA was absent.	Quinacrine	86-95	phospholipase A2 group IB	Rattus norvegicus	71-75
7759504-6	1995	Similarly, when the GH-induced liberation of [3H]AA was blocked by the PLA2 inhibitor mepacrine or the Ca2+ channel blocker verapamil, GH-induced accumulation of P4502C12 mRNA was absent.	Quinacrine	86-95	gonadotropin releasing hormone receptor	Rattus norvegicus	135-137
7759504-8	1995	The inhibitory effect of mepacrine on GH induction of P4502C12 mRNA was reversed by AA addition, further supporting a role for eicosanoids in the regulation of CYP2C12.	Quinacrine	25-34	gonadotropin releasing hormone receptor	Rattus norvegicus	38-40
7759504-8	1995	The inhibitory effect of mepacrine on GH induction of P4502C12 mRNA was reversed by AA addition, further supporting a role for eicosanoids in the regulation of CYP2C12.	Quinacrine	25-34	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	160-167
7537492-5	1995	On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2.	Quinacrine	54-64	phospholipase A2 group IB	Rattus norvegicus	82-86
7537492-5	1995	On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2.	Quinacrine	54-64	phospholipase A2 group IB	Rattus norvegicus	130-134
7537492-5	1995	On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2.	Quinacrine	54-64	phospholipase A2 group IB	Rattus norvegicus	130-134
7753489-2	1995	In comparison with the control group, the phospholipase A2 inhibitor mepacrine significantly decreased the ischemia-evoked efflux of transmitter amino acids into cortical superfusates.	Quinacrine	69-78	phospholipase A2 group IB	Rattus norvegicus	42-58
7602616-6	1995	Quinacrine, a phospholipase A2 inhibitor (250 microM), decreased the NMDA-evoked eicosanoid release by 30%, whereas 10 microM indomethacin, a cyclo-oxygenase inhibitor, completely suppressed the release.	Quinacrine	0-10	phospholipase A2	Oryctolagus cuniculus	14-30
7900800-3	1995	Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05).	Quinacrine	33-43	phospholipase A2 group IB	Rattus norvegicus	17-21
7900800-3	1995	Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05).	Quinacrine	33-43	phospholipase A2 group IB	Rattus norvegicus	103-107
7900800-4	1995	However, when quinacrine was administered after 2 h of reperfusion, circulating PMN priming and lung leak continued to evolve despite suppression of intestinal PLA2 activity.	Quinacrine	14-24	phospholipase A2 group IB	Rattus norvegicus	160-164
7663895-1	1995	Quinacrine (QU) is an inhibitor of phospholipase A2 (PLA2).	Quinacrine	0-10	phospholipase A2 group IIA	Gallus gallus	35-51
7663895-1	1995	Quinacrine (QU) is an inhibitor of phospholipase A2 (PLA2).	Quinacrine	0-10	phospholipase A2 group IIA	Gallus gallus	53-57
7878677-8	1995	This increase in [3H]AA release was inhibited by quinacrine (20 microM), which is a phospholipase (PLA2) inhibitor.	Quinacrine	49-59	phospholipase A2, group V	Mus musculus	99-103
7655056-4	1995	The PLA2 activity in A. americanum was reduced by the substrate analog, PLA2 inhibitor, oleyloxyethyl phosphorylcholine in a dose-dependent manner, but was insensitive to the other mammalian PLA2 inhibitors mepacrine (20 microM), aristolochic acid (45 microM), and dexamethasone (50 microM).	Quinacrine	207-216	phospholipase A2 group IIA	Homo sapiens	4-8
7851533-0	1995	Quinacrine mustard and lipophilic cations inhibitory to both vacuolar H(+)-ATPase and F0F1-ATP synthase.	Quinacrine	0-10	ATPase H+ transporting V1 subunit B2	Bos taurus	61-81
7851533-1	1995	Various lipophilic cations, such as quinacrine mustard and dequalinium, which are known to inhibit mitochondrial F1-ATPase, strongly inhibited vacuolar H(+)-ATPase purified from bovine adrenal chromaffin granules.	Quinacrine	36-46	ATPase H+ transporting V1 subunit B2	Bos taurus	143-163
7851533-2	1995	Quinacrine mustard bound irreversibly to vacuolar H(+)-ATPase subunit A, and the 115 kDa accessory polypeptide and dithiothreitol had no effect.	Quinacrine	0-10	ATPase H+ transporting V1 subunit B2	Bos taurus	41-61
7742810-4	1995	Various PL A2 inhibitors, such as manoalide, quinacrine and p-bromophenacyl bromide, suppressed the stimulatory release of lipoprotein lipase (LPL) activity from the fat pads by vanadate.	Quinacrine	45-55	lipoprotein lipase	Rattus norvegicus	123-141
7742810-4	1995	Various PL A2 inhibitors, such as manoalide, quinacrine and p-bromophenacyl bromide, suppressed the stimulatory release of lipoprotein lipase (LPL) activity from the fat pads by vanadate.	Quinacrine	45-55	lipoprotein lipase	Rattus norvegicus	143-146
7873389-13	1995	Thrombin induced mepacrine release in a dose-dependent manner from 0.003 to 0.4 U/ml.	Quinacrine	17-26	coagulation factor II, thrombin	Homo sapiens	0-8
7784893-3	1995	In the present work, it was demonstrated that pretreatment of rats with PLA2 inhibitor, quinacrine (20 mg/kg, I.P.	Quinacrine	88-98	phospholipase A2 group IB	Rattus norvegicus	72-76
7831318-7	1995	Interruption of the yeast gene, denoted as VMA8, resulted in the null mutant delta vma8::URA3 that, like all the other V-ATPase null mutants, did not grow on medium buffered at pH 7.5 and showed no accumulation of quinacrine into their vacuoles.	Quinacrine	214-224	H(+)-transporting V1 sector ATPase subunit D	Saccharomyces cerevisiae S288C	43-47
7655056-4	1995	The PLA2 activity in A. americanum was reduced by the substrate analog, PLA2 inhibitor, oleyloxyethyl phosphorylcholine in a dose-dependent manner, but was insensitive to the other mammalian PLA2 inhibitors mepacrine (20 microM), aristolochic acid (45 microM), and dexamethasone (50 microM).	Quinacrine	207-216	phospholipase A2 group IIA	Homo sapiens	72-76
7655056-4	1995	The PLA2 activity in A. americanum was reduced by the substrate analog, PLA2 inhibitor, oleyloxyethyl phosphorylcholine in a dose-dependent manner, but was insensitive to the other mammalian PLA2 inhibitors mepacrine (20 microM), aristolochic acid (45 microM), and dexamethasone (50 microM).	Quinacrine	207-216	phospholipase A2 group IIA	Homo sapiens	72-76
9251753-0	1995	Opposing effects of quinacrine and chloroquine on the development of TA3 transplanted tumors in mice.	Quinacrine	20-30	RIKEN cDNA 2700049A03 gene	Mus musculus	69-72
7833250-6	1995	The results confirm that delta SPD occurs commonly in MPD/MDS with 7/15 patients having reduced mepacrine staining but, like the findings in hereditary delta SPD, 3/7 patients with normal platelet aggregation had delta SPD.	Quinacrine	96-105	mevalonate diphosphate decarboxylase	Homo sapiens	54-57
8001364-12	1995	CONCLUSIONS: The observation that quinacrine and preshock diltiazem limited the extent of shock-induced mucosal injury and bacterial translocation indicate that calcium and phospholipase A2 are involved in the pathogenesis of shock-induced mucosal injury and bacterial translocation.	Quinacrine	34-44	phospholipase A2 group IB	Rattus norvegicus	173-189
7713816-1	1995	Mepacrine, a cell membrane stabilizer and inhibitor of phospholipase A2 (PLA2), exerts a protective effect on ischemia-reperfusion injury in heart; however, its effect in lungs has not been examined.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	55-71
7713816-1	1995	Mepacrine, a cell membrane stabilizer and inhibitor of phospholipase A2 (PLA2), exerts a protective effect on ischemia-reperfusion injury in heart; however, its effect in lungs has not been examined.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	73-77
7713816-8	1995	Mepacrine also dose-dependently inhibited production of tumor necrosis factor-alpha (TNF-alpha) by human monocytes; dexamethasone was much less effective in decreasing TNF-alpha production.	Quinacrine	0-9	tumor necrosis factor	Homo sapiens	56-83
7713816-8	1995	Mepacrine also dose-dependently inhibited production of tumor necrosis factor-alpha (TNF-alpha) by human monocytes; dexamethasone was much less effective in decreasing TNF-alpha production.	Quinacrine	0-9	tumor necrosis factor	Homo sapiens	85-94
7713816-10	1995	This protective effect of mepacrine may not be the result of its inhibition of PLA2 but rather of its downregulation of oxygen radical production by circulating or resident leukocytes or its attenuation of TNF-alpha production by macrophages.	Quinacrine	26-35	phospholipase A2 group IB	Rattus norvegicus	79-83
7713816-10	1995	This protective effect of mepacrine may not be the result of its inhibition of PLA2 but rather of its downregulation of oxygen radical production by circulating or resident leukocytes or its attenuation of TNF-alpha production by macrophages.	Quinacrine	26-35	tumor necrosis factor	Rattus norvegicus	206-215
7900098-6	1994	However, partially purified PSA was partially inhibited by preincubation with 50 microM mepacrine, a phospholipase A2 inhibitor.	Quinacrine	88-97	phospholipase A2 group IB	Homo sapiens	101-117
8200994-11	1994	When 10(-9) M ET-1 was added in the presence of 10(-5) M quinacrine, a phospholipase (PL) inhibitor, Jv also increased from 1.02 +/- 0.20 to 1.23 +/- 0.22 nl/mm/min (P < 0.03).	Quinacrine	57-67	endothelin 1	Homo sapiens	14-18
7889312-11	1994	This EDHF-type dilation was reversibly inhibited by the phospholipase A2 inhibitor, quinacrine (3 microM, 9 +/- 3% decrease in CPP, n = 6, P < 0.01) and by the cytochrome P450 inhibitor SKF525a (3 microM, 6 +/- 1% decrease in CPP, n = 6, P < 0.01).	Quinacrine	84-94	phospholipase A2 group IB	Rattus norvegicus	56-72
7846335-6	1994	TNF-alpha increased significantly after quinacrine instillation.	Quinacrine	40-50	tumor necrosis factor	Homo sapiens	0-9
7846335-8	1994	Concentrations of TNF-alpha correlate with the amount of pleural fluid production after quinacrine instillation, in that a higher level of TNF-alpha is associated with more pleural fluid production.	Quinacrine	88-98	tumor necrosis factor	Homo sapiens	18-27
7846335-8	1994	Concentrations of TNF-alpha correlate with the amount of pleural fluid production after quinacrine instillation, in that a higher level of TNF-alpha is associated with more pleural fluid production.	Quinacrine	88-98	tumor necrosis factor	Homo sapiens	139-148
7929071-8	1994	The delta vma7::URA3 null mutants are not able to grow on a medium buffered at pH 7.5, they fail to accumulate quinacrine into their vacuoles and the other subunits of the catalytic sector are not assembled onto the vacuolar membrane in its absence.	Quinacrine	111-121	H(+)-transporting V1 sector ATPase subunit F	Saccharomyces cerevisiae S288C	10-14
7809385-7	1994	Treatment of the BEAS cells with the phospholipase A2 (PLA2) inhibitor mepacrine (1 mM) prior to, and during, incubation with melittin inhibited the increase in 3H-AA and 3H-PAF release into the apical compartment by 65% and 100%, respectively.	Quinacrine	71-80	phospholipase A2 group IB	Homo sapiens	37-53
7809385-7	1994	Treatment of the BEAS cells with the phospholipase A2 (PLA2) inhibitor mepacrine (1 mM) prior to, and during, incubation with melittin inhibited the increase in 3H-AA and 3H-PAF release into the apical compartment by 65% and 100%, respectively.	Quinacrine	71-80	phospholipase A2 group IB	Homo sapiens	55-59
7809385-7	1994	Treatment of the BEAS cells with the phospholipase A2 (PLA2) inhibitor mepacrine (1 mM) prior to, and during, incubation with melittin inhibited the increase in 3H-AA and 3H-PAF release into the apical compartment by 65% and 100%, respectively.	Quinacrine	71-80	PCNA clamp associated factor	Homo sapiens	174-177
7811392-5	1994	Quinacrine and the quinoline-based antimalarials variously inhibit CDPK, PKC and MLCK albeit at relatively high concentrations (about 1 to 4 x 10(-4) M), the best inhibitors found being primaquine, pentaquine and mefloquine (IC50 values for MLCK 49, 103 and 33 microM, respectively).	Quinacrine	0-10	myosin light chain kinase 3	Rattus norvegicus	81-85
7811392-5	1994	Quinacrine and the quinoline-based antimalarials variously inhibit CDPK, PKC and MLCK albeit at relatively high concentrations (about 1 to 4 x 10(-4) M), the best inhibitors found being primaquine, pentaquine and mefloquine (IC50 values for MLCK 49, 103 and 33 microM, respectively).	Quinacrine	0-10	myosin light chain kinase 3	Rattus norvegicus	241-245
8039843-7	1994	The synthesis of vasoconstrictor prostaglandins, such as thromboxane A2, may be stimulated during acetylcholine treatment, resulting in the attenuation of acetylcholine relaxation, because the relaxation was abolished by treatment with the phospholipase A2 inhibitor quinacrine, cyclooxygenase inhibitor indomethacin, prostaglandin H2/thromboxane A2 receptor antagonist S1452, and thromboxane A2 synthase inhibitor dazmegrel.	Quinacrine	267-277	phospholipase A2 group IB	Rattus norvegicus	240-256
7918869-3	1994	This response could be fully prevented by pretreatment of cells with the PLA2 inhibitor, mepacrine.	Quinacrine	89-98	phospholipase A2 group IB	Rattus norvegicus	73-77
7918869-7	1994	The effect was inhibited by mepacrine, further supporting the pivotal role of PLA2 in the release of the eicosanoid precursor, AA.	Quinacrine	28-37	phospholipase A2 group IB	Rattus norvegicus	78-82
12288043-1	1994	Family Health International (FHI) recently announced that it is carrying out studies on a drug called quinacrine to determine whether it has potential as a safe, non-surgical method for female sterilization.	Quinacrine	102-112	cytochrome P450 family 11 subfamily B member 1	Homo sapiens	29-32
7826678-4	1994	Of the compounds tested, the intercalators coralyne and quinacrine provide the largest stabilization of the triplex dT19.dA19.dT19.	Quinacrine	56-66	Fat body protein 2	Drosophila melanogaster	116-120
7826678-4	1994	Of the compounds tested, the intercalators coralyne and quinacrine provide the largest stabilization of the triplex dT19.dA19.dT19.	Quinacrine	56-66	Fat body protein 2	Drosophila melanogaster	126-130
7826678-5	1994	Molecular modeling studies suggest that the large intercalating ring system of coralyne stacks well with the triplex bases whereas the alkylamino side chain of quinacrine fits snugly into the remaining space of the major groove of dT19.dA19.dT19 triplex and forms extensive van der Waals contacts with the thymine methyl groups that line the groove.	Quinacrine	160-170	Fat body protein 2	Drosophila melanogaster	231-235
8033515-6	1994	Blockade of cyclo-oxygenase with indomethacin or of lipoxygenase with ICI 207968 or of phospholipase A2 with mepacrine inhibited release of prostaglandin E2 or leukotriene C4 or both of these plus platelet-activating factor, respectively.	Quinacrine	109-118	phospholipase A2 group IB	Homo sapiens	87-103
7826678-5	1994	Molecular modeling studies suggest that the large intercalating ring system of coralyne stacks well with the triplex bases whereas the alkylamino side chain of quinacrine fits snugly into the remaining space of the major groove of dT19.dA19.dT19 triplex and forms extensive van der Waals contacts with the thymine methyl groups that line the groove.	Quinacrine	160-170	Fat body protein 2	Drosophila melanogaster	241-245
8174549-5	1994	The activation by OHzero depended on concomitant release of arachidonic acid and was blocked by the phospholipase A2 inhibitors mepacrine and aristolochic acid, and by the Na+/K+ antiporter inhibitor ethylisopropylamiloride.	Quinacrine	128-137	phospholipase A2 group IB	Homo sapiens	100-116
8166641-3	1994	AngII induced a rapid time-dependent release of [3H]arachidonic acid from prelabelled cells that was inhibited by mepacrine, a PLA2 inhibitor.	Quinacrine	114-123	angiotensinogen	Homo sapiens	0-5
8166641-3	1994	AngII induced a rapid time-dependent release of [3H]arachidonic acid from prelabelled cells that was inhibited by mepacrine, a PLA2 inhibitor.	Quinacrine	114-123	phospholipase A2 group IB	Homo sapiens	127-131
8166641-5	1994	This AngII-stimulated cPLA2 activity was also significantly inhibited by mepacrine.	Quinacrine	73-82	angiotensinogen	Homo sapiens	5-10
8166641-5	1994	This AngII-stimulated cPLA2 activity was also significantly inhibited by mepacrine.	Quinacrine	73-82	phospholipase A2 group IVA	Homo sapiens	22-27
8014598-1	1994	The phospholipase A2 (PLA2) inhibitors, quinacrine, p-bromophenacyl bromide, ONO-RS-082, aristolochic acid and chloracysine blocked the priming effect of LHRH, but not acute LHRH-induced gonadotrophin release measured in anterior pituitary pieces in pro-oestrous rats in vitro.	Quinacrine	40-50	gonadotropin releasing hormone 1	Rattus norvegicus	154-158
8135755-5	1994	This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system.	Quinacrine	207-217	angiotensinogen	Rattus norvegicus	51-57
8135755-5	1994	This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system.	Quinacrine	207-217	phospholipase A2 group IB	Rattus norvegicus	159-175
8118827-9	1994	In addition, quinacrine, which can inhibit phospholipase activity, blocked PDT induced c-fos mRNA expression.	Quinacrine	13-23	FBJ osteosarcoma oncogene	Mus musculus	87-92
8138923-5	1994	Inhibition of phospholipase A2 with quinacrine or by removal of extracellular Ca++ blocks the agonist-mediated loss of 5-HT1A receptor binding sites.	Quinacrine	36-46	phospholipase A2 group IB	Homo sapiens	14-30
8138923-5	1994	Inhibition of phospholipase A2 with quinacrine or by removal of extracellular Ca++ blocks the agonist-mediated loss of 5-HT1A receptor binding sites.	Quinacrine	36-46	5-hydroxytryptamine receptor 1A	Homo sapiens	119-134
8106442-2	1994	Monocyte Chemotactic Protein-1 (MCP-1), a member of the Cys-Cys branch of the chemokine superfamily, induced a mepacrine- and manoalide-sensitive increase in the release of [3H]arachidonic acid from prelabeled human monocytes and monocytic THP-1 leukemic cells.	Quinacrine	111-120	C-C motif chemokine ligand 2	Homo sapiens	0-30
8106442-2	1994	Monocyte Chemotactic Protein-1 (MCP-1), a member of the Cys-Cys branch of the chemokine superfamily, induced a mepacrine- and manoalide-sensitive increase in the release of [3H]arachidonic acid from prelabeled human monocytes and monocytic THP-1 leukemic cells.	Quinacrine	111-120	C-C motif chemokine ligand 2	Homo sapiens	32-37
8106442-8	1994	Phospholipase A2 inhibitors (mepacrine, p-bromophenacyl bromide, and manoalide) blocked monocyte polarization and chemotaxis induced by MCP-1.	Quinacrine	29-38	phospholipase A2 group IB	Homo sapiens	0-16
8106442-8	1994	Phospholipase A2 inhibitors (mepacrine, p-bromophenacyl bromide, and manoalide) blocked monocyte polarization and chemotaxis induced by MCP-1.	Quinacrine	29-38	C-C motif chemokine ligand 2	Homo sapiens	136-141
8294933-6	1994	Inhibition of MeHg-induced PLA2 activation by 100 microM mepacrine failed to modify cytotoxicity.	Quinacrine	57-66	phospholipase A2 group IB	Homo sapiens	27-31
7938614-14	1994	Quinacrine (a phospholipase A2 inhibitor) blocked DC-induced PGE2 release.	Quinacrine	0-10	phospholipase A2	Oryctolagus cuniculus	14-30
8014598-6	1994	Both gonadotrophin secretion and [3H]AA release responses to LHRH and to phorbol ester varied in parallel during the oestrous cycle and in ovariectomized/oestradiol-17 beta-replaced animals, as did their sensitivity to quinacrine and the protein synthesis inhibitor cycloheximide.	Quinacrine	219-229	gonadotropin releasing hormone 1	Rattus norvegicus	61-65
8121291-1	1994	We investigated the effects of 7 days" treatment with oral mepacrine hydrochloride 100 mg three times daily on fasting serum levels of glucose, insulin, lipids, lipoproteins, and apolipoproteins in 16 patients with non-insulin-dependent diabetes mellitus (NIDDM) in a double-blind placebo-controlled study.	Quinacrine	59-82	insulin	Homo sapiens	144-151
8122272-7	1994	The PLA2 inhibitors dibucaine (50 microM) and mepacrine (50 microM) inhibited KCN-mediated [3H]AA release.	Quinacrine	46-55	phospholipase A2 group IB	Rattus norvegicus	4-8
8312361-5	1994	Evidence suggesting that rbFGF-induced release of [3H]arachidonic acid was being mediated via a PLA2 pathway was obtained by pharmacological antagonism using mepacrine, a putative PLA2 inhibitor.	Quinacrine	158-167	phospholipase A2, group V	Mus musculus	96-100
8280102-2	1994	In spite of total inhibition of superoxide production in the presence of the PLA2 inhibitors, 10 microM bromophenacyl bromide (BPB) or 20 microM quinacrine, a maximal phosphorylation of p47 and translocation of p47 and p67 to the neutrophil membranes induced by PMA or OZ was observed.	Quinacrine	145-155	phospholipase A2 group IB	Homo sapiens	77-81
8280102-2	1994	In spite of total inhibition of superoxide production in the presence of the PLA2 inhibitors, 10 microM bromophenacyl bromide (BPB) or 20 microM quinacrine, a maximal phosphorylation of p47 and translocation of p47 and p67 to the neutrophil membranes induced by PMA or OZ was observed.	Quinacrine	145-155	pleckstrin	Homo sapiens	186-189
8280102-2	1994	In spite of total inhibition of superoxide production in the presence of the PLA2 inhibitors, 10 microM bromophenacyl bromide (BPB) or 20 microM quinacrine, a maximal phosphorylation of p47 and translocation of p47 and p67 to the neutrophil membranes induced by PMA or OZ was observed.	Quinacrine	145-155	pleckstrin	Homo sapiens	211-214
8280102-2	1994	In spite of total inhibition of superoxide production in the presence of the PLA2 inhibitors, 10 microM bromophenacyl bromide (BPB) or 20 microM quinacrine, a maximal phosphorylation of p47 and translocation of p47 and p67 to the neutrophil membranes induced by PMA or OZ was observed.	Quinacrine	145-155	CD33 molecule	Homo sapiens	219-222
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	phospholipase A2, group IB, pancreas	Mus musculus	31-47
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	jun proto-oncogene	Mus musculus	112-117
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	122-128
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	tumor necrosis factor	Mus musculus	204-213
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	leukemia inhibitory factor	Mus musculus	225-251
8282065-5	1994	Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF).	Quinacrine	58-68	leukemia inhibitory factor	Mus musculus	253-256
8282065-6	1994	In addition, quinacrine partially blocked IL-1 plus TNF-alpha induced 3H-arachidonic acid release from prelabeled stromal cells.	Quinacrine	13-23	tumor necrosis factor	Mus musculus	52-61
8282065-10	1994	In this system, quinacrine significantly inhibited IL-1 plus TNF-alpha induced GM-CSF transcription assayed with the reporter construct.	Quinacrine	16-26	tumor necrosis factor	Mus musculus	61-70
8282065-10	1994	In this system, quinacrine significantly inhibited IL-1 plus TNF-alpha induced GM-CSF transcription assayed with the reporter construct.	Quinacrine	16-26	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	79-85
7982028-5	1994	This effect was inhibited by MK-801 and quinacrine, suggesting an involvement of NMDA receptors and phospholipase A2.	Quinacrine	40-50	phospholipase A2 group IB	Rattus norvegicus	100-116
8108369-4	1994	This promoting effect of pancreatic and venom PLA2 required Ca2+ in the incubation medium and was inhibited by mepacrine (10(-5) M).	Quinacrine	111-120	phospholipase A2 group IB	Homo sapiens	46-50
7993881-12	1994	We conclude that phospholipase A2 inhibitor, mepacrine, is able to prevent IPRO-stimulated incorporation into phospholipids, suggesting a feedback relation between their biosynthesis and degradation in the myocardium.	Quinacrine	45-54	phospholipase A2, group IB, pancreas	Mus musculus	17-33
8250938-1	1993	The phospholipase A2 (PLA2) inhibitors quinacrine, manoalide and scalaradial inhibit the carbachol-stimulated secretion of the amyloid precursor protein (APP) from cells transfected with the human m1 muscarinic receptor.	Quinacrine	39-49	phospholipase A2 group IB	Homo sapiens	4-20
8250938-1	1993	The phospholipase A2 (PLA2) inhibitors quinacrine, manoalide and scalaradial inhibit the carbachol-stimulated secretion of the amyloid precursor protein (APP) from cells transfected with the human m1 muscarinic receptor.	Quinacrine	39-49	phospholipase A2 group IB	Homo sapiens	22-26
8250938-1	1993	The phospholipase A2 (PLA2) inhibitors quinacrine, manoalide and scalaradial inhibit the carbachol-stimulated secretion of the amyloid precursor protein (APP) from cells transfected with the human m1 muscarinic receptor.	Quinacrine	39-49	amyloid beta precursor protein	Homo sapiens	127-152
8409449-9	1993	Quinacrine and p-bromophenacylbromide, inhibitors of PLA2, blocked LPS priming but not the baseline O2- release from unprimed cells.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	53-57
8409449-9	1993	Quinacrine and p-bromophenacylbromide, inhibitors of PLA2, blocked LPS priming but not the baseline O2- release from unprimed cells.	Quinacrine	0-10	interferon regulatory factor 6	Homo sapiens	67-70
8312361-5	1994	Evidence suggesting that rbFGF-induced release of [3H]arachidonic acid was being mediated via a PLA2 pathway was obtained by pharmacological antagonism using mepacrine, a putative PLA2 inhibitor.	Quinacrine	158-167	phospholipase A2, group V	Mus musculus	180-184
8227189-6	1993	Quinacrine, a phospholipase A2 inhibitor, significantly suppressed the vasopressin-induced arachidonic acid release but had little effect on the formation of inositol phosphates.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
8227189-6	1993	Quinacrine, a phospholipase A2 inhibitor, significantly suppressed the vasopressin-induced arachidonic acid release but had little effect on the formation of inositol phosphates.	Quinacrine	0-10	arginine vasopressin	Rattus norvegicus	71-82
8263365-3	1993	It appears that the BK-induced [3H]arachidonic acid release was attributed to the activation of phospholipase A2, since a phospholipase A2 inhibitor, mepacrine, significantly inhibited the BK enhancement of [3H]arachidonic acid release whereas a diacylglycerol lipase inhibitor, RHC80267, failed to do so.	Quinacrine	150-159	phospholipase A2, group IB, pancreas	Mus musculus	96-112
8409901-10	1993	Sperm treated with the phospholipase A2 inhibitors quinacrine dihydrochloride and p-bromophenacyl-bromide showed an inhibition of the spontaneous occurrence of the acrosome reaction.	Quinacrine	51-77	phospholipase A2 group IB	Homo sapiens	23-39
8378085-4	1993	This stimulation was significantly inhibited by mepacrine, a phospholipase A2 (PLA2) inhibitor.	Quinacrine	48-57	phospholipase A2 group IB	Rattus norvegicus	61-77
8378085-4	1993	This stimulation was significantly inhibited by mepacrine, a phospholipase A2 (PLA2) inhibitor.	Quinacrine	48-57	phospholipase A2 group IB	Rattus norvegicus	79-83
8402133-7	1993	Intravenous administration of quinacrine 10 mg kg-1 at 30 min before instillation of acetic acid resulted in a normal mucosal appearance, normal MPO activity and a significantly reduced increase in plasma exudation into the colon.	Quinacrine	30-40	myeloperoxidase	Rattus norvegicus	145-148
8403225-0	1993	Differential inhibition of the DNA binding of transcription factors NF kappa B and OTF-1 by nitrogen mustard and quinacrine mustard: transcriptional implications.	Quinacrine	113-123	nuclear factor kappa B subunit 1	Homo sapiens	68-78
8403225-0	1993	Differential inhibition of the DNA binding of transcription factors NF kappa B and OTF-1 by nitrogen mustard and quinacrine mustard: transcriptional implications.	Quinacrine	113-123	POU class 2 homeobox 1	Homo sapiens	83-88
8403225-1	1993	Nitrogen mustard (HN2) and quinacrine mustard (QM) both inhibited the binding of NF kappa B to the GC-rich consensus sequence in the HIV long terminal repeat (LTR), as assessed by gel-shift assays.	Quinacrine	27-37	nuclear factor kappa B subunit 1	Homo sapiens	81-91
8315315-5	1993	Phase 2 was significantly inhibited by the PLA2 inhibitor, Mepacrine.	Quinacrine	59-68	phospholipase A2 group IB	Homo sapiens	43-47
8367414-8	1993	The phospholipase A2 inhibitor, quinacrine (10 microM), had no significant effect on PGE, PGFM, TxB2 or 6-keto-PGF1 alpha.	Quinacrine	32-42	phospholipase A2 group IB	Homo sapiens	4-20
8214092-5	1993	The phospholipase A2 (PLA2) inhibitor, mepacrine, also resulted in functional protection and reduction of cell FFA content from 20.2 +/- 2.3 to 15.9 +/- 1.7 micrograms/mg (P < 0.05).	Quinacrine	39-48	phospholipase A2 group IB	Canis lupus familiaris	4-20
8214092-5	1993	The phospholipase A2 (PLA2) inhibitor, mepacrine, also resulted in functional protection and reduction of cell FFA content from 20.2 +/- 2.3 to 15.9 +/- 1.7 micrograms/mg (P < 0.05).	Quinacrine	39-48	phospholipase A2 group IB	Canis lupus familiaris	22-26
8214099-8	1993	The PLA2 inhibitor mepacrine prevented the effect of all agents, and arachidonic acid produced a dose-dependent pump inhibition in each of the three segments studied.	Quinacrine	19-28	phospholipase A2 group IB	Homo sapiens	4-8
8393756-13	1993	Mepacrine (a phospholipase A2 inhibitor) reduced the A23187- and TPA-induced increase of PGE2.	Quinacrine	0-9	phospholipase A2	Oryctolagus cuniculus	13-29
8496167-6	1993	Addition of phospholipase A2 (PLA2) inhibitors (quinacrine, 4-bromophenacyl bromide, manoalide) to the perfusion medium inhibited K(+)-stimulated [3H]ACh and [3H]AA release in a dose-dependent manner.	Quinacrine	48-58	phospholipase A2 group IB	Rattus norvegicus	12-28
8496167-6	1993	Addition of phospholipase A2 (PLA2) inhibitors (quinacrine, 4-bromophenacyl bromide, manoalide) to the perfusion medium inhibited K(+)-stimulated [3H]ACh and [3H]AA release in a dose-dependent manner.	Quinacrine	48-58	phospholipase A2 group IB	Rattus norvegicus	30-34
8388321-3	1993	Eicosanoid generation is attributable to PLA2 activation since pretreatment with PLA2 irreversible inhibitors, such as mepacrine or para-bromophenacylbromide (pBPB), completely blocks AA metabolite generation.	Quinacrine	119-128	phospholipase A2 group IB	Rattus norvegicus	41-45
8388321-3	1993	Eicosanoid generation is attributable to PLA2 activation since pretreatment with PLA2 irreversible inhibitors, such as mepacrine or para-bromophenacylbromide (pBPB), completely blocks AA metabolite generation.	Quinacrine	119-128	phospholipase A2 group IB	Rattus norvegicus	81-85
8388321-5	1993	Treatment of effector cells with mepacrine or pBPB resulted in complete, irreversible, dose-dependent inhibition of both NK and ADCC activities, which were completely reversed by the addition of exogenous PLA2 or its hydrolysis products, AA and lysophosphatidylcholine (lysoPC).	Quinacrine	33-42	phospholipase A2 group IB	Rattus norvegicus	205-209
8387540-6	1993	Treatment of HE with 100 microM mepacrine before activation blocked EPO release (2.0 +/- 0.2 vs 10.2 +/- 2.1% cell content for activated HE, P < 0.004, n = 9), .O2- generation (2.6 +/- 0.9 vs 44.2 +/- 10.8 nmol/ml per 10(6) HE, P < 0.002, n = 5), and LTC4 secretion (68.2 +/- 32.2 vs 1,125.2 +/- 526.8 pg/ml per 10(6) HE, P < 0.04, n = 8).	Quinacrine	32-41	eosinophil peroxidase	Homo sapiens	68-71
8358025-1	1993	Several amphiphilic cations such as mepacrine, desipramine, didodecyldimethylamine, chlorpromazine, oleylamine and W-7 activated the phospholipase D (PLD) activity of cultured LA-N-2 cells.	Quinacrine	36-45	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	133-148
8358025-1	1993	Several amphiphilic cations such as mepacrine, desipramine, didodecyldimethylamine, chlorpromazine, oleylamine and W-7 activated the phospholipase D (PLD) activity of cultured LA-N-2 cells.	Quinacrine	36-45	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	150-153
8491398-8	1993	Inflamed tissue treated with a phospholipase A2 inhibitor (mepacrine) produced less PGE2, LTD4, and electrical responses when compared with inflamed tissue, either untreated (91%, 92%, and 79% respectively) or treated with cyclo-oxygenase and lipoxygenase inhibition.	Quinacrine	59-68	phospholipase A2 group IB	Rattus norvegicus	31-47
8263365-3	1993	It appears that the BK-induced [3H]arachidonic acid release was attributed to the activation of phospholipase A2, since a phospholipase A2 inhibitor, mepacrine, significantly inhibited the BK enhancement of [3H]arachidonic acid release whereas a diacylglycerol lipase inhibitor, RHC80267, failed to do so.	Quinacrine	150-159	phospholipase A2, group IB, pancreas	Mus musculus	122-138
8464709-2	1993	Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	59-63
8464709-2	1993	Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression.	Quinacrine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
7678793-3	1993	ET-1 dose-dependently (10(-9)-10(-6) M) stimulated cAMP formation in VSMC, whose effect was inhibited completely by ETA receptor antagonist (BQ-123) but not by indomethacin or quinacrine.	Quinacrine	176-186	endothelin receptor type A	Rattus norvegicus	116-119
8461044-6	1993	The addition of the phospholipase A2 inhibitors manoalide, mepacrine, or U-26384, or the phospholipase C inhibitor U-73122, reduced the severity of cell injury, but did not maintain cell viability.	Quinacrine	59-68	phospholipase A2 group IB	Homo sapiens	20-36
8500985-9	1993	Mepacrine, a phospholipase A2 inhibitor, completely inhibited PGD2 and LTC4/D4 generation, as well as AA release itself, without affecting serotonin release.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-29
8431204-7	1993	In the presence of either quinacrine, an inhibitor of PLA2 pathway activation, or neomycin, which binds to PI mono- and biphosphate thus blocking their degradation by phospholipases, AA and PGE2 secretion were reduced in a dose-dependent manner.	Quinacrine	26-36	phospholipase A2 group IB	Homo sapiens	54-58
8431204-10	1993	Addition of quinacrine was also demonstrated to abolish the IL-1-induced hydrolysis of PC and PE but not PI, indicating that PC and PE are the preferred substrates for PLA2 enzymatic activity in human synovial cells.	Quinacrine	12-22	phospholipase A2 group IB	Homo sapiens	168-172
8450566-5	1993	Treatment of cells with the phospholipase A2 inhibitor mepacrine (30 microM) inhibited basal (by 50%) and IL-1 stimulated (by 80%) NGF secretion.	Quinacrine	55-64	phospholipase A2 group IB	Rattus norvegicus	28-44
8424665-0	1993	Study of the mechanism of MF1 ATPase inhibition by fluorosulfonylbenzoyl inosine, quinacrine mustard, and efrapeptin using intermediate 18O exchange as a probe.	Quinacrine	82-92	flap structure-specific endonuclease 1	Homo sapiens	26-29
8424665-1	1993	The mitochondrial F1-ATPase (MF1) is known to be largely or totally inhibited by combination or reaction with one fluorosulfonylbenzoyl inosine (FSBI), quinacrine mustard, or efrapeptin per enzyme.	Quinacrine	152-162	flap structure-specific endonuclease 1	Homo sapiens	4-27
8424665-1	1993	The mitochondrial F1-ATPase (MF1) is known to be largely or totally inhibited by combination or reaction with one fluorosulfonylbenzoyl inosine (FSBI), quinacrine mustard, or efrapeptin per enzyme.	Quinacrine	152-162	flap structure-specific endonuclease 1	Homo sapiens	29-32
8215907-3	1993	Quinacrine (QUIN) is a well known inhibitor of PLA2.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	47-51
8215907-3	1993	Quinacrine (QUIN) is a well known inhibitor of PLA2.	Quinacrine	12-16	phospholipase A2 group IB	Homo sapiens	47-51
8215907-7	1993	QUIN concentrations in liver at times from 1 to 24 h are well over those required to inhibit PLA2 activity.	Quinacrine	0-4	phospholipase A2 group IB	Homo sapiens	93-97
8478207-0	1993	Ageing before mating and quinacrine ameliorate the expression of abnormal oocyte (abo) in homozygous Drosophila melanogaster females.	Quinacrine	25-35	abnormal oocyte	Drosophila melanogaster	65-80
8478207-0	1993	Ageing before mating and quinacrine ameliorate the expression of abnormal oocyte (abo) in homozygous Drosophila melanogaster females.	Quinacrine	25-35	abnormal oocyte	Drosophila melanogaster	82-85
8429273-5	1993	The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion.	Quinacrine	38-48	phospholipase A2 group IB	Rattus norvegicus	4-20
8429273-5	1993	The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion.	Quinacrine	38-48	phospholipase A2 group IB	Rattus norvegicus	22-26
8429273-5	1993	The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion.	Quinacrine	38-48	phospholipase A2 group IB	Rattus norvegicus	152-156
8445334-10	1993	Phospholipase inhibitors (4-bromophenacylbromide and mepacrine) added to the culture medium completely prevented the ox-LDL-induced stimulation of phosphatidylinositol degradation, [3H]arachidonate release, and PAI-1 secretion.	Quinacrine	53-62	serpin family E member 1	Homo sapiens	211-216
1335253-3	1992	The phospholipase A2 inhibitors p-bromophenacyl bromide and mepacrine did not affect the basal and ouabain-induced release, but dose-dependently blocked PGE2-evoked phosphoinositide metabolism and the consequent catecholamine release at an IC50 value of 3 microM.	Quinacrine	60-69	LOC104974671	Bos taurus	4-20
1295883-3	1992	BW755C, a dual inhibitor of cyclooxygenase and lipoxygenase, as well as p-bromophenacyl bromide and mepacrine, inhibitors of phospholipase A2, inhibited the aggregation induced by low concentrations of PASA, but not that induced by high concentrations.	Quinacrine	100-109	phospholipase A2	Oryctolagus cuniculus	125-141
1474344-5	1992	The effect of ET-1 was attenuated in the presence of the phospholipase A2 inhibitor quinacrine.	Quinacrine	84-94	endothelin 1	Homo sapiens	14-18
1474344-5	1992	The effect of ET-1 was attenuated in the presence of the phospholipase A2 inhibitor quinacrine.	Quinacrine	84-94	phospholipase A2 group IB	Homo sapiens	57-73
8290803-0	1993	Quinacrine-induced pleural inflammation in malignant pleurisy: relation between drainage time of pleural fluid and local interleukin-1 beta levels.	Quinacrine	0-10	interleukin 1 beta	Homo sapiens	121-139
8290803-2	1993	IL-1 beta levels increased significantly within 24 h after the instillation of quinacrine (p < 0.001).	Quinacrine	79-89	interleukin 1 beta	Homo sapiens	0-9
1332872-3	1992	Quinacrine (K0.5 = 6.7 x 10(-6) M, nH = 0.84, k-1 increased) inhibits the binding allosterically by an action compatible with binding to one site.	Quinacrine	0-10	keratin 1	Rattus norvegicus	46-49
1443868-5	1992	Diphenylamine-2-carboxylate, Cl-free medium, indomethacin, the phospholipase A2 inhibitor mepacrine, and the methyltransferase inhibitor 3-deazaadenosine reduced the change in ISC, whereas amiloride and the lipoxygenase inhibitor AA-861 did not.	Quinacrine	90-99	phospholipase A2 group IB	Canis lupus familiaris	63-79
1331280-0	1992	Mepacrine inhibits fMLP-induced activation of human neutrophil granulocytes, leukotriene B4 formation, and fMLP binding.	Quinacrine	0-9	formyl peptide receptor 1	Homo sapiens	19-23
1331280-0	1992	Mepacrine inhibits fMLP-induced activation of human neutrophil granulocytes, leukotriene B4 formation, and fMLP binding.	Quinacrine	0-9	formyl peptide receptor 1	Homo sapiens	107-111
1331280-2	1992	The present experiments were designed to study the effects of mepacrine on human neutrophils challenged with N-formylmethionyl-leucyl-phenylalanine (fMLP).	Quinacrine	62-71	formyl peptide receptor 1	Homo sapiens	149-153
1331280-3	1992	Mepacrine inhibited fMLP-induced superoxide production and degranulation in a dose-dependent manner with Kd values of 2.3 +/- 0.5 x 10(-7) M and 5.7 +/- 1.3 x 10(-6) M, respectively.	Quinacrine	0-9	formyl peptide receptor 1	Homo sapiens	20-24
1331280-7	1992	Furthermore, mepacrine inhibited the specific binding of [3H]fMLP to neutrophils with a Ki value of 1.4 +/- 0.4 x 10(-5) M. Mepacrine decreased the receptor binding affinity without altering the number of receptors.	Quinacrine	13-22	formyl peptide receptor 1	Homo sapiens	61-65
1331280-7	1992	Furthermore, mepacrine inhibited the specific binding of [3H]fMLP to neutrophils with a Ki value of 1.4 +/- 0.4 x 10(-5) M. Mepacrine decreased the receptor binding affinity without altering the number of receptors.	Quinacrine	124-133	formyl peptide receptor 1	Homo sapiens	61-65
1331280-8	1992	These findings demonstrate that the inhibitory effect of mepacrine is response dependent and suggest that this action of mepacrine could, in part, be attributed to a decrease in fMLP receptor affinity.	Quinacrine	57-66	formyl peptide receptor 1	Homo sapiens	178-191
1331280-8	1992	These findings demonstrate that the inhibitory effect of mepacrine is response dependent and suggest that this action of mepacrine could, in part, be attributed to a decrease in fMLP receptor affinity.	Quinacrine	121-130	formyl peptide receptor 1	Homo sapiens	178-191
1400315-8	1992	Moreover, phospholipase A2 inhibitors (p-bromophenacyl bromide and mepacrine) block the transacetylation process in whole cell system.	Quinacrine	67-76	phospholipase A2 group IB	Homo sapiens	10-26
1396679-8	1992	The effect of thrombin on carbohydrate output was also blocked by a phospholipase A2 inhibitor (quinacrine, 50 microM) and by an inhibitor of the cyclooxygenase (indomethacin, 20 microM), suggesting the involvement of cyclooxygenase in the mechanism of action of thrombin.	Quinacrine	96-106	coagulation factor II	Rattus norvegicus	14-22
1396679-8	1992	The effect of thrombin on carbohydrate output was also blocked by a phospholipase A2 inhibitor (quinacrine, 50 microM) and by an inhibitor of the cyclooxygenase (indomethacin, 20 microM), suggesting the involvement of cyclooxygenase in the mechanism of action of thrombin.	Quinacrine	96-106	phospholipase A2 group IB	Rattus norvegicus	68-84
1382129-2	1992	We evaluated the cardioprotective activity of two putative PLA2 inhibitors, quinacrine and 7,7-dimethyleicosadienoic acid (DEDA), in isolated globally ischemic rat hearts.	Quinacrine	76-86	phospholipase A2 group IB	Rattus norvegicus	59-63
1405334-5	1992	Mepacrine, a phospholipase A inhibitor, prevented TNF-beta stimulation of 3H release from 3H-arachidonic acid labeled cells and TNF-beta potentiation of adenylate cyclase activity.	Quinacrine	0-9	lymphotoxin alpha	Sus scrofa	50-58
1405334-5	1992	Mepacrine, a phospholipase A inhibitor, prevented TNF-beta stimulation of 3H release from 3H-arachidonic acid labeled cells and TNF-beta potentiation of adenylate cyclase activity.	Quinacrine	0-9	lymphotoxin alpha	Sus scrofa	128-136
1386368-6	1992	The phospholipase A2 inhibitor, mepacrine, had no effect on AVP-mediated AA release, but abolished the synergistic action of EGF-URO.	Quinacrine	32-41	phospholipase A2 group IB	Rattus norvegicus	4-20
1329113-5	1992	Quinacrine, a phospholipase A2 inhibitor, suppressed the PGE2-induced AA release but had little effect on the IP3 formation.	Quinacrine	0-10	phospholipase A2, group IB, pancreas	Mus musculus	14-30
1322564-3	1992	METHODS: Sprague-Dawley rats were pretreated with a PLA2 inhibitor, quinacrine (10 mg/kg, intravenously), before the induction of gut ischemia (45 minutes of superior mesenteric artery occlusion) followed by 6 hours of reperfusion.	Quinacrine	68-78	phospholipase A2 group IB	Rattus norvegicus	52-56
1382379-2	1992	Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms).	Quinacrine	183-192	phospholipase A2 group IB	Rattus norvegicus	13-29
1327821-10	1992	The dilator activity of scoparone was also inhibited by quinacrine (inhibitor of phospholipase A2) and indomethacin (inhibitor of cyclooxygenase).	Quinacrine	56-66	phospholipase A2 group IB	Rattus norvegicus	81-97
1425935-7	1992	The suppressive activity of scoparone was significantly reduced by quinacrine (a phospholipase A2 inhibitor), indomethacin (a cyclooxygenase inhibitor) and nordihydroguaiaretic acid (a lipoxygenase inhibitor).	Quinacrine	67-77	phospholipase A2 group IB	Homo sapiens	81-97
1382379-2	1992	Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms).	Quinacrine	183-192	phospholipase A2 group IB	Rattus norvegicus	31-35
1382379-5	1992	Dose-dependent histamine release by rat peritoneal cells was induced by PLA2 and by lysophosphatidylserine and this effect could be antagonized by aristolochic acid and mepacrine.	Quinacrine	169-178	phospholipase A2 group IB	Rattus norvegicus	72-76
1383617-5	1992	The ET-1-induced potentiation of the response to serotonin was prevented by nordihydroguaiaretic acid (3 x 10(-6) M), quinacrine (10(-6) M), and AA861 (10(-6) M), but not by indomethacin (10(-7) M) and baicalein (10(-6) M).	Quinacrine	118-128	endothelin 1	Rattus norvegicus	4-8
1619039-1	1992	The present work shows that the corticotropin-releasing factor (CRF)-releasing activity of interleukin-1 (IL-1) is partially inhibited by a phospholipase A2 (mepacrine) or a cyclooxygenase (indomethacin) inhibitor, but is not affected by inhibition of the lypoxygenase pathway with norhydroguaiaretic acid.	Quinacrine	158-167	corticotropin releasing hormone	Rattus norvegicus	32-62
1326745-5	1992	ET-1-induced Cl- secretion is completely inhibited by the loop diuretic bumetanide and by indomethacin and quinacrine, inhibitors of prostaglandin synthesis.	Quinacrine	107-117	endothelin-1	Oryctolagus cuniculus	0-4
1427593-8	1992	In Experiment II designed to study the cause of the exercise-induced decrease in PE and PC, intravenous quinacrine was used to inhibit PLA2.	Quinacrine	104-114	phospholipase A2 group IB	Rattus norvegicus	135-139
1427593-14	1992	These results suggest that quinacrine can partially prevent the decrease of phospholipid and partially inhibit the activity of PLA2 after prolonged exercise.	Quinacrine	27-37	phospholipase A2 group IB	Rattus norvegicus	127-131
1330464-2	1992	The phospholipase A2 inhibitor mepacrine at 25 and 50 mumol/l significantly inhibited glucagon secretion induced by 0.1 mumol/l clonidine (P less than 0.01, respectively), whereas 5 mumol/l mepacrine did not affect clonidine-induced glucagon secretion.	Quinacrine	31-40	phospholipase A2 group IB	Rattus norvegicus	4-20
1315360-4	1992	CD69-induced arachidonic acid release and TXA2 production were essentially PLA2 dependent because they could be blocked by the PLA2 inhibitor quinacrine.	Quinacrine	142-152	CD69 molecule	Homo sapiens	0-4
1332181-2	1992	Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release.	Quinacrine	75-85	phospholipase A2 group IB	Rattus norvegicus	60-64
1332181-2	1992	Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release.	Quinacrine	75-85	thyrotropin releasing hormone	Rattus norvegicus	99-128
1332181-2	1992	Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release.	Quinacrine	75-85	thyrotropin releasing hormone	Rattus norvegicus	130-133
1332181-2	1992	Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release.	Quinacrine	75-85	vasoactive intestinal peptide	Rattus norvegicus	170-173
1315360-4	1992	CD69-induced arachidonic acid release and TXA2 production were essentially PLA2 dependent because they could be blocked by the PLA2 inhibitor quinacrine.	Quinacrine	142-152	phospholipase A2 group IB	Homo sapiens	75-79
1315360-4	1992	CD69-induced arachidonic acid release and TXA2 production were essentially PLA2 dependent because they could be blocked by the PLA2 inhibitor quinacrine.	Quinacrine	142-152	phospholipase A2 group IB	Homo sapiens	127-131
1315360-6	1992	Finally, direct measurement of enzymatic activity in vitro using radiolabeled phospholipid vesicles showed that CD69 cross-linking resulted in PLA2-dependent arachidonic acid and lysophosphatidylcholine generation from phosphatidylcholine, which was sensitive to quinacrine but not to R68070.	Quinacrine	263-273	CD69 molecule	Homo sapiens	112-116
1315360-6	1992	Finally, direct measurement of enzymatic activity in vitro using radiolabeled phospholipid vesicles showed that CD69 cross-linking resulted in PLA2-dependent arachidonic acid and lysophosphatidylcholine generation from phosphatidylcholine, which was sensitive to quinacrine but not to R68070.	Quinacrine	263-273	phospholipase A2 group IB	Homo sapiens	143-147
1315576-4	1992	The production of arachidonic acid is not inhibited by neomycin, a PI-cycle inhibitor, but is completely abolished by mepacrine, an inhibitor of both phospholipase A2 and C. At low concentration of fluoroaluminate (10 mM NaF) phospholipase A2 but not phospholipase C is activated.	Quinacrine	118-127	phospholipase A2 group IB	Homo sapiens	150-166
1349027-6	1992	To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP.	Quinacrine	127-136	phospholipase A2 group IB	Rattus norvegicus	94-110
1349027-6	1992	To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP.	Quinacrine	127-136	phospholipase A2 group IB	Rattus norvegicus	112-116
1349027-6	1992	To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP.	Quinacrine	127-136	phospholipase A2 group IB	Rattus norvegicus	140-144
1373616-1	1992	In intact rat pancreatic acini, the phospholipase A2 inhibitor mepacrine did not affect basal amylase release but dose-dependently inhibited the carbachol (IC50 65 microM) and CCK-8 (IC50 210 microM)-stimulated amylase release.	Quinacrine	63-72	phospholipase A2 group IB	Rattus norvegicus	36-52
1563542-5	1992	Chloroquine and quinacrine treatment also increases the insulin receptor content of endosomal fractions and, in rats injected by native insulin, the ligand-induced accumulation of receptors in endosomal fractions at late times after injection.	Quinacrine	16-26	insulin receptor	Rattus norvegicus	56-72
12106434-4	1992	The ET-1-evoked release of AA probably resulted from the activation of a phospholipase A2, since it required extracellular Ca2+ and was prevented by mepacrine but not by RHC 80267, an inhibitor of diacylglycerol lipase.	Quinacrine	149-158	phospholipase A2, group IB, pancreas	Mus musculus	73-89
1640804-5	1992	The possibility that NMDA receptor mediated activation of phospholipase A2 and release of arachidonic acid might mediate this ODC response was investigated in this study by treatment with the phospholipase inhibitors quinacrine and dexamethasone.	Quinacrine	217-227	phospholipase A2 group IB	Homo sapiens	58-74
1640804-5	1992	The possibility that NMDA receptor mediated activation of phospholipase A2 and release of arachidonic acid might mediate this ODC response was investigated in this study by treatment with the phospholipase inhibitors quinacrine and dexamethasone.	Quinacrine	217-227	ornithine decarboxylase 1	Homo sapiens	126-129
1640804-6	1992	Treatment of animals with quinacrine (100 mg/kg) at the time of injection of kainate into the nucleus basalis caused a significant attenuation of the induction of ODC in cerebral cortex of 43%.	Quinacrine	26-36	ornithine decarboxylase 1	Homo sapiens	163-166
1426529-8	1992	The release of arachidonate was blocked by quinacrine which is a specific inhibitor of phospholipase A2.	Quinacrine	43-53	phospholipase A2 group IB	Homo sapiens	87-103
1583386-6	1992	In platelets prelabeled with tritiated arachidonic acid, H2O2 induced tritium release in a dose-dependent fashion; this effect was prevented by mepacrine, an inhibitor of the phospholipase A2 enzyme.	Quinacrine	144-153	phospholipase A2 group IB	Homo sapiens	175-191
1315576-6	1992	Under identical conditions both neomycin and mepacrine suppress the release of arachidonic acid and beta-TG induced by thrombin.	Quinacrine	45-54	pro-platelet basic protein	Homo sapiens	100-107
1315576-6	1992	Under identical conditions both neomycin and mepacrine suppress the release of arachidonic acid and beta-TG induced by thrombin.	Quinacrine	45-54	coagulation factor II, thrombin	Homo sapiens	119-127
1312031-3	1992	However, a decrease in cytoplasmic pH was accompanied by an increase in phospholipase A2 activity; (iii) membrane cholesterol-modulated changes in intra-platelet pH, as well as phospholipase A2 activity, was completely inhibited when platelets were pretreated with quinacrine (a specific phospholipase A2 inhibitor) before exposure to various types of liposomes.	Quinacrine	265-275	phospholipase A2 group IB	Homo sapiens	177-193
1312031-3	1992	However, a decrease in cytoplasmic pH was accompanied by an increase in phospholipase A2 activity; (iii) membrane cholesterol-modulated changes in intra-platelet pH, as well as phospholipase A2 activity, was completely inhibited when platelets were pretreated with quinacrine (a specific phospholipase A2 inhibitor) before exposure to various types of liposomes.	Quinacrine	265-275	phospholipase A2 group IB	Homo sapiens	177-193
1521562-1	1992	Using a perfused rat hindleg system, release of tissue-type plasminogen activator (t-PA) from endothelial cells could be induced by platelet-activating factor (PAF), bradykinin, substance P, thrombin, carbachol and A23187, while this release was inhibited by mepacrine and by nor-dihydroguaiaretic acid.	Quinacrine	259-268	plasminogen activator, tissue type	Rattus norvegicus	48-81
1521562-1	1992	Using a perfused rat hindleg system, release of tissue-type plasminogen activator (t-PA) from endothelial cells could be induced by platelet-activating factor (PAF), bradykinin, substance P, thrombin, carbachol and A23187, while this release was inhibited by mepacrine and by nor-dihydroguaiaretic acid.	Quinacrine	259-268	plasminogen activator, tissue type	Rattus norvegicus	83-87
1355446-5	1992	NMDA-evoked arachidonic acid release was inhibited by MK-801 and TCP (two NMDA receptor-type antagonists), or by mepacrine, an inhibitor of phospholipase A2.	Quinacrine	113-122	phospholipase A2 group IB	Rattus norvegicus	140-156
1537295-6	1992	PTH secretion inhibited by 2 mM Ca2+ was restored by two PL-A2 inhibitors, indomethacin (30 microM) and mepacrine (50 microM).	Quinacrine	104-113	parathyroid hormone	Homo sapiens	0-3
1537295-6	1992	PTH secretion inhibited by 2 mM Ca2+ was restored by two PL-A2 inhibitors, indomethacin (30 microM) and mepacrine (50 microM).	Quinacrine	104-113	phospholipase A2 group IB	Homo sapiens	57-62
1400612-6	1992	Quinacrine, a phospholipase A2 inhibitor, showed partial inhibitory effect on PGF2 alpha-induced AA release, while it suppressed the amplification by OAG of PGF2 alpha-induced AA release almost to the control level.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	14-30
1375638-16	1992	The combined application of a cyclo-oxygenase inhibitor, indomethacin (50 microM), and a lipoxygenase inhibitor, esculetin (100 microM), increased the Cl- current, whereas the administration of a phospholipase A2 inhibitor, mepacrine (100 microM), significantly decreased the whole-cell Cl- current.	Quinacrine	224-233	polyunsaturated fatty acid lipoxygenase ALOX15	Oryctolagus cuniculus	89-101
1311959-7	1992	The increase in [Ca2+]i elicited by ATP apparently caused the activation of a calmodulin-dependent phospholipase A2 since trifluoperazine, an inhibitor of calmodulin, and quinacrine, an inhibitor of phospholipase A2, prevented the stimulation of PGI2 release by ATP.	Quinacrine	171-181	LOC104974671	Bos taurus	99-115
1311959-7	1992	The increase in [Ca2+]i elicited by ATP apparently caused the activation of a calmodulin-dependent phospholipase A2 since trifluoperazine, an inhibitor of calmodulin, and quinacrine, an inhibitor of phospholipase A2, prevented the stimulation of PGI2 release by ATP.	Quinacrine	171-181	LOC104974671	Bos taurus	199-215
1320593-1	1992	We examined the effect of quinacrine, an anti-malarial drug which inhibits phospholipase A2, on phorbol myristate acetate (PMA) stimulated alveolar macrophage oxygen radical secretion.	Quinacrine	26-36	phospholipase A2 group IB	Homo sapiens	75-91
1311688-4	1992	This conclusion is supported by our findings that inhibition of GTPase by mepacrine amplified bradykinin-stimulated Ca2+ influx, but did not interfere with the effect of the Ca2+ ionophore A23187.	Quinacrine	74-83	kininogen 1	Homo sapiens	94-104
1311688-5	1992	Similar to its effect on Ca2+ influx, mepacrine also potentiated endothelium-derived relaxing factor (EDRF) formation by bradykinin and sodium fluoride, but did not affect A23187-induced EDRF biosynthesis.	Quinacrine	38-47	alpha hemoglobin stabilizing protein	Homo sapiens	102-106
1311688-5	1992	Similar to its effect on Ca2+ influx, mepacrine also potentiated endothelium-derived relaxing factor (EDRF) formation by bradykinin and sodium fluoride, but did not affect A23187-induced EDRF biosynthesis.	Quinacrine	38-47	kininogen 1	Homo sapiens	121-131
1727652-6	1992	Another phospholipase A2 inhibitor, mepacrine, poorly inhibited both microsomal and pool-B"-promoted lipid peroxidation, but did block both iron-ascorbate-driven and ABAP-promoted lipid peroxidation.	Quinacrine	36-45	phospholipase A2 group IB	Homo sapiens	8-24
1315576-4	1992	The production of arachidonic acid is not inhibited by neomycin, a PI-cycle inhibitor, but is completely abolished by mepacrine, an inhibitor of both phospholipase A2 and C. At low concentration of fluoroaluminate (10 mM NaF) phospholipase A2 but not phospholipase C is activated.	Quinacrine	118-127	phospholipase A2 group IB	Homo sapiens	226-242
1662619-4	1991	Three lines of evidence indicate phospholipase A2 activity to be involved in arachidonic acid release: (a) its inhibition by mepacrine, (b) the concomitant generation of lysophosphatidylcholine from [3H]choline-labeled cells and (c) an increase in arachidonic acid release from 14C-labeled phosphatidylcholine in particulate fractions from PMA-treated and bradykinin-treated keratinocytes.	Quinacrine	125-134	phospholipase A2, group IB, pancreas	Mus musculus	33-49
21043868-7	1992	Furthermore this activation seems to be dependent on arachidonic acid mobilization from platelet phospholipids by phospholipase A(2) since mepacrine is able to block H(2)O(2)-mediated platelet activation.	Quinacrine	139-148	phospholipase A2 group IB	Homo sapiens	114-131
1721808-2	1991	Mepacrine, a known inhibitor of phospholipase A2, at concentrations below 10(-5) M and anti-rat 14-kDa group II phospholipase A2 antibody inhibited histamine release, while they did not affect the prostaglandin generation.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	32-48
1667913-8	1991	Quinacrine (phospholipase A2 inhibitor), indomethacin (cyclooxygenase inhibitor) and nordihydroguaiaretic acid (NDGA, lipoxygenase inhibitor) potentiated the relaxation induced by emodin.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	12-28
1951711-4	1991	The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation.	Quinacrine	222-231	nerve growth factor	Rattus norvegicus	156-159
1951711-4	1991	The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation.	Quinacrine	222-231	nerve growth factor	Rattus norvegicus	191-194
1951711-4	1991	The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation.	Quinacrine	222-231	phospholipase A2 group IB	Rattus norvegicus	267-283
1951711-4	1991	The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation.	Quinacrine	222-231	nerve growth factor	Rattus norvegicus	191-194
1681548-3	1991	It required external calcium and was selectively antagonized by both mepacrine, an inhibitor of phospholipase A2, and 5,8,11,14-eicosatetraynoic acid, a nonmetabolizable analog of arachidonic acid.	Quinacrine	69-78	phospholipase A2 group IB	Homo sapiens	96-112
1910075-3	1991	Quinacrine, an inhibitor of phospholipase A2 (PLA2), suppressed AA release by about 60% and neomycin, a putative inhibitor of phospholipase C (PLC), reduced AA release by about 30%.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	28-44
1811338-6	1991	In addition, the inhibitors of phospholipase A2, quinacrine and 4-bromophenacylbromide, respectively inhibited t-PA production as well as glucocorticoids.	Quinacrine	49-59	plasminogen activator, tissue type	Homo sapiens	111-115
1833985-6	1991	Inhibition of phospholipase A2 (PLA2) activity with quinacrine (100 microM) completely blocked the dopamine-stimulated PGE2 production, whereas inhibition of polyphosphoinositol hydrolysis with neomycin (100 microM) or inhibition of protein kinase C with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM) did not.	Quinacrine	52-62	phospholipase A2 group IB	Rattus norvegicus	14-30
1833985-6	1991	Inhibition of phospholipase A2 (PLA2) activity with quinacrine (100 microM) completely blocked the dopamine-stimulated PGE2 production, whereas inhibition of polyphosphoinositol hydrolysis with neomycin (100 microM) or inhibition of protein kinase C with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM) did not.	Quinacrine	52-62	phospholipase A2 group IB	Rattus norvegicus	32-36
1910075-3	1991	Quinacrine, an inhibitor of phospholipase A2 (PLA2), suppressed AA release by about 60% and neomycin, a putative inhibitor of phospholipase C (PLC), reduced AA release by about 30%.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	46-50
19215501-3	1991	The NMDA-induced effects (arachidonic acid release and somatostatin secretion) were both inhibited by MK-801, an NMDA receptor-type antagonist, or mepacrine, a phospholipase A(2) inhibitor.	Quinacrine	147-156	phospholipase A and acyltransferase 1	Homo sapiens	160-175
1720878-1	1991	The release of acetylcholine (ACh) from myenteric plexus evoked by 5-hydroxytryptamine (5-HT) and senktide (a selective neurokinin3 (NK3) agonist) was depressed by mepacrine, an inhibitor for phospholipase A2 activity.	Quinacrine	164-173	phospholipase A2 group IB	Homo sapiens	192-208
1860838-1	1991	A peptide mitogen bombesin, which activates the phospholipase C-protein kinase C signaling pathway, induces a mepacrine-sensitive, dose-dependent increase in the release of [3H]arachidonic acid and its metabolites ([3H]AA) from prelabeled Swiss 3T3 fibroblasts.	Quinacrine	110-119	gastrin releasing peptide	Homo sapiens	18-26
2018523-2	1991	Ram sperm PLA2 activity was Ca2(+)-dependent and was inhibited by dexamethasone, chloracysine and compounds Ro 31-4493 and Ro 31-4639; mepacrine, however, did not inhibit PLA2 activity.	Quinacrine	135-144	phospholipase A2 group IB	Homo sapiens	10-14
1934272-0	1991	Dose-dependent enhancing effects of quinacrine on induction of preneoplastic glutathione S-transferase placental form positive liver cell foci in male F344 rats.	Quinacrine	36-46	hematopoietic prostaglandin D synthase	Rattus norvegicus	77-102
1934272-7	1991	The numbers and unit areas of GST-P-positive foci per cm2 were significantly increased in the DEN/quinacrine (500 p.p.m.)	Quinacrine	98-108	glutathione S-transferase pi 1	Rattus norvegicus	30-35
1934272-13	1991	The results thus demonstrated that quinacrine treatment enhances GST-P-positive liver cell foci development in a dose-dependent way, this effect presumably being related to the induction of lipidosis.	Quinacrine	35-45	glutathione S-transferase pi 1	Rattus norvegicus	65-70
1933128-4	1991	Nordihydroguaiaretic acid (NDGA; 5 x 10(-6) M), an inhibitor of lipoxygenase and quinacrine (10(-5) M), which blocks the release of arachidonic acid from phospholipids by inhibiting the enzyme phospholipase A2, blocked hypoxia-induced contractions.	Quinacrine	81-91	phospholipase A2 group IB	Canis lupus familiaris	193-209
1944607-2	1991	In the preparation with the submucosal plexus, quinacrine and indomethacin completely blocked the effect of melittin, indicating activation of phospholipase A2 and production of prostaglandins induced by the drug.	Quinacrine	47-57	phospholipase A2 group IB	Rattus norvegicus	143-159
1944607-8	1991	The results provide evidence for the presence of a quinacrine-sensitive phospholipase A2 in the preparation with and that without the submucosa.	Quinacrine	51-61	phospholipase A2 group IB	Rattus norvegicus	72-88
2009286-5	1991	Mepacrine, a membrane stabilizer and a phospholipase inhibitor, reduced the release of H-FABP from the heart and prevented the accumulation of nonesterified fatty acids in the tissue during ischemia and reperfusion.	Quinacrine	0-9	fatty acid binding protein 3	Rattus norvegicus	87-93
2010033-10	1991	NGF-like immunoreactivity colocalized to cells containing quinacrine fluorescence in situ and in vitro.	Quinacrine	58-68	nerve growth factor	Rattus norvegicus	0-3
1848278-9	1991	Moreover, the inhibitory effect of 8-OH-DPAT on the carbachol response was blocked by 10 microM quinacrine (a phospholipase A2 inhibitor) but not by BW 755C (100 microM), a cyclooxygenase and lipoxygenase inhibitor.	Quinacrine	96-106	phospholipase A2 group IB	Rattus norvegicus	110-126
1901939-7	1991	This concentration- and time-dependent effect of Et3PbCl might be due to a stimulated liberation of fatty acids via phospholipase A2, because this stimulation could be totally prevented by the phospholipase inhibitors quinacrine and p-bromophenacylbromide.	Quinacrine	218-228	phospholipase A2 group IB	Homo sapiens	116-132
1646955-5	1991	On the other hand, the L(+)-lactate-evoked supersensitivity could be blocked by the phospholipase A2 inhibitors mepacrine and n-bromophenacyl-bromide, suggesting an involvement of phospholipase A2 in the process of beta-adrenergic sensitization.	Quinacrine	112-121	phospholipase A2 group IB	Rattus norvegicus	84-100
1646955-5	1991	On the other hand, the L(+)-lactate-evoked supersensitivity could be blocked by the phospholipase A2 inhibitors mepacrine and n-bromophenacyl-bromide, suggesting an involvement of phospholipase A2 in the process of beta-adrenergic sensitization.	Quinacrine	112-121	phospholipase A2 group IB	Rattus norvegicus	180-196
2095437-3	1990	Cumene hydroperoxide-induced damage was reduced or prevented by several compounds: the application of Trolox C, a water-soluble vitamin E analogue, and of phospholipase A2 inhibitors chlorpromazine and (to a lesser extent) quinacrine prevented alpha-HBDH release.	Quinacrine	223-233	phospholipase A2 group IB	Rattus norvegicus	155-171
1869120-1	1991	Intrapleural instillation of quinacrine HC1 (Atabrine) was used to treat spontaneous pneumothorax in 2 young men, aged 26 and 36 years, respectively, with advanced pulmonary disease due to cystic fibrosis.	Quinacrine	29-39	CYCS pseudogene 39	Homo sapiens	40-43
1869120-1	1991	Intrapleural instillation of quinacrine HC1 (Atabrine) was used to treat spontaneous pneumothorax in 2 young men, aged 26 and 36 years, respectively, with advanced pulmonary disease due to cystic fibrosis.	Quinacrine	45-53	CYCS pseudogene 39	Homo sapiens	40-43
1905234-2	1991	Gly-Gln but not the related dipeptide, glycyl-glutamic acid, caused a 2-fold elevation of AAM release which was blocked in the absence of extracellular calcium, in the presence of 5 mM magnesium and by the phospholipase A2 (PLA2) inhibitor, mepacrine.	Quinacrine	241-250	phospholipase A2, group IB, pancreas	Mus musculus	206-222
1845801-6	1991	Moreover, the bradykinin-induced arachidonic acid release was unaffected by pertussis toxin and markedly inhibited by two treatments ineffective on glucose transport, the blockade of [Ca2+]i increases elicited by the peptide and the administration of the phospholipase A2 blocker, quinacrine.	Quinacrine	281-291	kininogen 1	Homo sapiens	14-24
1937914-1	1991	In a test of adoptive cutaneous anaphylaxis, the influence of the phospholipase A2 inhibitor mepacrine, on the intensity of the local anaphylactic reaction was investigated in the skin of recipients following intracutaneous injection of syngenic immune splenocytes.	Quinacrine	93-102	phospholipase A2 group IB	Homo sapiens	66-82
1659882-8	1991	Similarly, the PLA2 inhibitors quinacrine, dexamethasone and corticosterone, added to the Leydig cells in vitro, inhibited LH-stimulated testosterone production but not cyclic AMP production.	Quinacrine	31-41	phospholipase A2 group IB	Rattus norvegicus	15-19
1649917-9	1991	5) A phospholipase A2 (PL A2) inhibitor, quinacrine, significantly depressed the endothelin-induced contractions, suggesting a possible involvement of PL A2.	Quinacrine	41-51	LOC104974671	Bos taurus	5-21
1649917-9	1991	5) A phospholipase A2 (PL A2) inhibitor, quinacrine, significantly depressed the endothelin-induced contractions, suggesting a possible involvement of PL A2.	Quinacrine	41-51	LOC104974671	Bos taurus	23-28
1649917-9	1991	5) A phospholipase A2 (PL A2) inhibitor, quinacrine, significantly depressed the endothelin-induced contractions, suggesting a possible involvement of PL A2.	Quinacrine	41-51	LOC104974671	Bos taurus	151-156
1823713-4	1991	Under the same condition, the release of PAF was also inhibited by mepacrine at 100 mumol/L.	Quinacrine	67-76	PCNA clamp associated factor	Rattus norvegicus	41-44
2172463-2	1990	The agonist-induced [3H]AA release was reduced by quinacrine at concentrations that inhibited phospholipase A2 (PLA2) but affected neither the activity of phospholipase C (PLC) nor the hydrolysis of phosphoinositides induced by glutamate or quisqualate.	Quinacrine	50-60	phospholipase A2 group IB	Homo sapiens	94-110
2172463-2	1990	The agonist-induced [3H]AA release was reduced by quinacrine at concentrations that inhibited phospholipase A2 (PLA2) but affected neither the activity of phospholipase C (PLC) nor the hydrolysis of phosphoinositides induced by glutamate or quisqualate.	Quinacrine	50-60	phospholipase A2 group IB	Homo sapiens	112-116
2264993-9	1990	Quinacrine was a noncompetitive PLA2 inhibitor with Kis for low- and high-Km activities of 0.42 mM and 0.49 mM, respectively.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	32-36
1663633-7	1991	Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs.	Quinacrine	75-84	phospholipase A2 group IB	Rattus norvegicus	41-57
1663633-7	1991	Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs.	Quinacrine	75-84	phospholipase A2 group IB	Rattus norvegicus	59-63
2249891-6	1990	While the 2 phospholipase A2 inhibitors, quinacrine and dexamethasone, were efficient in inhibiting TNF-mediated cell lysis, only quinacrine was efficient in selectively abrogating the TNF/VP-16 cell killing pathway.	Quinacrine	41-51	tumor necrosis factor	Mus musculus	100-103
2249891-6	1990	While the 2 phospholipase A2 inhibitors, quinacrine and dexamethasone, were efficient in inhibiting TNF-mediated cell lysis, only quinacrine was efficient in selectively abrogating the TNF/VP-16 cell killing pathway.	Quinacrine	130-140	tumor necrosis factor	Mus musculus	185-188
2249891-7	1990	The inhibitory effect of quinacrine on VP-16/TNF-mediated cell lysis was accompanied by a marked decrease in VP-16-mediated DNA single-strand break generation.	Quinacrine	25-35	tumor necrosis factor	Mus musculus	45-48
2090584-4	1990	Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was blocked (50%) by phospholipase A2 (PLA2) inhibitors quinacrine and dimethyleicosadienoic acid at 5 min.	Quinacrine	111-121	phospholipase A2 group IB	Rattus norvegicus	76-92
2090584-4	1990	Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was blocked (50%) by phospholipase A2 (PLA2) inhibitors quinacrine and dimethyleicosadienoic acid at 5 min.	Quinacrine	111-121	phospholipase A2 group IB	Rattus norvegicus	94-98
2254900-5	1990	Further, chondrocyte PLA2 was sensitive to inhibition by mepacrine, a compound with PLA2 inhibitory activity.	Quinacrine	57-66	phospholipase A2	Oryctolagus cuniculus	21-25
2254900-5	1990	Further, chondrocyte PLA2 was sensitive to inhibition by mepacrine, a compound with PLA2 inhibitory activity.	Quinacrine	57-66	phospholipase A2	Oryctolagus cuniculus	84-88
2241906-2	1990	Pre-treatment with the phospholipase A2 inhibitors mepacrine or dexamethasone prevented this stimulation and decreased the release of prostaglandin F2 alpha, implicating the action of phospholipase A2 and the subsequent metabolism of arachidonic acid to prostaglandins in the stimulation of protein synthesis by physiological doses of insulin.	Quinacrine	51-60	phospholipase A2 group IB	Homo sapiens	23-39
2241906-2	1990	Pre-treatment with the phospholipase A2 inhibitors mepacrine or dexamethasone prevented this stimulation and decreased the release of prostaglandin F2 alpha, implicating the action of phospholipase A2 and the subsequent metabolism of arachidonic acid to prostaglandins in the stimulation of protein synthesis by physiological doses of insulin.	Quinacrine	51-60	phospholipase A2 group IB	Homo sapiens	184-200
2241906-2	1990	Pre-treatment with the phospholipase A2 inhibitors mepacrine or dexamethasone prevented this stimulation and decreased the release of prostaglandin F2 alpha, implicating the action of phospholipase A2 and the subsequent metabolism of arachidonic acid to prostaglandins in the stimulation of protein synthesis by physiological doses of insulin.	Quinacrine	51-60	insulin	Homo sapiens	335-342
2241906-3	1990	Higher concentrations of insulin (500-1000 mu-units/ml) stimulated protein synthesis in the presence of mepacrine or dexamethasone, suggesting that an alternative pathway may become important in insulin action when phospholipase A2 is inhibited.	Quinacrine	104-113	insulin	Homo sapiens	25-32
2231411-6	1990	However, melittin-stimulated renin secretion is independent of melittin-stimulated phospholipase A2 activity, arachidonic acid release, and PG synthesis, since 20 microM-quinacrine (a phospholipase A2 antagonist) and 50 microM-meclofenamate (a cyclooxygenase antagonist) antagonized basal and melittin-stimulated PGE2 synthesis but had no effects on basal or melittin-stimulated renin secretion.	Quinacrine	170-180	renin	Rattus norvegicus	29-34
1980544-4	1990	The contraction could be blocked by the cyclooxygenase inhibitor indomethacin and the phospholipase A2 inhibitor quinacrine, suggesting a role for prostaglandins in the response.	Quinacrine	113-123	phospholipase A2 group IB	Rattus norvegicus	86-102
2174147-3	1990	The repolarization has been blunted by the phospholipase A2 inhibitor mepacrine, but not by the cyclooxygenase inhibitor indomethacin.	Quinacrine	70-79	phospholipase A2 group IB	Homo sapiens	43-59
2104489-8	1990	On the same condition PAF release was also significantly inhibited by quinacrine at 500 mumol/L.	Quinacrine	70-80	patchy fur	Mus musculus	22-25
2114045-1	1990	We observed that the growth of human umbilical artery smooth muscle cells was inhibited by the phospholipase A2 inhibitors p-bromophenacylbromide and mepacrine.	Quinacrine	150-159	phospholipase A2 group IB	Homo sapiens	95-111
2156930-7	1990	In contrast, there was no detectable effect of LPS on activation of protein kinase C. We also demonstrate that inhibition of phospholipase A2 activity with bromophenacyl bromide or quinacrine blocks the induction of TNF transcripts by LPS.	Quinacrine	181-191	phospholipase A2 group IB	Homo sapiens	125-141
2156930-7	1990	In contrast, there was no detectable effect of LPS on activation of protein kinase C. We also demonstrate that inhibition of phospholipase A2 activity with bromophenacyl bromide or quinacrine blocks the induction of TNF transcripts by LPS.	Quinacrine	181-191	tumor necrosis factor	Homo sapiens	216-219
2156930-7	1990	In contrast, there was no detectable effect of LPS on activation of protein kinase C. We also demonstrate that inhibition of phospholipase A2 activity with bromophenacyl bromide or quinacrine blocks the induction of TNF transcripts by LPS.	Quinacrine	181-191	interferon regulatory factor 6	Homo sapiens	235-238
2107184-7	1990	The PLase inhibitors--quinacrine, hydrocortisone, dexamethasone, and indomethacin--were potent inhibitors of LT- and TNF-mediated cell destruction, suggesting that selective deacylation of specific membrane PL by PLase activation is an important step in the events that lead to LT- and TNF-mediated cellular destruction in vitro.	Quinacrine	22-32	tumor necrosis factor	Homo sapiens	117-120
16667359-4	1990	The formation of a proton gradient across the membrane vesicle, measured by quinacrine fluorescence quench, was inhibited about 20% by CaM.	Quinacrine	76-86	calmodulin1	Zea mays	135-138
2123093-2	1990	The phospholipase A2 inhibitors mepacrine, nordihydroguaiaretic acid and indomethacin had no effect on either arachidonic acid release or secretion.	Quinacrine	32-41	LOC104974671	Bos taurus	4-20
2117049-6	1990	Quinacrine, a nonselective phospholipase A2 inhibitor, reduced the carbachol stimulation of adenylate cyclase activity, but this inhibition appeared to be competitive with a Ki of 0.2 microM.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	27-43
2231411-6	1990	However, melittin-stimulated renin secretion is independent of melittin-stimulated phospholipase A2 activity, arachidonic acid release, and PG synthesis, since 20 microM-quinacrine (a phospholipase A2 antagonist) and 50 microM-meclofenamate (a cyclooxygenase antagonist) antagonized basal and melittin-stimulated PGE2 synthesis but had no effects on basal or melittin-stimulated renin secretion.	Quinacrine	170-180	phospholipase A2 group IB	Rattus norvegicus	184-200
1977095-7	1990	A phospholipase A2 inhibitor (10(-6) M, quinacrine) completely abolished the stimulatory effect of GRF on both AA and SRIF release.	Quinacrine	40-50	phospholipase A2 group IB	Rattus norvegicus	2-18
1977095-7	1990	A phospholipase A2 inhibitor (10(-6) M, quinacrine) completely abolished the stimulatory effect of GRF on both AA and SRIF release.	Quinacrine	40-50	growth hormone releasing hormone	Rattus norvegicus	99-102
1974033-7	1990	We find that the IM-augmenting effects of somatostatin are abolished by two substances that can inhibit phospholipase A2, quinacrine and 4-bromophenacyl bromide, and that both arachidonic acid and leukotriene C4 mimic the effects of somatostatin-14 on hippocampal pyramidal neurons in vitro.	Quinacrine	122-132	somatostatin	Homo sapiens	42-54
1974033-7	1990	We find that the IM-augmenting effects of somatostatin are abolished by two substances that can inhibit phospholipase A2, quinacrine and 4-bromophenacyl bromide, and that both arachidonic acid and leukotriene C4 mimic the effects of somatostatin-14 on hippocampal pyramidal neurons in vitro.	Quinacrine	122-132	phospholipase A2 group IB	Homo sapiens	104-120
2115300-7	1990	Mepacrine (10 microM) decreased PLA2 activity by 60% but had no effect on increased Pmann after exposure to A23187.	Quinacrine	0-9	phospholipase A2 group IB	Canis lupus familiaris	32-36
2195545-4	1990	Ethidium bromide, acridine orange, and quinacrine inhibit RecA protein binding to single-stranded DNA.	Quinacrine	39-49	RAD51 recombinase	Homo sapiens	58-62
2162128-4	1990	Nifedipine, Ca2(+)-free medium, indomethacin and the phospholipase A2 inhibitor mepacrine, but not nordihydroguaiaretic acid, reduced the change in CBF.	Quinacrine	80-89	phospholipase A2	Oryctolagus cuniculus	53-69
2111570-5	1990	The phospholipase A2 inhibitor quinacrine was able to prevent the TPA-induced increase in PGE2 synthesis even in the presence of exogenous arachidonic acid suggesting that phospholipase A2 may be a target for PKC action.	Quinacrine	31-41	phospholipase A2 group IB	Homo sapiens	4-20
2111570-5	1990	The phospholipase A2 inhibitor quinacrine was able to prevent the TPA-induced increase in PGE2 synthesis even in the presence of exogenous arachidonic acid suggesting that phospholipase A2 may be a target for PKC action.	Quinacrine	31-41	phospholipase A2 group IB	Homo sapiens	172-188
1968928-4	1990	This release is largely independent of PLC activation and is mediated by a PLA2 because: 1) phosphatidylcholine is the preferential source of [3H]arachidonate release; 2) [3H]arachidonic acid release and phosphatidylcholine hydrolysis are blocked by two inhibitors of solubilized PLA2, mepacrine, and 4-p-bromophenacylbromide; and 3) we evidenced a PLA2 activity in cell homogenates.	Quinacrine	286-295	phospholipase A2 group IB	Homo sapiens	75-79
2105339-6	1990	Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA.	Quinacrine	33-43	phospholipase A2 group IB	Homo sapiens	59-75
2105339-6	1990	Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA.	Quinacrine	33-43	tumor necrosis factor	Homo sapiens	94-97
2105339-6	1990	Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA.	Quinacrine	33-43	colony stimulating factor 1	Homo sapiens	119-124
2105339-6	1990	Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA.	Quinacrine	33-43	arachidonate 5-lipoxygenase	Homo sapiens	242-256
2105339-6	1990	Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA.	Quinacrine	33-43	colony stimulating factor 1	Homo sapiens	307-312
2108808-2	1990	It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine.	Quinacrine	205-214	phospholipase A2 group IB	Rattus norvegicus	35-51
2128431-3	1990	Quinacrine, inhibitor of phospholipase A2 (PLA2), suppressed AA release by 60% and neomycin, inhibitor of phospholipase C (PLC) by about 30%.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	25-41
2128431-3	1990	Quinacrine, inhibitor of phospholipase A2 (PLA2), suppressed AA release by 60% and neomycin, inhibitor of phospholipase C (PLC) by about 30%.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	43-47
2108808-2	1990	It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine.	Quinacrine	205-214	phospholipase A2 group IB	Rattus norvegicus	53-57
2108808-2	1990	It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine.	Quinacrine	205-214	phospholipase A2 group IB	Rattus norvegicus	172-176
34243615-0	2021	Altered expression of ERK, Cytochrome-c, and HSP70 triggers apoptosis in Quinacrine-exposed human invasive ductal carcinoma cells.	Quinacrine	73-83	mitogen-activated protein kinase 1	Homo sapiens	22-25
2097100-2	1990	In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs.	Quinacrine	47-56	phospholipase A2 group IB	Rattus norvegicus	74-90
1636736-7	1992	Conversely, 10 microM of the PLA2 antagonist quinacrine applied apically decreased Po.	Quinacrine	45-55	phospholipase A2	Oryctolagus cuniculus	29-33
34843984-0	2022	NIR irradiation enhances the apoptotic potentiality of Quinacrine-gold hybrid nanoparticles by modulation of HSP-70 in oral cancer stem cells.	Quinacrine	55-65	NOC2 like nucleolar associated transcriptional repressor	Mus musculus	0-3
34843984-0	2022	NIR irradiation enhances the apoptotic potentiality of Quinacrine-gold hybrid nanoparticles by modulation of HSP-70 in oral cancer stem cells.	Quinacrine	55-65	heat shock protein 1B	Mus musculus	109-115
34639002-0	2021	Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway.	Quinacrine	0-10	sirtuin 1	Rattus norvegicus	74-83
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	sirtuin 1	Rattus norvegicus	65-74
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	sirtuin 1	Rattus norvegicus	76-82
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	intercellular adhesion molecule 1	Rattus norvegicus	119-152
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	intercellular adhesion molecule 1	Rattus norvegicus	154-160
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	tumor necrosis factor	Rattus norvegicus	166-193
34639002-8	2021	Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha).	Quinacrine	13-23	tumor necrosis factor	Rattus norvegicus	195-204
34639002-9	2021	Moreover, quinacrine significantly blocked cisplatin-induced apoptosis, which was made evident by downregulating renal apoptotic proteins (BAX and p53) and upregulating the renal anti-apoptotic protein BCL2, compared with the cisplatin group.	Quinacrine	10-20	BCL2 associated X, apoptosis regulator	Rattus norvegicus	139-142
34639002-9	2021	Moreover, quinacrine significantly blocked cisplatin-induced apoptosis, which was made evident by downregulating renal apoptotic proteins (BAX and p53) and upregulating the renal anti-apoptotic protein BCL2, compared with the cisplatin group.	Quinacrine	10-20	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	147-150
34639002-9	2021	Moreover, quinacrine significantly blocked cisplatin-induced apoptosis, which was made evident by downregulating renal apoptotic proteins (BAX and p53) and upregulating the renal anti-apoptotic protein BCL2, compared with the cisplatin group.	Quinacrine	10-20	BCL2, apoptosis regulator	Rattus norvegicus	202-206
34639002-10	2021	In conclusion, this study demonstrates, for the first time, that quinacrine alleviates cisplatin-induced renal toxicity via upregulating SIRT-1, downregulating inflammatory markers (ICAM-1 and TNF-alpha), reducing oxidative stress, and inhibiting apoptosis.	Quinacrine	65-75	sirtuin 1	Rattus norvegicus	137-143
34639002-10	2021	In conclusion, this study demonstrates, for the first time, that quinacrine alleviates cisplatin-induced renal toxicity via upregulating SIRT-1, downregulating inflammatory markers (ICAM-1 and TNF-alpha), reducing oxidative stress, and inhibiting apoptosis.	Quinacrine	65-75	intercellular adhesion molecule 1	Rattus norvegicus	182-188
34639002-10	2021	In conclusion, this study demonstrates, for the first time, that quinacrine alleviates cisplatin-induced renal toxicity via upregulating SIRT-1, downregulating inflammatory markers (ICAM-1 and TNF-alpha), reducing oxidative stress, and inhibiting apoptosis.	Quinacrine	65-75	tumor necrosis factor	Rattus norvegicus	193-202
2303407-5	1990	Phospholipase A2 activity measured in the 1246 cells was inhibited in a dose-dependent fashion by incubation with ONO-RS-082 and quinacrine which are inhibitors of phospholipase A2 activity.	Quinacrine	129-139	phospholipase A2 group IB	Homo sapiens	0-16
2303407-5	1990	Phospholipase A2 activity measured in the 1246 cells was inhibited in a dose-dependent fashion by incubation with ONO-RS-082 and quinacrine which are inhibitors of phospholipase A2 activity.	Quinacrine	129-139	phospholipase A2 group IB	Homo sapiens	164-180
2403930-10	1990	Finally, quinacrine secretion was stimulated by two nutrients with onset times similar to those recorded for [Ca2+]i elevations.	Quinacrine	9-19	carbonic anhydrase 2	Rattus norvegicus	110-113
1703978-4	1990	This enhancement of the release of radioactivity was inhibited by phospholipase A2 inhibitors, quinacrine (1 mM) and p-bromophenacyl bromide (10 microM), suggesting that polyethylenimine and polyallylamine activates phospholipase A2 to generate arachidonate and its metabolites.	Quinacrine	95-105	phospholipase A2 group IB	Rattus norvegicus	66-82
1703978-4	1990	This enhancement of the release of radioactivity was inhibited by phospholipase A2 inhibitors, quinacrine (1 mM) and p-bromophenacyl bromide (10 microM), suggesting that polyethylenimine and polyallylamine activates phospholipase A2 to generate arachidonate and its metabolites.	Quinacrine	95-105	phospholipase A2 group IB	Rattus norvegicus	216-232
2299401-8	1990	The phospholipase A2 inhibitors quinacrine hydrochloride, trifluoperazine, and 4-bromophenacylbromide dose-dependently inhibited potassium depolarization-induced activation of specific 3H-HCh-3 binding in slices of rat brain in vitro.	Quinacrine	32-56	phospholipase A2 group IB	Rattus norvegicus	4-20
2314485-5	1990	Phospholipase A2 inhibitors such as quinacrine and ONO-RS-082 abolished the relaxation induced by ACh but did not affect that by PAF.	Quinacrine	36-46	phospholipase A2 group IB	Rattus norvegicus	0-16
2128375-3	1990	We found that, in normal skin, bradykinin hyperalgesia is inhibited by the phospholipase A2 inhibitor, mepacrine, but not by the phospholipase C inhibitor, neomycin and is mimicked by phospholipase A2.	Quinacrine	103-112	phospholipase A2 group IB	Rattus norvegicus	75-91
2135207-7	1990	The phospholipase A2 (PLA2) inhibitor quinacrine had no significant effect on endothelin-induced contractions.	Quinacrine	38-48	phospholipase A2	Oryctolagus cuniculus	22-26
7843128-14	1994	Quinacrine, which is thought to be an inhibitor of phospholipase A2 (PLA2), prevented the AA liberation from membrane phospholipids induced by organometals.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	51-67
7843128-14	1994	Quinacrine, which is thought to be an inhibitor of phospholipase A2 (PLA2), prevented the AA liberation from membrane phospholipids induced by organometals.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	69-73
34621176-0	2021	Quinacrine Has Preferential Anticancer Effects on Mesothelioma Cells With Inactivating NF2 Mutations.	Quinacrine	0-10	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	87-90
34621176-5	2021	Unexpectedly, we discovered cells with NF2 mutations were very sensitive to quinacrine.	Quinacrine	76-86	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	39-42
34621176-6	2021	This change of quinacrine sensitivity was confirmed by NF2 ectopic expression and knockdown in NF2 mutant and wildtype cell lines, respectively.	Quinacrine	15-25	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	55-58
34621176-6	2021	This change of quinacrine sensitivity was confirmed by NF2 ectopic expression and knockdown in NF2 mutant and wildtype cell lines, respectively.	Quinacrine	15-25	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	95-98
34621176-8	2021	We found quinacrine alters the expression of over 3000 genes in NF2-mutated cells that were significantly different than quinacrine-induced changes in NF2 wildtype cells.	Quinacrine	9-19	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	64-67
34621176-8	2021	We found quinacrine alters the expression of over 3000 genes in NF2-mutated cells that were significantly different than quinacrine-induced changes in NF2 wildtype cells.	Quinacrine	121-131	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	151-154
34621176-10	2021	Additionally, quinacrine induces a G1 phase cell cycle arrest in NF2-mutated cells versus the S phase arrest in NF2-wildtype cells.	Quinacrine	14-24	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	65-68
34243615-0	2021	Altered expression of ERK, Cytochrome-c, and HSP70 triggers apoptosis in Quinacrine-exposed human invasive ductal carcinoma cells.	Quinacrine	73-83	cytochrome c, somatic	Homo sapiens	27-39
34243615-0	2021	Altered expression of ERK, Cytochrome-c, and HSP70 triggers apoptosis in Quinacrine-exposed human invasive ductal carcinoma cells.	Quinacrine	73-83	heat shock protein family A (Hsp70) member 4	Homo sapiens	45-50
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	nucleoporin 62	Homo sapiens	260-263
35460941-0	2022	Low doses of niclosamide and quinacrine combination yields synergistic effect in melanoma via activating autophagy-mediated p53-dependent apoptosis.	Quinacrine	29-39	tumor protein p53	Homo sapiens	124-127
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	tumor protein p53	Homo sapiens	117-120
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	caspase 3	Homo sapiens	130-139
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	collagen type XI alpha 2 chain	Homo sapiens	152-156
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	microtubule associated protein 1 light chain 3 beta	Homo sapiens	187-191
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Quinacrine	106-116	tumor protein p53	Homo sapiens	326-329
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Quinacrine	233-243	tumor protein p53	Homo sapiens	326-329
2606905-4	1989	Addition of an inhibitor of mitochondrial phospholipase A2, such as quinacrine, dibucaine, or chlorpromazine, also prevented increase in the respiration rate without affecting Ca2+ release from mitochondria during anoxic incubation.	Quinacrine	68-78	phospholipase A2 group IB	Homo sapiens	42-58
2817601-6	1989	Before treatment the concentration of PAI-1 was 21.7 +/- 12.0 (mean +/- SD) AU/ml and it increased to 86.9 +/- 25.9 AU/ml 6 h after quinacrine instillation.	Quinacrine	132-142	serpin family E member 1	Homo sapiens	38-43
2695506-2	1989	This LHRH-A-induced T secretion was completely blocked by quinacrine and chloroquine, inhibitors of phospholipase A2.	Quinacrine	58-68	gonadotropin releasing hormone 1	Rattus norvegicus	5-9
2695506-2	1989	This LHRH-A-induced T secretion was completely blocked by quinacrine and chloroquine, inhibitors of phospholipase A2.	Quinacrine	58-68	phospholipase A2 group IB	Rattus norvegicus	100-116
2808369-11	1989	Quinacrine, a phospholipase inhibitor, inhibited both cytotoxicity and DNA synthesis in response to TNF, and melittin, a phospholipase activator, mimicked both the cytotoxic and mitogenic actions of TNF in quiescent BALB/c 3T3 cells.	Quinacrine	0-10	tumor necrosis factor	Mus musculus	100-103
2808369-11	1989	Quinacrine, a phospholipase inhibitor, inhibited both cytotoxicity and DNA synthesis in response to TNF, and melittin, a phospholipase activator, mimicked both the cytotoxic and mitogenic actions of TNF in quiescent BALB/c 3T3 cells.	Quinacrine	0-10	tumor necrosis factor	Mus musculus	199-202
34998856-4	2022	Here, we have precisely evaluated the mechanism of PARP trapping mediated anti-cancer action of Quinacrine (QC), BMN-673, and their combination (QC + BMN-673) in breast cancer cells.	Quinacrine	96-106	poly(ADP-ribose) polymerase 1	Homo sapiens	51-55
2482349-7	1989	p-Bromophenacyl bromide and mepacrine, PLA2 inhibitors, inhibited the release of histamine caused by PLA2.	Quinacrine	28-37	phospholipase A2 group IB	Rattus norvegicus	39-43
2482349-7	1989	p-Bromophenacyl bromide and mepacrine, PLA2 inhibitors, inhibited the release of histamine caused by PLA2.	Quinacrine	28-37	phospholipase A2 group IB	Rattus norvegicus	101-105
2674942-6	1989	A recessive nuclear mutation, vph1-1, caused an abnormally high vacuolar pH of 6.9, as assayed by flow cytometry, and eliminated vacuolar uptake of the weak base quinacrine.	Quinacrine	162-172	H(+)-transporting V0 sector ATPase subunit a	Saccharomyces cerevisiae S288C	30-36
2545786-5	1989	The inhibitors of phospholipase A2, mepacrine and 2-(p-amylcinnamoyl)-amino-4-chlorobenzoic acid, effectively suppressed the liberation of [3H]AA from phospholipids, indicating that liberation of AA is mainly catalyzed by the action of phospholipase A2.	Quinacrine	36-45	phospholipase A2 group IB	Homo sapiens	18-34
2545786-5	1989	The inhibitors of phospholipase A2, mepacrine and 2-(p-amylcinnamoyl)-amino-4-chlorobenzoic acid, effectively suppressed the liberation of [3H]AA from phospholipids, indicating that liberation of AA is mainly catalyzed by the action of phospholipase A2.	Quinacrine	36-45	phospholipase A2 group IB	Homo sapiens	236-252
2503825-8	1989	This muscle depolarization also involves phospholipase A2 activation because dexamethasone and quinacrin, but not indomethacin, protect against depolarization.	Quinacrine	95-104	phospholipase A2, group IB, pancreas	Mus musculus	41-57
2764379-4	1989	Nifedipine, Ca2+-free medium, indomethacin, the phospholipase A2 inhibitor mepacrine, and the methyltransferase inhibitor 3-deazaadenosine reduced the change in CBF.	Quinacrine	75-84	phospholipase A2	Oryctolagus cuniculus	48-64
2570849-1	1989	p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes.	Quinacrine	32-42	phospholipase A2 group IB	Rattus norvegicus	75-91
2519894-8	1989	Quinacrine, the inhibitor of phospholipase A2, completely inhibits carbachol- and guanine nucleotide-activated AA release and greatly (by about 60-70%) decreases Ca(2+)-dependent AA liberation from phosphatidylinositol.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	29-45
2542466-7	1989	A role for phospholipase A2 is also possible, because pretreatment of cultures with quinacrine partially blocked arachidonic acid release.	Quinacrine	84-94	phospholipase A2 group IB	Rattus norvegicus	11-27
2570849-1	1989	p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes.	Quinacrine	32-42	phospholipase A2 group IB	Rattus norvegicus	93-97
3143415-4	1988	Evidence for LPS activation of phospholipase A2 included a time-dependent LPS-induced generation of [32P]lysophosphatidylcholine and the inhibitory effects of a phospholipase A2 inhibitor, mepacrine, on LPS-induced PGE2 formation.	Quinacrine	189-198	phospholipase A2 group IB	Rattus norvegicus	31-47
2545840-4	1989	Mepacrine, an inhibitor of phospholipase A2 (PLA2) activity and hence of arachidonic acid (AA) formation from membrane phospholipids, markedly inhibits (IC50 of approximately 15 microM) the release of VIP evoked by 4-AP.	Quinacrine	0-9	phospholipase A2, group IB, pancreas	Mus musculus	27-43
2545840-4	1989	Mepacrine, an inhibitor of phospholipase A2 (PLA2) activity and hence of arachidonic acid (AA) formation from membrane phospholipids, markedly inhibits (IC50 of approximately 15 microM) the release of VIP evoked by 4-AP.	Quinacrine	0-9	phospholipase A2, group IB, pancreas	Mus musculus	45-49
2545840-4	1989	Mepacrine, an inhibitor of phospholipase A2 (PLA2) activity and hence of arachidonic acid (AA) formation from membrane phospholipids, markedly inhibits (IC50 of approximately 15 microM) the release of VIP evoked by 4-AP.	Quinacrine	0-9	vasoactive intestinal polypeptide	Mus musculus	201-204
2545840-5	1989	The inhibitory effect of mepacrine is not additive to that of TTX, thus indicating an involvement of PLA2 activation in the TTX-sensitive component of the 4-AP-evoked release.	Quinacrine	25-34	phospholipase A2, group IB, pancreas	Mus musculus	101-105
2779545-2	1989	Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo.	Quinacrine	76-85	phospholipase A and acyltransferase 1	Rattus norvegicus	51-66
2542410-7	1989	Treatment of cells with phospholipase A2 inhibitors, mepacrine and bromophenacyl bromide, abolished AA release by C5b-9.	Quinacrine	53-62	phospholipase A2 group IB	Rattus norvegicus	24-40
2544450-3	1989	Addition of neomycin (an inhibitor of phospholipase C), as well as mepacrine (an inhibitor of phospholipase A2) to IFN-treated cells inhibited the antiviral activity of Hu-IFN alpha in the vesicular stomatitis virus (VSV)-UAC system used.	Quinacrine	67-76	interferon alpha 1	Homo sapiens	115-118
2544450-3	1989	Addition of neomycin (an inhibitor of phospholipase C), as well as mepacrine (an inhibitor of phospholipase A2) to IFN-treated cells inhibited the antiviral activity of Hu-IFN alpha in the vesicular stomatitis virus (VSV)-UAC system used.	Quinacrine	67-76	interferon alpha 1	Homo sapiens	172-175
2543228-3	1989	All these effects of ischemia were efficiently inhibited by the PLA2 inhibitor quinacrine.	Quinacrine	79-89	phospholipase A2 group IB	Homo sapiens	64-68
2543618-9	1989	Quinacrine, a phospholipase A2 inhibitor, suppressed the incorporation of [32P]Pi into this phospholipid on dose dependently.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
2918318-3	1989	Whereas ATP-stimulated 3H-IP accumulation was unaffected, its ability to promote TXA2 release was markedly reduced by mepacrine, an inhibitor of phospholipase A2 (PLA2).	Quinacrine	118-127	phospholipase A2 group IB	Homo sapiens	145-161
2918318-3	1989	Whereas ATP-stimulated 3H-IP accumulation was unaffected, its ability to promote TXA2 release was markedly reduced by mepacrine, an inhibitor of phospholipase A2 (PLA2).	Quinacrine	118-127	phospholipase A2 group IB	Homo sapiens	163-167
2570543-11	1989	Results obtained with the phospholipase A-2 inhibitor mepacrine and the acyltransferase inhibitor THC suggest that NE attenuates PL acylation by activating phospholipase A-2, but it concomitantly enhances PI acylation by selectively stimulating a PI-specific arachidonyl transferase via mechanisms that have not yet been elucidated.	Quinacrine	54-63	phospholipase A2 group IB	Rattus norvegicus	26-43
2611891-0	1989	Selective reduction of anaphase B in quinacrine-treated PtK1 cells.	Quinacrine	37-47	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	56-60
2611891-3	1989	In the study presented here, mitotic PtK1 cells were treated in early anaphase with concentrations of quinacrine ranging from 2 to 12 microM to determine energy requirements for chromosome motion.	Quinacrine	102-112	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	37-41
2551803-3	1989	Pretreatment of animals with quinacrine, a known inhibitor of phospholipase A2, prevented the increases in the luminal N-acetyl-beta-glucosaminidase activity, mucosal permeability, malondialdehyde and myeloperoxidase activity after deposition of phospholipase C in the gut lumen.	Quinacrine	29-39	phospholipase A2 group IB	Rattus norvegicus	62-78
2551803-3	1989	Pretreatment of animals with quinacrine, a known inhibitor of phospholipase A2, prevented the increases in the luminal N-acetyl-beta-glucosaminidase activity, mucosal permeability, malondialdehyde and myeloperoxidase activity after deposition of phospholipase C in the gut lumen.	Quinacrine	29-39	O-GlcNAcase	Rattus norvegicus	119-148
2551803-3	1989	Pretreatment of animals with quinacrine, a known inhibitor of phospholipase A2, prevented the increases in the luminal N-acetyl-beta-glucosaminidase activity, mucosal permeability, malondialdehyde and myeloperoxidase activity after deposition of phospholipase C in the gut lumen.	Quinacrine	29-39	myeloperoxidase	Rattus norvegicus	201-216
2551803-5	1989	Part of its action may be mediated via phospholipase A2 activation since pretreatment with quinacrine afforded protection.	Quinacrine	91-101	phospholipase A2 group IB	Rattus norvegicus	39-55
2474147-5	1989	Furthermore, the effect of A23187 was inhibited in the presence of quinacrine, indicating that the activation of the cyclooxygenase pathway is dependent on phospholipase A2 activity.	Quinacrine	67-77	phospholipase A2 group IB	Homo sapiens	156-172
2765476-4	1989	Several lipophilic compounds, including alkanols, substituted butyrophenones, aristolochic acid, and mepacrine apparently reduce the rate of lipolysis by promoting the desorption of phospholipase A2 from the interface.	Quinacrine	101-110	phospholipase A2 group IB	Homo sapiens	182-198
2719638-5	1989	Formation of lysophospholipids in [3H]glycerol-labelled membranes and decrease in [3H]AA liberated by the phospholipase A2 inhibitors mepacrine and ONO-RS-082 suggest that [3H]AA release is mainly catalysed by phospholipase A2.	Quinacrine	134-143	phospholipase A2 group IB	Homo sapiens	106-122
2499570-3	1989	To further investigate the mechanism of thromboxane generation, we studied the influence of the phospholipase A2 inhibitor, mepacrine, in a dose known to inhibit the enzyme in other systems, on t-bu-OOH-induced pulmonary arterial vasoconstriction.	Quinacrine	124-133	phospholipase A2	Oryctolagus cuniculus	96-112
2495005-1	1989	In view of the fact that mepacrine (Mp) is usually used as an inhibitor of the endogenous phospholipase A2, and since this enzyme produces the release of arachidonic acid (AA) from membrane phospholipids, we studied the effect of different concentrations of Mp on the mobilization of [1-14C]AA in rat renomedullary phospholipids.	Quinacrine	25-34	phospholipase A2 group IB	Rattus norvegicus	90-106
2495005-1	1989	In view of the fact that mepacrine (Mp) is usually used as an inhibitor of the endogenous phospholipase A2, and since this enzyme produces the release of arachidonic acid (AA) from membrane phospholipids, we studied the effect of different concentrations of Mp on the mobilization of [1-14C]AA in rat renomedullary phospholipids.	Quinacrine	36-38	phospholipase A2 group IB	Rattus norvegicus	90-106
2920033-3	1989	When PlA2 was inhibited with chlorpromazine, mepacrine, or p-bromphenacyl bromide, the accumulation of thiobarbituric acid reactive substances (TBARS) was reduced in a dose dependent manner.	Quinacrine	45-54	phospholipase A2 group IB	Rattus norvegicus	5-9
3143415-4	1988	Evidence for LPS activation of phospholipase A2 included a time-dependent LPS-induced generation of [32P]lysophosphatidylcholine and the inhibitory effects of a phospholipase A2 inhibitor, mepacrine, on LPS-induced PGE2 formation.	Quinacrine	189-198	phospholipase A2 group IB	Rattus norvegicus	161-177
3143714-8	1988	Activation of phospholipase A2 by melittin increased LH and FSH secretion, whereas blockade of this enzyme by quinacrine reduced GnRH-stimulated hormone release.	Quinacrine	110-120	gonadotropin releasing hormone 1	Rattus norvegicus	129-133
3218612-0	1988	Quinacrine prevention of intestinal ischaemic mucosal damage is partly mediated through inhibition of intraluminal phospholipase A2.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	115-131
3218612-4	1988	Pretreatment of animals with the phospholipase A2 inhibitor, quinacrine prevented the increases in luminal phospholipase A2 activity and mucosal damage following ischaemia and revascularization.	Quinacrine	61-71	phospholipase A2 group IB	Rattus norvegicus	33-49
3218612-4	1988	Pretreatment of animals with the phospholipase A2 inhibitor, quinacrine prevented the increases in luminal phospholipase A2 activity and mucosal damage following ischaemia and revascularization.	Quinacrine	61-71	phospholipase A2 group IB	Rattus norvegicus	107-123
3218612-6	1988	Again, quinacrine pretreatment of animals prevented the increases in mucosal permeability and activity of N-acetyl-beta-glucosaminidase after intraluminal injection of purified phospholipase A2.	Quinacrine	7-17	O-GlcNAcase	Rattus norvegicus	106-135
3218612-6	1988	Again, quinacrine pretreatment of animals prevented the increases in mucosal permeability and activity of N-acetyl-beta-glucosaminidase after intraluminal injection of purified phospholipase A2.	Quinacrine	7-17	phospholipase A2 group IB	Rattus norvegicus	177-193
3196359-3	1988	The effect of PLA2 on [3H]HCh-3 binding was inhibited by quinacrine, a PLA2 inhibitor, and by removal of calcium.	Quinacrine	57-67	phospholipase A2 group IB	Homo sapiens	14-18
3196359-3	1988	The effect of PLA2 on [3H]HCh-3 binding was inhibited by quinacrine, a PLA2 inhibitor, and by removal of calcium.	Quinacrine	57-67	phospholipase A2 group IB	Homo sapiens	71-75
2460617-3	1988	The endothelium-dependent contraction induced by A-23187 was attenuated by a phospholipase A2 inhibitor (quinacrine), cyclooxygenase inhibitors (aspirin and indomethacin), a thromboxane A2 (TXA2) synthetase inhibitor (OKY-046) and a TXA2 antagonist (ONO-3708).	Quinacrine	105-115	phospholipase A2 group IB	Canis lupus familiaris	77-93
3180226-4	1988	Quinacrine dim PBL, which are devoid of lytic NK cells, are capable of developing LAK activity following culture with IL-2.	Quinacrine	0-10	interleukin 2	Homo sapiens	118-122
3164726-15	1988	This evidence, together with inhibition of acylhydrolase activity with phospholipase A2 inhibitors, dibucaine and mepacrine, indicates that the primary acylhydrolase activity was due to phospholipase A2.	Quinacrine	114-123	phospholipase A2 group IB	Rattus norvegicus	186-202
3145981-6	1988	Drugs that inhibit arachidonate liberation from membrane phospholipids (mepacrine or 4-bromphenacyl bromide) block NGF-stimulated nerve fiber growth by PC12 cells.	Quinacrine	72-81	nerve growth factor	Rattus norvegicus	115-118
3220836-2	1988	In contrast, such an inhibition was not seen in the rats given DAP from 0 to 4 h; it occurred when quinacrine, a polyamine oxidase inhibitor, was concomitantly dosed, and disappeared with further addition of putrescine.	Quinacrine	99-109	polyamine oxidase	Rattus norvegicus	113-130
3129942-9	1988	Furthermore, alpha-1 but not beta-1 adrenergic receptor stimulated PG synthesis is inhibited by mepacrine, a phospholipase A2 and C inhibitor.	Quinacrine	96-105	adrenoceptor alpha 1D	Homo sapiens	13-20
3259847-4	1988	The actions of the endothelium-dependent and -independent vasodilators, ATP and nitroprusside, respectively, were studied before and after administration of quinacrine (an inhibitor of phospholipase A2), which blocks formation and/or release of endothelium-derived relaxing factor (EDRF).	Quinacrine	157-167	phospholipase A2 group IB	Canis lupus familiaris	185-201
3131280-3	1988	A phospholipase A2 inhibitor, quinacrine (2 X 10(-6) M), also inhibited the TNF cytotoxicity.	Quinacrine	30-40	phospholipase A2 group IB	Homo sapiens	2-18
3131280-3	1988	A phospholipase A2 inhibitor, quinacrine (2 X 10(-6) M), also inhibited the TNF cytotoxicity.	Quinacrine	30-40	tumor necrosis factor	Homo sapiens	76-79
2447244-4	1988	The effect of PLA2 was prevented by EGTA and two nonselective PLA2 inhibitors, mepacrine and bromophenacyl bromide.	Quinacrine	79-88	phospholipase A2 group IB	Rattus norvegicus	14-18
3124931-3	1988	The neuronal responses to IL-1 were blocked or attenuated by concurrent application of mepacrine (a phospholipase inhibitor) or sodium salicylate (a cyclooxygenase inhibitor).	Quinacrine	87-96	interleukin 1 alpha	Homo sapiens	26-30
2830996-3	1988	All these effects were efficiently inhibited by the PLA2 inhibitor quinacrine.	Quinacrine	67-77	phospholipase A2 group IB	Rattus norvegicus	52-56
2838694-3	1988	Similar inhibitory effects are observed with mepacrine, an inhibitor of phospholipase A2 (PLA2).	Quinacrine	45-54	phospholipase A2 group IB	Rattus norvegicus	72-88
2838694-3	1988	Similar inhibitory effects are observed with mepacrine, an inhibitor of phospholipase A2 (PLA2).	Quinacrine	45-54	phospholipase A2 group IB	Rattus norvegicus	90-94
3068748-3	1988	Mepacrine sharply diminished neutrophil migration, O2 and elastase release.	Quinacrine	0-9	immunoglobulin kappa variable 1D-39	Homo sapiens	51-66
3428670-3	1987	Pretreatment with the phospholipase A2 inhibitor, quinacrine, prevented the increases in mucosal phospholipase A2 activity and lysophosphatidylcholine/phosphatidylcholine ratio after ischaemia and morphological examinations revealed that the mucosa was then also protected against ischaemic injury.	Quinacrine	50-60	phospholipase A2 group IB	Rattus norvegicus	22-38
3428670-3	1987	Pretreatment with the phospholipase A2 inhibitor, quinacrine, prevented the increases in mucosal phospholipase A2 activity and lysophosphatidylcholine/phosphatidylcholine ratio after ischaemia and morphological examinations revealed that the mucosa was then also protected against ischaemic injury.	Quinacrine	50-60	phospholipase A2 group IB	Rattus norvegicus	97-113
3120519-5	1987	Quinacrine, a non specific inhibitor of phospholipase A2 impaired PAF-acether formation in a dose-dependent manner.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	40-56
3660410-10	1987	Dantrolene and mepacrine antagonized the synergism between halothane and phospholipase A2 most likely by reducing the lytic action of halothane in the presence of arachidonic acid.	Quinacrine	15-24	phospholipase A2 group IB	Homo sapiens	73-89
3660410-11	1987	The red blood cell is a useful model for studying the antagonism of halothane and phospholipase A2 toxicity by dantrolene and mepacrine.	Quinacrine	126-135	phospholipase A2 group IB	Homo sapiens	82-98
3112143-5	1987	Treatment of C62B cells with two other glucocorticoids, betamethasone and cortisone, produced results similar to those of dexamethasone as did treatment with quinacrine, a phospholipase A2-selective inhibitor.	Quinacrine	158-168	phospholipase A2 group IB	Homo sapiens	172-188
3116708-0	1987	The inhibitory action of quinacrine on endotoxin-induced tissue factor expression in cultured human endothelial cells is due to cell injury.	Quinacrine	25-35	coagulation factor III, tissue factor	Homo sapiens	57-70
3133309-2	1988	In this study, the involvement of arachidonate metabolism has been investigated further with the following results: (i) Cytolysis of human U937 tumour cells by recombinant TNF was reduced by dexamethasone and quinacrine, agents which inhibit phospholipase A2.	Quinacrine	209-219	tumor necrosis factor	Homo sapiens	172-175
3133309-2	1988	In this study, the involvement of arachidonate metabolism has been investigated further with the following results: (i) Cytolysis of human U937 tumour cells by recombinant TNF was reduced by dexamethasone and quinacrine, agents which inhibit phospholipase A2.	Quinacrine	209-219	phospholipase A2 group IB	Homo sapiens	242-258
2834949-2	1988	Inhibition of phospholipase A2 with para-bromophenacyl bromide, dexamethasone or quinacrine, alone or in combination, blocked arachidonate release by 50%-60% but had no effect on EDRF production as assessed by cyclic GMP accumulation in mixed- or co-cultures of endothelial and vascular smooth muscle cells.	Quinacrine	81-91	LOC104974671	Bos taurus	14-30
2829912-0	1988	Effects of quinacrine on vasopressin-induced changes in glycogen phosphorylase activity, Ca2+ transport and phosphoinositide metabolism in isolated hepatocytes.	Quinacrine	11-21	arginine vasopressin	Homo sapiens	25-36
2829912-1	1988	In isolated hepatocytes, quinacrine (150-250 microM) inhibited vasopressin-induced increases in glucose release, glycogen phosphorylase a activity and 45Ca2+ efflux; and glucagon-induced increases in glucose release and cyclic AMP formation.	Quinacrine	25-35	arginine vasopressin	Homo sapiens	63-74
2829912-2	1988	These results indicate that a phospholipase A2 enzyme sensitive to quinacrine is unlikely to be involved in the process by which vasopressin stimulates glycogen phosphorylase activity in the liver cell.	Quinacrine	67-77	phospholipase A2 group IB	Homo sapiens	30-46
2829912-3	1988	In cells labelled with [3H]inositol, much lower concentrations of quinacrine (20-50 microM) inhibited the stimulation by vasopressin of the accumulation of [3H]inositol.	Quinacrine	66-76	arginine vasopressin	Homo sapiens	121-132
3335042-1	1988	Mammary carcinogenesis studies were conducted to determine the chemopreventive activity of quinacrine, an antimalarial drug which suppresses the production of arachidonic acid from phospholipid through inhibition of phospholipase A2.	Quinacrine	91-101	phospholipase A2 group IB	Rattus norvegicus	216-232
3690677-4	1987	PA-2 inhibitors, quinacrine and p-bromophenacyl bromide, inhibited NK CMC at the effector cell level, but affected neither initial target-effector cell binding nor dissociated conjugates during the length of the NK assay, suggesting that they block post-binding lytic events.	Quinacrine	17-27	phospholipase A2 group IB	Homo sapiens	0-4
2824717-9	1987	Fourth, mepacrine blockade of the Ca2+-dependent enzyme phospholipase A2, which releases endogenous oleate from membrane phospholipids, inhibited the time-course of a persistent LTP response.	Quinacrine	8-17	phospholipase A2 group IB	Homo sapiens	56-72
3120703-6	1987	A transient appearance of radiolabelled phosphatidic acid and diacylglycerol indicated phosphatidylinositol hydrolysis by phospholipase C. Pretreatment with a phospholipase A2 inhibitor, mepacrine, substantially prevented the antigen-induced liberation of [3H]arachidonic acid from phosphatidylcholine.	Quinacrine	187-196	phospholipase A2 group IB	Rattus norvegicus	159-175
3660410-0	1987	Dantrolene and mepacrine antagonize the hemolysis of human red blood cells by halothane and bee venom phospholipase A2.	Quinacrine	15-24	phospholipase A2 group IB	Homo sapiens	102-118
3660410-8	1987	Dantrolene (10 microM) and mepacrine (10 microM) significantly antagonized hemolysis induced by halothane and phospholipase A2 or halothane and exogenously added arachidonic acid and lysophosphatidylcholine.	Quinacrine	27-36	phospholipase A2 group IB	Homo sapiens	110-126
3119146-3	1987	This effect was inhibited by the protein kinase inhibitor 1-(-5-isoquinolinylsulfonyl)-2-methylpiperizine (IC50 = 25 microM) and the phospholipase A2 inhibitor, mepacrine (IC50 = 5 microM).	Quinacrine	161-170	phospholipase A2 group IB	Rattus norvegicus	133-149
2887563-10	1987	The effects of norepinephrine, A23187, and protein kinase C activators appear to be mediated by phospholipase A2 because the effects of these compounds on [3H]arachidonic acid release are blocked by an established inhibitor of this enzyme, mepacrine, and because these compounds stimulate the formation of 32P- and 14C-labeled lysophosphatidylcholine by glands incubated with 32Pi or [14C]choline.	Quinacrine	240-249	phospholipase A2 group IB	Homo sapiens	96-112
3594767-2	1987	These compounds were administered before and after a 30 min intracoronary infusion of the phospholipase A2 inhibitor quinacrine (300 micrograms/min).	Quinacrine	117-127	phospholipase A2 group IB	Canis lupus familiaris	90-106
3106986-3	1987	Quinacrine at concentrations of 1-5 microM attenuated the magnitude of the PRL stimulation of cell division; at concentrations of 10 microM and above quinacrine abolished the PRL response.	Quinacrine	150-160	prolactin	Homo sapiens	175-178
3129942-9	1988	Furthermore, alpha-1 but not beta-1 adrenergic receptor stimulated PG synthesis is inhibited by mepacrine, a phospholipase A2 and C inhibitor.	Quinacrine	96-105	phospholipase A2 group IB	Homo sapiens	109-125
3475493-13	1987	Mepacrine, a phospholipase A2 inhibitor, more potently inhibited the bradykinin- and ATP-induced contractions than the ACh-induced one.	Quinacrine	0-9	phospholipase A2	Oryctolagus cuniculus	13-29
3588973-7	1987	Phospholipase A2 activity was inhibited by bromophenacyl bromide, chlorpromazine and mepacrine in decreasing order of effectiveness.	Quinacrine	85-94	phospholipase A2	Oryctolagus cuniculus	0-16
3101507-1	1987	Quinacrine either inhibited or stimulated Na-Ca exchange in cardiac sarcolemmal vesicles, depending on the experimental conditions.	Quinacrine	0-10	nascent polypeptide associated complex subunit alpha	Homo sapiens	42-47
3101507-2	1987	When present in the assay medium for Na-Ca exchange, quinacrine inhibited both Nai-dependent Ca2+ uptake (Ki = 50 microM) and Nao-dependent Ca2+ efflux.	Quinacrine	53-63	nascent polypeptide associated complex subunit alpha	Homo sapiens	37-42
3101507-5	1987	The inhibitory effects of quinacrine on Na-Ca exchange activity are qualitatively similar to those reported previously for amiloride derivatives.	Quinacrine	26-36	nascent polypeptide associated complex subunit alpha	Homo sapiens	40-45
3101507-6	1987	When Na-loaded vesicles were preincubated with quinacrine and then assayed for Na-Ca exchange in a quinacrine-free medium, stimulation of exchange activity was observed.	Quinacrine	47-57	nascent polypeptide associated complex subunit alpha	Homo sapiens	79-84
3101507-6	1987	When Na-loaded vesicles were preincubated with quinacrine and then assayed for Na-Ca exchange in a quinacrine-free medium, stimulation of exchange activity was observed.	Quinacrine	99-109	nascent polypeptide associated complex subunit alpha	Homo sapiens	79-84
3101507-9	1987	Since Ca2+, quinacrine and tetraphenylphosphonium all bind strongly to sarcolemmal membranes, it is suggested that the observed stimulation of exchange activity involves a local electrostatic effect of the bound cations in accelerating a rate-limiting step in the reaction mechanism for Na-Ca exchange.	Quinacrine	12-22	nascent polypeptide associated complex subunit alpha	Homo sapiens	287-292
3815542-0	1987	Quinacrine-induced changes in mitotic PtK1 spindle microtubule organization.	Quinacrine	0-10	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	38-42
3594487-5	1987	Therefore separation of interleukin-2-incubated cells for LAK activity could be accomplished using sorting after quinacrine staining.	Quinacrine	113-123	interleukin 2	Mus musculus	24-37
3815542-1	1987	Quinacrine, an acridine derivative which competitively binds to ATP binding sites, has been used to study the role of ATP requiring molecules in microtubule organization in mitotic PtK1 cells.	Quinacrine	0-10	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	181-185
3038761-2	1987	The generation of these lysophosphatidylcholine-like molecules appears to represent an essential step in the activation of the oxidative burst of the PMNL triggered by PMA since inhibition of phospholipase A2 (PLA2) by p-bromophenacylbromide (BB) or mepacrine results in an inhibition of the O-2 release.	Quinacrine	250-259	phospholipase A2 group IB	Homo sapiens	192-208
3038761-2	1987	The generation of these lysophosphatidylcholine-like molecules appears to represent an essential step in the activation of the oxidative burst of the PMNL triggered by PMA since inhibition of phospholipase A2 (PLA2) by p-bromophenacylbromide (BB) or mepacrine results in an inhibition of the O-2 release.	Quinacrine	250-259	phospholipase A2 group IB	Homo sapiens	210-214
3102257-2	1986	Mepacrine, a phospholipase A2 inhibitor (3 X 10(-5) M) and the lipoxygenase inhibitor nordihydroguaiaretic acid (10(-5) M) inhibited this response whereas the cyclooxygenase inhibitor, diclofenac sodium (10(-5) M), and the thromboxane synthetase inhibitor imidazole (10(-5) M) did not.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-29
3503494-6	1987	The co-existence of PLA2 with its inhibitors--quinacrine (3 microM), cortisone (0.01 microM) and tetracaine (30 microM)--significantly overcame the PLA2-induced inhibition of both indices.	Quinacrine	46-56	phospholipase A2, group IB, pancreas	Mus musculus	20-24
3503494-6	1987	The co-existence of PLA2 with its inhibitors--quinacrine (3 microM), cortisone (0.01 microM) and tetracaine (30 microM)--significantly overcame the PLA2-induced inhibition of both indices.	Quinacrine	46-56	phospholipase A2, group IB, pancreas	Mus musculus	148-152
2875734-3	1986	However, the rebound crosslinked ATPase differed from the native enzyme in lacking the ability to restore NADH oxidation - and ATP hydrolysis-dependent quenching of the fluorescence of quinacrine to ATPase-stripped membrane vesicles.	Quinacrine	185-195	ATPase	Escherichia coli	33-39
3553641-5	1986	PG I2 synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A2.	Quinacrine	52-61	phospholipase A2 group IB	Rattus norvegicus	78-94
2429133-12	1986	But the release was also inhibited by the calmodulin antagonists, W-7 and mepacrine, suggesting that the influx of calcium in the permeabilized cells acts primarily through calmodulin-mediated enzyme activation.	Quinacrine	74-83	calmodulin 1	Homo sapiens	42-52
2429133-12	1986	But the release was also inhibited by the calmodulin antagonists, W-7 and mepacrine, suggesting that the influx of calcium in the permeabilized cells acts primarily through calmodulin-mediated enzyme activation.	Quinacrine	74-83	calmodulin 1	Homo sapiens	173-183
3106986-3	1987	Quinacrine at concentrations of 1-5 microM attenuated the magnitude of the PRL stimulation of cell division; at concentrations of 10 microM and above quinacrine abolished the PRL response.	Quinacrine	0-10	prolactin	Homo sapiens	75-78
2875734-3	1986	However, the rebound crosslinked ATPase differed from the native enzyme in lacking the ability to restore NADH oxidation - and ATP hydrolysis-dependent quenching of the fluorescence of quinacrine to ATPase-stripped membrane vesicles.	Quinacrine	185-195	ATPase	Escherichia coli	199-205
3091592-4	1986	With phorbol diesters as stimuli, the following inhibitors of phospholipase A2 and lipoxygenase suppressed release of H2O2 at nontoxic concentrations (microM range): p-bromophenacyl bromide, quinacrine, eicosatetraenoic acid, nordihydroguaiaretic acid, and phenidone.	Quinacrine	191-201	phospholipase A2, group IB, pancreas	Mus musculus	62-78
3766758-4	1986	Pretreatment with the phospholipase A2 inhibitor quinacrine reduced the pulmonary vascular responses to ACh without affecting systemic arterial pressure.	Quinacrine	49-59	phospholipase A2	Oryctolagus cuniculus	22-38
3756201-6	1986	Indomethacin (500 microM), mepacrine (500 microM) and N-ethylmaleimide (4 mM) inhibited the phospholipase A2 by 69, 62 and 19%, respectively.	Quinacrine	27-36	phospholipase A2 group IB	Homo sapiens	92-108
3781471-0	1986	Prolactin actions on casein and lipid biosynthesis in mouse and rabbit mammary gland explants are abolished by p-bromphenacyl bromide and quinacrine, phospholipase A2 inhibitors.	Quinacrine	138-148	prolactin	Mus musculus	0-9
3781471-0	1986	Prolactin actions on casein and lipid biosynthesis in mouse and rabbit mammary gland explants are abolished by p-bromphenacyl bromide and quinacrine, phospholipase A2 inhibitors.	Quinacrine	138-148	phospholipase A2	Oryctolagus cuniculus	150-166
3781471-1	1986	p-Bromphenacyl bromide (BPB) at concentrations of 50 microM and above and quinacrine (50 microM) abolished the actions of prolactin (PRL) on casein and lipid biosynthesis in cultured mouse mammary gland explants.	Quinacrine	74-84	prolactin	Mus musculus	122-131
3781471-3	1986	Since BPB and quinacrine are known to inhibit the enzyme phospholipase A2 (PLA2), it is possible that ongoing PLA2 activity is essential for prolactin to express its actions on at least certain lactogenic processes.	Quinacrine	14-24	phospholipase A2, group IB, pancreas	Mus musculus	57-73
3781471-3	1986	Since BPB and quinacrine are known to inhibit the enzyme phospholipase A2 (PLA2), it is possible that ongoing PLA2 activity is essential for prolactin to express its actions on at least certain lactogenic processes.	Quinacrine	14-24	phospholipase A2, group IB, pancreas	Mus musculus	75-79
3781471-3	1986	Since BPB and quinacrine are known to inhibit the enzyme phospholipase A2 (PLA2), it is possible that ongoing PLA2 activity is essential for prolactin to express its actions on at least certain lactogenic processes.	Quinacrine	14-24	prolactin	Mus musculus	141-150
2431915-5	1986	Mepacrine only blocked substance P relaxation.	Quinacrine	0-9	tachykinin precursor 1	Homo sapiens	23-34
2413502-7	1985	It seems probable that chloroquine and mepacrine inhibit leukotriene release by inhibition of phospholipase A2 in lung.	Quinacrine	39-48	phospholipase A2 group IB	Homo sapiens	94-110
2429529-0	1986	Effects of mepacrine and p-bromophenacyl bromide on anti-IgE and phospholipase A2-induced histamine release from human basophils.	Quinacrine	11-20	phospholipase A2 group IB	Homo sapiens	65-81
2429529-2	1986	Low concentrations of mepacrine and p-bromophenacyl bromide (BPB) inhibited both phospholipase A2- and anti-IgE-induced histamine release.	Quinacrine	22-31	phospholipase A2 group IB	Homo sapiens	81-97
3709328-7	1986	In contrast, indomethacin (5 mg/kg) and aspirin (200 mg/kg) as cyclooxygenase inhibitors or quinacrine (100 mg/kg) as a phospholipase A2 inhibitor significantly decreased both the pH and acid neutralizing capacity.	Quinacrine	92-102	phospholipase A2 group IB	Rattus norvegicus	120-136
16664845-2	1986	The H(+)-PPase catalyzed the electrogenic transport of H(+) into the vesicles, generating a pH gradient, inside acid (quinacrine fluorescence quenching), and a membrane potential, inside positive (Oxonol V fluorescence quenching).	Quinacrine	118-128	inorganic pyrophosphatase 1	Homo sapiens	9-14
2867452-4	1986	Quinacrine, a phospholipase A2 inhibitor, reduced both basal and GRF-stimulated free arachidonate levels as well as GH release.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	14-30
2867452-4	1986	Quinacrine, a phospholipase A2 inhibitor, reduced both basal and GRF-stimulated free arachidonate levels as well as GH release.	Quinacrine	0-10	growth hormone releasing hormone	Homo sapiens	65-68
3779108-8	1986	Quinacrine, an inhibitor of phospholipase A2, attenuated the dilation response in a dose-dependent manner.	Quinacrine	0-10	phospholipase A2 group IB	Canis lupus familiaris	28-44
3879308-4	1985	Quinacrine, a phospholipase A2 inhibitor, methylene blue, a guanylate cyclase inhibitor and tetraethylammonium, a potassium permeability inhibitor, inhibited carbachol-induced relaxation and augmented the magnitude of norepinephrine-induced contraction only when endothelium was present.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	14-30
3832018-1	1985	Four compounds: amodiaquine, quinacrine, 1,4-(tele)-methylhistamine and metoprine, which in vitro effectively inhibit histamine N-methyltransferase (HMT) activity, were tested for their effects on histamine (HI) levels in the rat brain and ex vivo HMT activity.	Quinacrine	29-39	histamine N-methyltransferase	Rattus norvegicus	149-152
3832018-3	1985	Amodiaquine, quinacrine and 1,4-(tele)-methyl-HI weakly inhibited HMT activity ex vivo and they failed to alter HI levels in the rat brain.	Quinacrine	13-23	histamine N-methyltransferase	Rattus norvegicus	66-69
3931692-0	1985	Mepacrine (quinacrine) inhibition of thrombin-induced platelet responses can be overcome by lysophosphatidic acid.	Quinacrine	0-9	coagulation factor II, thrombin	Homo sapiens	37-45
3931692-0	1985	Mepacrine (quinacrine) inhibition of thrombin-induced platelet responses can be overcome by lysophosphatidic acid.	Quinacrine	11-21	coagulation factor II, thrombin	Homo sapiens	37-45
3931692-2	1985	Such synthesis of lysophosphatidic acid can be inhibited by mepacrine, an inhibitor of the phospholipase A2 which attacks phosphatidic acid to give lysophosphatidic acid.	Quinacrine	60-69	phospholipase A2 group IB	Homo sapiens	91-107
3931692-3	1985	In the present study, mepacrine was used at a concentration of 2.5-20 microM, sufficient to block aggregation and lysophosphatidic acid formation induced by 0.1 U/ml thrombin.	Quinacrine	22-31	coagulation factor II, thrombin	Homo sapiens	166-174
3931692-4	1985	Mepacrine, at this concentration, also blocked thrombin-induced phosphorylation of platelet myosin light chain and a 47 kDa protein, thrombin-induced secretion and thrombin-induced release of arachidonic acid from platelet phospholipids.	Quinacrine	0-9	coagulation factor II, thrombin	Homo sapiens	47-55
3931692-4	1985	Mepacrine, at this concentration, also blocked thrombin-induced phosphorylation of platelet myosin light chain and a 47 kDa protein, thrombin-induced secretion and thrombin-induced release of arachidonic acid from platelet phospholipids.	Quinacrine	0-9	coagulation factor II, thrombin	Homo sapiens	133-141
3931692-4	1985	Mepacrine, at this concentration, also blocked thrombin-induced phosphorylation of platelet myosin light chain and a 47 kDa protein, thrombin-induced secretion and thrombin-induced release of arachidonic acid from platelet phospholipids.	Quinacrine	0-9	coagulation factor II, thrombin	Homo sapiens	133-141
3931692-5	1985	However, mepacrine also partly inhibited the formation of phosphatidic acid in response to thrombin, consistent with some simultaneous inhibition of phospholipase C. Lysophosphatidic acid (2.5-22 microM) overcame the mepacrine block in thrombin-stimulated aggregation, protein phosphorylation and secretion without stimulating the release of arachidonic acid from platelet phospholipids or the formation of lysophosphatidic acid, and only slightly increasing phosphatidic acid formation.	Quinacrine	9-18	coagulation factor II, thrombin	Homo sapiens	91-99
3931692-5	1985	However, mepacrine also partly inhibited the formation of phosphatidic acid in response to thrombin, consistent with some simultaneous inhibition of phospholipase C. Lysophosphatidic acid (2.5-22 microM) overcame the mepacrine block in thrombin-stimulated aggregation, protein phosphorylation and secretion without stimulating the release of arachidonic acid from platelet phospholipids or the formation of lysophosphatidic acid, and only slightly increasing phosphatidic acid formation.	Quinacrine	9-18	coagulation factor II, thrombin	Homo sapiens	236-244
3931692-6	1985	The results suggest that lysophosphatidic acid primarily acts distal to mepacrine inhibition of phospholipase A2 and phospholipase C and are consistent with the possibility that lysophosphatidic acid might be a mediator of part of the effects of low-dose thrombin on human platelets.	Quinacrine	72-81	phospholipase A2 group IB	Homo sapiens	96-112
2995124-2	1985	NADH-dependent activation of 5"-nucleotidase was significantly suppressed by atebrine, an inhibitor of NADH dehydrogenase of plasma membranes, and completely abolished by 2,4-dinitrophenol (2 X 10(-4)M) and Triton X-100 (2%).	Quinacrine	77-85	5' nucleotidase, ecto	Rattus norvegicus	29-44
4016141-3	1985	Each of these lipolytic enzymes could be inhibited by antimalarial drugs (chloroquine, mepacrine, primaquine) at concentrations above 1 x 10(-4) M. Inhibition of the alkaline cytosolic lysophospholipase by these drugs was noncompetitive with respect to the substrate, and the inhibitory potency increased, when the pH was raised.	Quinacrine	87-96	asparaginase	Rattus norvegicus	185-202
3017321-4	1986	Similar inhibitory effects are observed with mepacrine, a PLA2-inhibitor, suggesting that PLA2-activation could be related to these secretory process.	Quinacrine	45-54	phospholipase A2 group IB	Homo sapiens	58-62
3017321-4	1986	Similar inhibitory effects are observed with mepacrine, a PLA2-inhibitor, suggesting that PLA2-activation could be related to these secretory process.	Quinacrine	45-54	phospholipase A2 group IB	Homo sapiens	90-94
3015148-7	1986	Other effective inhibitors of the cyclic GMP response were methylene blue, catalase, bromphenacyl bromide, retinal, dithiothreitol, quinacrine, and oxidized glutathione.	Quinacrine	132-142	5'-nucleotidase, cytosolic II	Mus musculus	41-44
3015425-4	1986	The membrane modulators mepacrine, chlorpromazine and cepharanthine inhibited the superoxide generation produced by chemotactic peptide, FMLP, and/or digitonin in neutrophils.	Quinacrine	24-33	formyl peptide receptor 1	Homo sapiens	137-141
3015753-7	1986	Mepacrine, a phospholipase A2 inhibitor, strongly inhibited it.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-29
3955065-5	1986	In control experiments with microsomal membranes employing quinacrine, an inhibitor of phospholipase A2, the increased lysophosphatidylcholine concentration was still observed in clofibrate-treated animals.	Quinacrine	59-69	phospholipase A2, group IB, pancreas	Mus musculus	87-103
2425595-8	1986	There was apparently an increase in the cytoplasmic calcium concentration, which acted through calmodulin, since the histamine release induced by calcium from the permeabilized mast cells could be inhibited by a calmodulin-antagonist, mepacrine (10-30 microM).	Quinacrine	235-244	calmodulin 1	Rattus norvegicus	95-105
2425595-8	1986	There was apparently an increase in the cytoplasmic calcium concentration, which acted through calmodulin, since the histamine release induced by calcium from the permeabilized mast cells could be inhibited by a calmodulin-antagonist, mepacrine (10-30 microM).	Quinacrine	235-244	calmodulin 1	Rattus norvegicus	212-222
3455595-11	1986	was inhibitory at 10(-5) M and showed no effects at 10(-6) M. However, after washing quinacrine, normal elongation rate was recovered by those previously treated with 10(-5) M and axon growth was enhanced in those treated with 10(-6) M. Since three different phospholipase A2 inhibitors, tested in different situations, produce a similar biphasic effect on axon elongation rate, we postulate that this enzymatic activity is involved in the motility of axon growth cones.	Quinacrine	85-95	phospholipase A2 group IB	Rattus norvegicus	259-275
3080438-7	1986	Melittin disruption of vinculin was inhibited by (in order of decreasing effectiveness) mepacrine greater than TMB-8 greater than TFP greater than leupeptin greater than PMSF, whereas A23187 and amiloride had no effect.	Quinacrine	88-97	vinculin	Mus musculus	23-31
3080438-9	1986	The observation that both PDGF- and melittin-induced removal of vinculin from adhesion plaques is inhibited by mepacrine suggests that phospholipase activation may be an early and important step in PDGF-induced disruption of vinculin from adhesion plaques.	Quinacrine	111-120	vinculin	Mus musculus	64-72
3080438-9	1986	The observation that both PDGF- and melittin-induced removal of vinculin from adhesion plaques is inhibited by mepacrine suggests that phospholipase activation may be an early and important step in PDGF-induced disruption of vinculin from adhesion plaques.	Quinacrine	111-120	vinculin	Mus musculus	225-233
3929616-5	1985	Similar results were obtained with 50 microM quinacrine, a phospholipase A2 inhibitor.	Quinacrine	45-55	phospholipase A2 group IB	Homo sapiens	59-75
3919107-4	1985	The stimulatory effect of EGF was partially inhibited by the addition of mepacrine (70% inhibition at 10 microM) and by the pretreatment of hydrocortisone (60% inhibition at 1.0 microM).	Quinacrine	73-82	epidermal growth factor	Sus scrofa	26-29
3924121-2	1985	The effect of melittin on insulin secretion was dependent on extracellular calcium, was inhibited by the phospholipase A2 inhibitor quinacrine and by the lipoxygenase inhibitor nordihydroguaiaretic acid.	Quinacrine	132-142	phospholipase A2 group IB	Rattus norvegicus	105-121
2992446-3	1985	Furthermore, the inhibitors against CANP, NCO-700 (2 and 20 micrograms/ml) that was demonstrated to permeate sarcolemma using 14C-labelled reagent, against CDP, mepacrine (1 and 10 micrograms/ml) or against cyclooxygenase, indomethacin (1 and 10 micrograms/ml) caused no effect on the Ca entry, nigrosin intake nor CPK release under hypoxia.	Quinacrine	161-170	calpain 1	Homo sapiens	36-40
4025667-7	1985	Placental PAO can be inhibited by quinacrine a typical inhibitor of flavoprotein enzymes but not by isoniazid, an inhibitor of pyridoxal enzymes; this would suggest that the enzymes in human placenta are of a tissular rather than seric origin.	Quinacrine	34-44	polyamine oxidase	Homo sapiens	10-13
2986027-3	1985	A phospholipase A2 inhibitor quinacrine (30 microM) increased cellular cAMP content while decreasing GH release.	Quinacrine	29-39	phospholipase A2 group IB	Homo sapiens	2-18
2983324-3	1985	The phospholipase A2 blockers mepacrine and p-bromophenacylbromide inhibited the ACTH release induced by secretagogues.	Quinacrine	30-39	phospholipase A2, group IB, pancreas	Mus musculus	4-20
2983324-3	1985	The phospholipase A2 blockers mepacrine and p-bromophenacylbromide inhibited the ACTH release induced by secretagogues.	Quinacrine	30-39	pro-opiomelanocortin-alpha	Mus musculus	81-85
2981065-7	1985	Quinacrine, a phospholipase A2 inhibitor, also abolished the stimulatory effect of phospholipase A2 or TRH on PRL release.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	14-30
2578123-3	1985	For verapamil, diltiazem, trifluoperazine, dibucaine, and quinacrine, there is complete agreement between the relative potencies as inhibitors of phospholipase A2 and the two other processes.	Quinacrine	58-68	phospholipase A2 group IB	Rattus norvegicus	146-162
3917874-9	1985	Prostaglandin output induced by angiotensin II and bradykinin were inhibited by mepacrine and indomethacin, whereas, the prostaglandin output caused by exogenous arachidonic acid (33 nmol) was abolished by indomethacin but was unaltered by mepacrine, calcium antagonists, and calmodulin inhibitors.	Quinacrine	80-89	angiotensinogen	Rattus norvegicus	32-46
3917874-9	1985	Prostaglandin output induced by angiotensin II and bradykinin were inhibited by mepacrine and indomethacin, whereas, the prostaglandin output caused by exogenous arachidonic acid (33 nmol) was abolished by indomethacin but was unaltered by mepacrine, calcium antagonists, and calmodulin inhibitors.	Quinacrine	240-249	angiotensinogen	Rattus norvegicus	32-46
2981387-4	1985	Quinacrine antagonized the stimulatory effects of ouabain, vanadate, and K-free medium on prostaglandin E2 release (consistent with phospholipase A2 involvement), but did not antagonize their inhibitory effects on renin secretion.	Quinacrine	0-10	phospholipase A2 group IB	Rattus norvegicus	132-148
4096539-4	1985	Phenothiazines (trifluoperazine and chlorpromazine), mepacrine, propranolol, and colchicine inhibited the effect of the purified epidermal calmodulin on the calmodulin-deficient phosphodiesterase of bovine heart.	Quinacrine	53-62	calmodulin-3	Sus scrofa	139-149
4096539-4	1985	Phenothiazines (trifluoperazine and chlorpromazine), mepacrine, propranolol, and colchicine inhibited the effect of the purified epidermal calmodulin on the calmodulin-deficient phosphodiesterase of bovine heart.	Quinacrine	53-62	calmodulin-3	Sus scrofa	157-167
2981065-7	1985	Quinacrine, a phospholipase A2 inhibitor, also abolished the stimulatory effect of phospholipase A2 or TRH on PRL release.	Quinacrine	0-10	phospholipase A2 group IB	Homo sapiens	83-99
2981065-7	1985	Quinacrine, a phospholipase A2 inhibitor, also abolished the stimulatory effect of phospholipase A2 or TRH on PRL release.	Quinacrine	0-10	prolactin	Homo sapiens	110-113
2981065-8	1985	In cultured cells, quinacrine inhibits basal PRL release, but does not affect PRL release induced by arachidonate or (Bu)2 cAMP.	Quinacrine	19-29	prolactin	Homo sapiens	45-48
20493019-2	1985	Chloroquine and quinacrine, which block the action of phospholipase A(2), inhibited either the phospholipase A(2)-stimulated or the high potassium-stimulated release of [(3)H]norepinephrine from synaptosomes.	Quinacrine	16-26	phospholipase A2 group IB	Rattus norvegicus	54-72
20493019-2	1985	Chloroquine and quinacrine, which block the action of phospholipase A(2), inhibited either the phospholipase A(2)-stimulated or the high potassium-stimulated release of [(3)H]norepinephrine from synaptosomes.	Quinacrine	16-26	phospholipase A2 group IB	Rattus norvegicus	95-113
6147162-0	1984	Mepacrine-induced inhibition of human platelet cyclic-GMP phosphodiesterase.	Quinacrine	0-9	5'-nucleotidase, cytosolic II	Homo sapiens	54-57
6149270-4	1984	In addition, this event was inhibited by quinacrine, 5,8,11,14-eicosatetraynoic acid, and nordi-hydroguaiaretic acid, suggesting involvement of phospholipase A2 with subsequent formation of lipoxygenase metabolities of arachidonic acid.	Quinacrine	41-51	phospholipase A2, group IB, pancreas	Mus musculus	144-160
6497852-7	1984	Three different additives, quinacrine, p-chloromercuribenzoate and cetyltrimethylammonium bromide, strongly inhibited O2.- generation; they also inhibited the reduction by NADPH of cytochrome b at the same low concentrations.	Quinacrine	27-37	cytochrome b	Sus scrofa	181-193
6094288-8	1984	Phospholipase A2 inhibitors (quinacrine, bromophenacylbromide) block maturation; inhibition is reversed by increasing the 1-MeAde concentration and only occurs during the hormone-dependent period.	Quinacrine	29-39	phospholipase A2 group IB	Homo sapiens	0-16
6488390-2	1984	The N-demethylation of benzphetamine (cytochrome P-450) was inhibited by chloroquine only while the O-deethylation of ethoxyresorufin (cytochrome P-448) was inhibited by primaquine and quinacrine.	Quinacrine	185-195	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	135-151
6488390-5	1984	These observations demonstrate that chloroquine and quinacrine are specific inhibitors of cytochromes P-450 and P-448, respectively.	Quinacrine	52-62	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	102-117
6147162-9	1984	Mepacrine blocks arachidonate release from human platelets by inhibiting phosphatidylinositol-specific phospholipase C. The increase in cyclic-GMP levels produced by addition of mepacrine will explain part of the pharmacological action of this drug.	Quinacrine	178-187	5'-nucleotidase, cytosolic II	Homo sapiens	143-146
6147162-1	1984	The effect of mepacrine (DL-quinacrine-HCI), a specific inhibitor of phospholipase C, on cyclic-GMP levels in human platelets was investigated.	Quinacrine	14-23	5'-nucleotidase, cytosolic II	Homo sapiens	96-99
6147162-3	1984	Addition of mepacrine to human platelet suspension resulted in increases in cyclic GMP.	Quinacrine	12-21	5'-nucleotidase, cytosolic II	Homo sapiens	83-86
6147162-5	1984	Mepacrine did not stimulate guanylate cyclase, but did specifically inhibit human platelet cyclic-GMP phosphodiesterase, separated from cyclic-AMP phosphodiesterase or other forms of phosphodiesterase on DEAE-cellulose columns.	Quinacrine	0-9	5'-nucleotidase, cytosolic II	Homo sapiens	98-101
6147162-8	1984	Mepacrine was 30-times more potent as an inhibitor of human platelet cyclic GMP than of cyclic-AMP phosphodiesterase.	Quinacrine	0-9	5'-nucleotidase, cytosolic II	Homo sapiens	76-79
6147162-9	1984	Mepacrine blocks arachidonate release from human platelets by inhibiting phosphatidylinositol-specific phospholipase C. The increase in cyclic-GMP levels produced by addition of mepacrine will explain part of the pharmacological action of this drug.	Quinacrine	0-9	5'-nucleotidase, cytosolic II	Homo sapiens	143-146
6430571-1	1984	The reagents quinacrine, hydrocortisone, and dexamethasone have been assumed to affect phospholipase A2 (PA2) when they reduce natural killer (NK) activity.	Quinacrine	13-23	phospholipase A2 group IB	Homo sapiens	87-103
6430571-1	1984	The reagents quinacrine, hydrocortisone, and dexamethasone have been assumed to affect phospholipase A2 (PA2) when they reduce natural killer (NK) activity.	Quinacrine	13-23	phospholipase A2 group IB	Homo sapiens	105-108
6589024-7	1984	Addition of mepacrine (2.1 X 10(-5)M) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A-23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced.	Quinacrine	12-21	angiotensinogen	Rattus norvegicus	210-213
6328532-3	1984	Instead, we have found that muscarinic or histamine H1 receptor stimulation elicits the release of arachidonic acid through a quinacrine-sensitive mechanism, possibly phospholipase A2.	Quinacrine	126-136	histamine receptor H1	Homo sapiens	42-63
6383404-2	1984	The phospholipase A2 was activated by Ca2+ (Ka approximately 0.5 mM) and inhibited by mepacrine.	Quinacrine	86-95	phospholipase A2 group IB	Rattus norvegicus	4-20
6328532-3	1984	Instead, we have found that muscarinic or histamine H1 receptor stimulation elicits the release of arachidonic acid through a quinacrine-sensitive mechanism, possibly phospholipase A2.	Quinacrine	126-136	phospholipase A2 group IB	Homo sapiens	167-183
6428500-5	1984	Mepacrine, a phospholipase A2 inhibitor, at 2.5 microM reduced PGAP -induced MDA formation and [14C]-5-HT release by the resuspended platelets without affecting irreversible aggregation; higher concentrations of mepacrine abolished all three responses.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	13-29
6428500-11	1984	Thrombin-induced aggregation was accompanied by substantial loss of 14C from phospholipids and equivalent gains of 14C in free fatty acids and TxB2; mepacrine pretreatment caused partial inhibition of thrombin-induced aggregation, halved the net 14C loss from phospholipids, but had little effect on the appearance of 14C in TxB2.	Quinacrine	149-158	coagulation factor II, thrombin	Homo sapiens	0-8
6428500-11	1984	Thrombin-induced aggregation was accompanied by substantial loss of 14C from phospholipids and equivalent gains of 14C in free fatty acids and TxB2; mepacrine pretreatment caused partial inhibition of thrombin-induced aggregation, halved the net 14C loss from phospholipids, but had little effect on the appearance of 14C in TxB2.	Quinacrine	149-158	coagulation factor II, thrombin	Homo sapiens	201-209
6147931-3	1984	Mepacrine, a phospholipase A2 inhibitor, suppressed the generation of both leukotrienes (SRS) and prostaglandins (PG), whereas the lipoxygenase inhibitor BW 755C reduced the generation of SRS, and the cyclooxygenase inhibitor indomethacin significantly suppressed the generation of PG.	Quinacrine	0-9	phospholipase A2 group IB	Rattus norvegicus	13-29
6607286-3	1984	Because other phospholipase A2 inhibitors such as tetracaine and p-bromophenacyl bromide could inhibit these reactions, the inhibition of cytotoxic T lymphocyte responses by quinacrine appeared to be attributable to the inhibition of phospholipase A2 in these cells.	Quinacrine	174-184	phospholipase A2 group IB	Homo sapiens	234-250
6425068-4	1984	Conversely, quinacrine (50 microM), an inhibitor of phospholipase A2 activity, inhibited basal and stimulated TSH release from pituitary cells perifused in columns.	Quinacrine	12-22	phospholipase A2 group IB	Homo sapiens	52-68
6141801-4	1984	Venoconstriction caused by U46619, bradykinin and 5-hydroxytryptamine was reduced during inhibition of phospholipase A2 with mepacrine.	Quinacrine	125-134	kininogen 1	Homo sapiens	35-45
6418521-4	1984	The phospholipase A2 inhibitors quinacrine and dibromoacetophenone blocked stimulation of PRL release by melittin and by themselves inhibited spontaneous PRL secretion.	Quinacrine	32-42	LOC104974671	Bos taurus	4-20
6091414-6	1984	The phospholipase A2 inhibitor, mepacrine, tended to decrease carbachol actions.	Quinacrine	32-41	phospholipase A2 group IB	Homo sapiens	4-20
6088738-5	1984	These changes in beta-adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor.	Quinacrine	72-82	phospholipase A2 group IB	Rattus norvegicus	86-102
6607286-2	1984	These observations were further supported by the finding that quinacrine inhibited the expression of Tac antigen, the receptor for growth factor(s).	Quinacrine	62-72	interleukin 2 receptor subunit alpha	Homo sapiens	101-112
6641623-5	1983	The action of PRL on ODC activity was significantly attenuated by quinacrine, an inhibitor of PLC and PLA2 activities.	Quinacrine	66-76	prolactin	Mus musculus	14-17
6641623-5	1983	The action of PRL on ODC activity was significantly attenuated by quinacrine, an inhibitor of PLC and PLA2 activities.	Quinacrine	66-76	ornithine decarboxylase, structural 1	Mus musculus	21-24
6641623-5	1983	The action of PRL on ODC activity was significantly attenuated by quinacrine, an inhibitor of PLC and PLA2 activities.	Quinacrine	66-76	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	94-97
6641623-5	1983	The action of PRL on ODC activity was significantly attenuated by quinacrine, an inhibitor of PLC and PLA2 activities.	Quinacrine	66-76	phospholipase A2, group V	Mus musculus	102-106
6626566-9	1983	Indomethacin, sodium meclofenamate and mepacrine, but not dexamethasone or aspirin, inhibited the sperm phospholipase A2 activity.	Quinacrine	39-48	phospholipase A2, group IB, pancreas	Mus musculus	104-120
6197128-6	1983	Calmodulin inhibitors, phenothiazines, R24571 and mepacrine, inhibited the histamine release induced by either calcium or lanthanides.	Quinacrine	50-59	calmodulin 1	Rattus norvegicus	0-10
6887013-2	1983	In the heart, the phospholipase A2 inhibitor mepacrine (10(-4) M) reduced the choline efflux (1.1 nmol g-1 min-1) by 51 +/- 5% (N = 3), whereas several cholinesterase inhibitors (physostigmine, neostigmine and diisopropylfluorophosphate) and muscarinic agonists (acetylcholine, oxotremorine and bethanechol) caused an increase.	Quinacrine	45-54	phospholipase A2 group IB	Rattus norvegicus	18-34
6887013-2	1983	In the heart, the phospholipase A2 inhibitor mepacrine (10(-4) M) reduced the choline efflux (1.1 nmol g-1 min-1) by 51 +/- 5% (N = 3), whereas several cholinesterase inhibitors (physostigmine, neostigmine and diisopropylfluorophosphate) and muscarinic agonists (acetylcholine, oxotremorine and bethanechol) caused an increase.	Quinacrine	45-54	butyrylcholinesterase	Rattus norvegicus	152-166
6413878-2	1983	Agents that decrease its production by blocking phospholipase A2 activity, i.e., quinacrine and 4-bromophenacylbromide, significantly decreased prolactin secretion from anterior pituitary glands in vitro and from dispersed pituitary cells in a perifusion column.	Quinacrine	81-91	phospholipase A2 group IB	Homo sapiens	48-64
6413878-2	1983	Agents that decrease its production by blocking phospholipase A2 activity, i.e., quinacrine and 4-bromophenacylbromide, significantly decreased prolactin secretion from anterior pituitary glands in vitro and from dispersed pituitary cells in a perifusion column.	Quinacrine	81-91	prolactin	Homo sapiens	144-153
6306770-3	1983	Thrombin-stimulated cyclic GMP formation was inhibited by mepacrine and nordihydroguaiaretic acid but unaffected by indomethacin, suggesting that lipoxygenase metabolites of arachidonic acid are involved in the response.	Quinacrine	58-67	coagulation factor II	Mus musculus	0-8
6306770-3	1983	Thrombin-stimulated cyclic GMP formation was inhibited by mepacrine and nordihydroguaiaretic acid but unaffected by indomethacin, suggesting that lipoxygenase metabolites of arachidonic acid are involved in the response.	Quinacrine	58-67	5'-nucleotidase, cytosolic II	Mus musculus	27-30
6352447-6	1983	Both quinacrine (an inhibitor of phospholipase A2 activity) and indomethacin (an inhibitor of prostaglandin biosynthesis) abolished the action of prolactin on [3H]-thymidine incorporation into DNA.	Quinacrine	5-15	phospholipase A2, group IB, pancreas	Mus musculus	33-49
6311573-5	1983	The prostaglandin synthetase inhibitors acetyl salicylic acid and indomethacin and the phospholipase A2 inhibitor quinacrine all abolished the increase in adenylate cyclase activity produced by delta 9-THC, suggesting the involvement of prostaglandins in this cannabinoid action.	Quinacrine	114-124	phospholipase A2, group IB, pancreas	Mus musculus	87-103
6870935-6	1983	Quantitative analysis of these mepacrine effects, together with the known inhibitory effects of this compound on phospholipase A2 and phosphatidylinositol-specific phospholipase C, suggests that mepacrine also inhibits phosphatidic acid phosphatase, thereby shunting the flux of phosphatidic acid away from diglyceride formation and into synthesis of phosphatidylinositol.	Quinacrine	195-204	phospholipase A2 group IB	Homo sapiens	113-129
16663096-11	1983	The NO(3) (-)-sensitive ATPase was stimulated by gramicidin and was associated with NO(3) (-)-inhibitable H(+) transport measured as quenching of quinacrine fluorescence.	Quinacrine	146-156	ATPase	Zea mays	24-30
6859870-5	1983	Increased lysophosphatidylcholine formation was evident following lipid peroxidation in phospholipase A2-containing liposomes which was inhibited by p-bromophenacyl bromide and mepacrine.	Quinacrine	177-186	phospholipase A2 group IB	Rattus norvegicus	88-104
6354779-6	1983	These glucose-induced increases in 3H-arachidonic acid-derived radioactivity in both the phospholipid and the prostaglandin fractions were eliminated by the inhibition of phospholipase A2 activity with mepacrine or by the inhibition of cyclooxygenase activity with sodium salicylate.	Quinacrine	202-211	phospholipase A2 group IB	Rattus norvegicus	171-187
6887041-1	1983	Injection of two chemically dissimilar inhibitors of phospholipase A2 (mepacrine and parabromophenacylbromide) into the cerebral ventricles of rabbits inhibited the febrile response to endogenous pyrogen given by the same route.	Quinacrine	71-80	phospholipase A2	Oryctolagus cuniculus	53-69
6303851-4	1983	Quinacrine inhibited membrane depolarization, superoxide (O-2) generation, and net phosphatidylserine production with ID50-values of 16 microM and greater than 500 microM, respectively.	Quinacrine	0-10	immunoglobulin kappa variable 1D-39	Homo sapiens	58-61
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Quinacrine	0-9	kininogen 1	Homo sapiens	46-56
6575779-1	1983	Lipid peroxidation induced by ascorbic acid and Fe2+ was inhibited by mepacrine (phospholipase A2 inhibitor) and aspirin (prostaglandin cyclo-oxygenase inhibitor) in rabbit kidney-medulla slices.	Quinacrine	70-79	phospholipase A2	Oryctolagus cuniculus	81-97
6847709-3	1983	Phospholipase A2 inhibitors, such as quinacrine, chloroquine, quinine and p-bromophenacyl bromide, all inhibited the secretion of catecholamines evoked by carbamylcholine in a dose-dependent manner.	Quinacrine	37-47	LOC104974671	Bos taurus	0-16
6401298-7	1983	The stimulatory effect of zymosan and the ionophore on alkylacetyl-GPC release was prevented by mepacrine (0.1 mM), an agent that inhibits the release of fatty acids from phospholipids.	Quinacrine	96-105	glycophorin C	Rattus norvegicus	67-70
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.	Quinacrine	140-150	calmodulin 1	Homo sapiens	216-226
6297604-5	1983	Exposure of isolated type II cells to the phospholipase A2 inhibitors 4-bromophenacylbromide or quinacrine dihydrochloride led to a decreased synthesis of total phosphatidylcholines from various labelled precursors.	Quinacrine	96-122	phospholipase A2 group IB	Rattus norvegicus	42-58
6147364-1	1983	Mepacrine, a phospholipase A2 inhibitor, caused concentration-dependent elevations of cyclic GMP levels without changing cyclic AMP levels in washed rabbit platelets.	Quinacrine	0-9	phospholipase A2	Oryctolagus cuniculus	13-29
6819863-2	1982	Calmodulin antagonists, such as trifluoperazine, dibucaine and quinacrine, inhibited the secretion of N-acetyl-beta-d-glucosaminidase from cytochalasin B-treated macrophages when the macrophages were stimulated by the chemotactic peptide, formylmethionyl-leucyl-phenylalanine (f Met-Leu-Phe) or the Ca(2+) ionophore A23187.	Quinacrine	63-73	calmodulin-3	Cavia porcellus	0-10
6129307-0	1982	Stimulation of polymorphonuclear leucocyte phospholipase A2 activity by chloroquine and mepacrine.	Quinacrine	88-97	phospholipase A2 group IB	Homo sapiens	43-59
7138896-4	1982	Contrary to previous reports, a biphasic modulatory role of mepacrine on phospholipase A2 activity and platelet aggregation was demonstrated.	Quinacrine	60-69	phospholipase A2 group IB	Rattus norvegicus	73-89
7126467-5	1982	The pellet of isolated mepacrine-fluorescent granules consisted almost entirely of granules with the typical appearance of dense bodies, as shown by electron microscopy, and was relatively free from membranes and other granule populations as evaluated by the presence of the different markers (tritiated lectin, beta-glucuronidase, monoamine oxidase, platelet factor 4).	Quinacrine	23-32	platelet factor 4	Homo sapiens	312-368
6752047-8	1982	Nonetheless, arachidonate metabolites were critical for the LAI phenomenon since BPB and mepacrine, inhibitors of phospholipase A2, negated the LAI response.	Quinacrine	89-98	phospholipase A2 group IB	Homo sapiens	114-130
6807980-10	1982	Indomethacin and aspirin, which inhibit the cyclooxygenase, and mepacrine, which inhibits the Ca2+-activated phospholipase A2, markedly reduced the increase in prostaglandin production.	Quinacrine	64-73	phospholipase A2 group IB	Rattus norvegicus	109-125
6810948-6	1982	Both bradykinin and ionophore A23187 stimulated [3H]arachidonate release from endothelial cell phospholipids, an effect which was abolished in a dose-dependent manner by mepacrine.	Quinacrine	170-179	kininogen 1	Homo sapiens	5-15
6805948-5	1982	More specific phospholipase A2 inhibitors, mepacrine (20 mumol/mouse) and p-bromophenacyl bromide (10 mumol/mouse), also inhibited the ODC induction.	Quinacrine	43-52	phospholipase A2, group IB, pancreas	Mus musculus	14-30
6805948-5	1982	More specific phospholipase A2 inhibitors, mepacrine (20 mumol/mouse) and p-bromophenacyl bromide (10 mumol/mouse), also inhibited the ODC induction.	Quinacrine	43-52	ornithine decarboxylase, structural 1	Mus musculus	135-138
6805948-6	1982	The TPA-induced ODC inhibited by mepacrine was not restored by the treatment of mice with PGE2.	Quinacrine	33-42	ornithine decarboxylase, structural 1	Mus musculus	16-19
6805948-7	1982	TPA-induced ODC inhibited by either mepacrine or p-bromophenacyl bromide was partially but significantly restored by treatment with arachidonic acid (1 to 40 mumol/mouse).	Quinacrine	36-45	ornithine decarboxylase, structural 1	Mus musculus	12-15
6895907-4	1982	In addition, 3-deaza-SIBA, an inhibitor of transmethylation reactions and quinacrine, an inhibitor of phospholipase A2, appear to act before the Ca2+-dependent programming for lysis.	Quinacrine	74-84	phospholipase A2, group IB, pancreas	Mus musculus	102-118
6286943-2	1982	Active Cl, but not Na, transport across the toad cornea was inhibited by mepacrine, which is a phospholipase A2 inhibitor; trifluoperazine, which blocks the action of calmodulin; and meclofenamic acid, which inhibits synthesis of prostaglandins.	Quinacrine	73-82	phospholipase A2 group IB	Homo sapiens	95-111
7037068-5	1982	Aggregation and release of 14C-serotonin and PF4 were inhibited by the metabolic inhibitors 2-deoxyglucose (16.7 mM) and antimycin-A (8.3 micrograms/ml), by the membrane-active drugs mepacrine (10 microM) and chlorpromazine (0.025 mM), by PGI2 (5.34 nM), which elevates intracellular c-AMP, by indomethacin (10 microM) or aspirin (100 microM).	Quinacrine	183-192	platelet factor 4	Homo sapiens	45-48
6701402-1	1984	Human platelets appear to accumulate quinacrine both in a thrombin-releasable compartment (dense bodies or amine storage vesicles) and in another compartment from which it is released by agents known to collapse pH gradients (possibly lysosomes with an acidic interior).	Quinacrine	37-47	coagulation factor II, thrombin	Homo sapiens	58-66
6803530-2	1981	The initial thrombin-activated phospholipase C-mediated reaction is quinacrine insensitive and is followed by quinacrine-sensitive phospholipase A2 activities.	Quinacrine	68-78	coagulation factor II, thrombin	Homo sapiens	12-20
6284950-4	1982	In the present study the effects of reported inhibitors of phospholipase A2 (quinacrine, chlorpromazine, dexamethasone, and dibutyryl cyclic AMP) on diethyl maleate (DEM)-induced lipid peroxidation, reduced glutathione (GSH) depletion, and cellular injury were examined in isolated hepatocyte suspensions.	Quinacrine	77-87	phospholipase A2 group IB	Rattus norvegicus	59-75
6281811-2	1982	Mepacrine (20 microgram/ml), an inhibitor of phospholipase A2, abolished the action of LTB4 on parenchymal strips.	Quinacrine	0-9	prostaglandin reductase 1	Cavia porcellus	87-91
6803530-2	1981	The initial thrombin-activated phospholipase C-mediated reaction is quinacrine insensitive and is followed by quinacrine-sensitive phospholipase A2 activities.	Quinacrine	68-78	phospholipase A2 group IB	Homo sapiens	131-147
6803530-2	1981	The initial thrombin-activated phospholipase C-mediated reaction is quinacrine insensitive and is followed by quinacrine-sensitive phospholipase A2 activities.	Quinacrine	110-120	coagulation factor II, thrombin	Homo sapiens	12-20
6803530-2	1981	The initial thrombin-activated phospholipase C-mediated reaction is quinacrine insensitive and is followed by quinacrine-sensitive phospholipase A2 activities.	Quinacrine	110-120	phospholipase A2 group IB	Homo sapiens	131-147
7053072-3	1981	Indeed, the PLA2 inhibitors, bromophenacyl bromide (BPB), mepacrine, 874CB (100 microM), and EDTA (5 mM), blocked the zymosan-induced release of PAF-acether from PC.	Quinacrine	58-67	phospholipase A2, group IB, pancreas	Mus musculus	12-16
6117560-4	1981	The combination of 3-deazaadenosine and homocysteine thiolactone, which inhibits phospholipid methylation, and quinacrine, an inhibitor of phospholipase A2, also abolishes the response to the peptide.	Quinacrine	111-121	phospholipase A2	Oryctolagus cuniculus	139-155
6798947-6	1981	Inhibitors of phospholipase A2 (mepacrine, p-bromophenacyl bromide) abolished the noradrenaline-induced PGE2-release and reduced the effect of A 23187; the stimulation of PGE2-release by arachidonic acid was not affected.	Quinacrine	32-41	phospholipase A2	Oryctolagus cuniculus	14-30
6271829-3	1981	The release reaction could be antagonized by phospholipase A2 inhibitors such as quinacrine and quinine, suggesting that THC can stimulate the activity of this enzyme.	Quinacrine	81-91	phospholipase A2 group IB	Homo sapiens	45-61
6112882-8	1981	Daily injection of quinacrine (16 mg/kg), an antimalarial agent that inhibits phospholipase A2, blocked the subsensitivity to the chronotropic effect of epinephrine, but not that to the pressor effect of epinephrine.	Quinacrine	19-29	phospholipase A2 group IB	Rattus norvegicus	78-94
7281105-1	1981	We have examined whether inhibition by mepacrine or freeing of arachidonic acid from platelet phospholipids inhibits platelet aggregation to collagen, thrombin or ADP, and the release reaction induced by thrombin or collagen.	Quinacrine	39-48	coagulation factor II, thrombin	Homo sapiens	151-159
7281105-5	1981	Mepacrine inhibited ADP-induced platelet aggregation by inhibiting the association of fibrinogen with platelets during aggregation.	Quinacrine	0-9	fibrinogen beta chain	Homo sapiens	86-96
7281105-6	1981	The effect of mepacrine on fibrinogen binding could be considerably decreased by washing the platelets but the inhibition of 14C loss persisted.	Quinacrine	14-23	fibrinogen beta chain	Homo sapiens	27-37
7281105-8	1981	Thus, mepacrine has two effects; 1. it inhibits phospholipases, 2. it inhibits fibrinogen binding.	Quinacrine	6-15	fibrinogen beta chain	Homo sapiens	79-89
6785276-8	1981	The data thus indicate the existence of a quinacrine-insensitive phospholipase C which can initially convert a given amount of PI to PA and which is closely associated to the thrombin receptor.	Quinacrine	42-52	coagulation factor II, thrombin	Homo sapiens	175-183
6785276-9	1981	The further breakdown of PI and production of arachidonic acid might result from the action of quinacrine-sensitive activities (i.e. phospholipase A2).	Quinacrine	95-105	phospholipase A2 group IB	Homo sapiens	133-149
6785276-10	1981	The simplest scheme is one in which thrombin specifically produces an active fraction of PA which in some way results in the subsequent production of arachidonic acid from various phospholipids (including PI), perhaps by activation of quinacrine-sensitive phospholipase A2.	Quinacrine	235-245	coagulation factor II, thrombin	Homo sapiens	36-44
6785276-10	1981	The simplest scheme is one in which thrombin specifically produces an active fraction of PA which in some way results in the subsequent production of arachidonic acid from various phospholipids (including PI), perhaps by activation of quinacrine-sensitive phospholipase A2.	Quinacrine	235-245	phospholipase A2 group IB	Homo sapiens	256-272
7007379-6	1981	The phospholipase A2 inhibitors, chloroquine and quinacrine, prevented the effect of GnRH on arachidonic acid formation and LH release.	Quinacrine	49-59	phospholipase A2 group IB	Homo sapiens	4-20
7007379-6	1981	The phospholipase A2 inhibitors, chloroquine and quinacrine, prevented the effect of GnRH on arachidonic acid formation and LH release.	Quinacrine	49-59	gonadotropin releasing hormone 1	Homo sapiens	85-89
6257888-3	1981	These changes in beta adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor, although the drug had no effect on beta adrenoceptors when given alone.	Quinacrine	72-82	phospholipase A2 group IB	Rattus norvegicus	86-102
6258719-6	1981	Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells.	Quinacrine	93-102	phospholipase A2 group IB	Rattus norvegicus	65-81
6258719-6	1981	Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells.	Quinacrine	104-114	phospholipase A2 group IB	Rattus norvegicus	65-81
922007-1	1977	The interactions of a quinacrine derivative, methylated at both the aromatic and aliphatic nitrogens, and propidium diiodide with the dinucleoside monophosphates CpG, GpC, UpA and ApU have been investigated using 13C-NMR (for the quinacrine derivative prepared with [13C]methyl substituents and 1H-NMR and ultraviolet-visible spectroscopy.	Quinacrine	22-32	glycophorin C (Gerbich blood group)	Homo sapiens	167-170
6262771-0	1981	Local anesthetics, mepacrine, and propranolol are antagonists of calmodulin.	Quinacrine	19-28	calmodulin 1	Homo sapiens	65-75
7313587-5	1981	A 1-week course of metronidazole (200 mg 3 times daily) was successful in 8/9 failures; 1 patient was finally cured with mepacrine.	Quinacrine	121-130	BCL2 related protein A1	Homo sapiens	0-3
6109256-4	1980	PG release was abolished by indometacin (1-3 microgram/ml) and reduced by the phospholipase A2 inhibitor quinacrine (10 microgram/ml) as well as by perfusing with calcium-free, 1 mM EGTA containing solution.	Quinacrine	105-115	LOC104974671	Bos taurus	78-94
6263163-0	1980	Antagonism of calmodulin by local anesthetics, mepacrine, and propranolol.	Quinacrine	47-56	calmodulin 1	Homo sapiens	14-24
533666-3	1979	Studies done with quinacrine staining of seven day old pupal foot-pad polytene nuclei showed that the granules fluoresced very brightly while the chromosomal bands to which the granules were attached did not.	Quinacrine	18-28	Partner of Bursicon	Drosophila melanogaster	55-60
533666-6	1979	Most of the label on these slides was concentrated on the centromeric heterochromatin of chromosomes C and E. Quinacrine staining of the foot-pad cells at very early stages of pupal development showed that when granules were present, they were always closely associated with the same two centromeric regions, those of chromosomes C and E. Since the highly repetitive DNA located in these centromeric regions is underreplicated, we conclude that the granules result from an extrusion process which takes place early during the polytenization of these cells.	Quinacrine	110-120	Partner of Bursicon	Drosophila melanogaster	176-181
225265-2	1979	Both these bradykinin-induced reactions are inhibited by quinacrine, an inhibitor of phospholipase A activity.	Quinacrine	57-67	kininogen 1	Homo sapiens	11-21
95126-1	1979	Quinacrine at concentrations of 0.025 mM and greater significantly reduced or abolished the prolactin stimulation of RNA synthesis in mouse mammary gland explants.	Quinacrine	0-10	prolactin	Mus musculus	92-101
95126-3	1979	The possible relationship of these actions of quinacrine to its inhibition of phospholipase A2 and/or prostaglandin biosynthesis is discussed.	Quinacrine	46-56	phospholipase A2, group IB, pancreas	Mus musculus	78-94
111464-3	1979	The liberation of arachidonic acid from membrane-bound phospholipids, induced by the enzyme phospholipase A2, may be inhibited by mepacrine and the steroidal anti-inflammatory agents.	Quinacrine	130-139	phospholipase A2 group IB	Homo sapiens	92-108
6818615-5	1982	Mepacrine (phospholipase A2 inhibitor) also suppressed collagen dissolution.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	11-27
6257896-24	1980	These data suggest that quinacrine"s main action is a slow, voltage dependent blockade of open end-plate channels, though there are probably additional effects on acetylcholinesterase and channel opening.	Quinacrine	24-34	acetylcholinesterase (Cartwright blood group)	Homo sapiens	163-183
6246490-5	1980	Mepacrine and tetracaine, both inhibitors of this phospholipase A2, are able to block l-isoproterenol-induced desensitization of cyclic AMP production and the decrease in beta-adrenergic receptors.	Quinacrine	0-9	phospholipase A2 group IB	Homo sapiens	50-66
225265-0	1979	Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 and F2 alpha in human synovial fibroblasts.	Quinacrine	56-66	kininogen 1	Homo sapiens	14-24
922007-1	1977	The interactions of a quinacrine derivative, methylated at both the aromatic and aliphatic nitrogens, and propidium diiodide with the dinucleoside monophosphates CpG, GpC, UpA and ApU have been investigated using 13C-NMR (for the quinacrine derivative prepared with [13C]methyl substituents and 1H-NMR and ultraviolet-visible spectroscopy.	Quinacrine	22-32	proline rich acidic protein 1	Homo sapiens	172-175
17672-5	1977	Such aggregation was inhibited by two phospholipase A2 inhibitors, bromophenacyl bromide and mepacrine.	Quinacrine	93-102	phospholipase A2	Oryctolagus cuniculus	38-54
13413145-9	1957	The action of mepacrine on plasmodial hexokinase was reduced by raising the concentration of ATP, but, as with yeast hexokinase, the inhibition by 10,732 was independent of the ATP concentration.From a consideration of the results, it seems doubtful whether this type of inhibitory effect plays more than a minor part in the mechanism of antimalarial action in vivo.	Quinacrine	14-23	hexokinase	Saccharomyces cerevisiae S288C	38-48
837023-6	1977	6 Mepacrine, a drug which possesses weak anti-phospholipase activity in platelets, also prevents aggregation by collagen or thrombin, but seems to do so by preventing substrate release from the phosphatide fraction.	Quinacrine	2-11	prothrombin	Oryctolagus cuniculus	124-132
415534-4	1977	The phospholipase A2 inhibitors bromophenacyl bromide and mepacrine, the chymotrypsin inhibitor tosylphenylalaninechloromethylketone, catalase and dithiothreitol also inhibited aggregation, whereas inhibitors of trypsin failed to do so.	Quinacrine	58-67	phospholipase A2	Oryctolagus cuniculus	4-20
61819-11	1976	The identity of the quinacrine-positive fibers is discussed with respect to recent suggestions that "purinergic", substance P, enkephalin, and somatosin-containing nerves, in addition to adrenergic and cholinergic nerves, are present in the gut wall.	Quinacrine	20-30	proenkephalin	Rattus norvegicus	127-137
11946657-0	1972	Energy transduction in photosynthetic bacteria V. Role of coupling factor ATPase in energy conversion as revealed by light or ATP-induced quenching of atebrine fluorescence.	Quinacrine	151-159	dynein axonemal heavy chain 8	Homo sapiens	74-80
4388687-20	1968	The dehydrogenase is inhibited by semicarbazide (K(i) 3.35mum), isoniazid (K(i) 1.17mum), cuprizone (K(i) 0.49mum), p-chloromercuribenzoate (K(i) 0.45mm) and quinacrine (K(i) 12.1mm).	Quinacrine	158-168	MEXAM1_RS21720	Methylobacterium extorquens AM1	4-17
4285331-11	1965	The reduction of cytochrome c by purified preparations of MP differs from its reduction of tetrazolium salts in that the cytochrome reaction is completely inhibited by BAL and partially inhibited by amytal, atabrine, and antimycin A.	Quinacrine	207-215	cytochrome c, somatic	Gallus gallus	17-29
1200845-1	1975	The antiviral activity and induction of interferon-like substance by mepacrine (quinacrine, Atabrine) and Acranil in mice, described previuosly, was studied in more detail and compared with tilorone.	Quinacrine	69-78	interferon	Gallus gallus	40-50
1200845-1	1975	The antiviral activity and induction of interferon-like substance by mepacrine (quinacrine, Atabrine) and Acranil in mice, described previuosly, was studied in more detail and compared with tilorone.	Quinacrine	80-90	interferon	Gallus gallus	40-50
1200845-1	1975	The antiviral activity and induction of interferon-like substance by mepacrine (quinacrine, Atabrine) and Acranil in mice, described previuosly, was studied in more detail and compared with tilorone.	Quinacrine	92-100	interferon	Gallus gallus	40-50
1200845-4	1975	Mepacrine was found to be a wealer interferon inducer than either tilorone or Acranil.	Quinacrine	0-9	interferon	Gallus gallus	35-45
13413145-9	1957	The action of mepacrine on plasmodial hexokinase was reduced by raising the concentration of ATP, but, as with yeast hexokinase, the inhibition by 10,732 was independent of the ATP concentration.From a consideration of the results, it seems doubtful whether this type of inhibitory effect plays more than a minor part in the mechanism of antimalarial action in vivo.	Quinacrine	14-23	hexokinase	Saccharomyces cerevisiae S288C	117-127
33939112-7	2021	RESULTS: We identified Auranofin, Colchicine, Monensin, Niclosamide, Podophyllotoxin, Quinacrine and Thiostrepton as efficient inhibitors of invasive growth of 2nd line HER2 inhibitor lapatinib resistant breast cancer spheroids and ovarian cancer organoids.	Quinacrine	86-96	erb-b2 receptor tyrosine kinase 2	Homo sapiens	169-173
33795785-3	2021	In vitro, the off-patent antibiotic Quinacrine efficiently suppressed PRMT5 transcription, causing chromatin remodelling with reduced global histone H4 symmetrical demethylation.	Quinacrine	36-46	protein arginine methyltransferase 5	Homo sapiens	70-75
33919392-0	2021	Quinacrine-Induced Autophagy in Ovarian Cancer Triggers Cathepsin-L Mediated Lysosomal/Mitochondrial Membrane Permeabilization and Cell Death.	Quinacrine	0-10	cathepsin L	Homo sapiens	56-67
33795785-4	2021	Quinacrine phenocopied PRMT5 RNA interference and small molecule PRMT5 inhibition, reducing clonogenicity in an MTAP-dependent manner.	Quinacrine	0-10	protein arginine methyltransferase 5	Homo sapiens	23-28
33795785-4	2021	Quinacrine phenocopied PRMT5 RNA interference and small molecule PRMT5 inhibition, reducing clonogenicity in an MTAP-dependent manner.	Quinacrine	0-10	protein arginine methyltransferase 5	Homo sapiens	65-70
33795785-4	2021	Quinacrine phenocopied PRMT5 RNA interference and small molecule PRMT5 inhibition, reducing clonogenicity in an MTAP-dependent manner.	Quinacrine	0-10	methylthioadenosine phosphorylase	Homo sapiens	112-116
33795785-6	2021	We identified c-jun as an essential PRMT5 transcription factor and a probable target for Quinacrine.	Quinacrine	89-99	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19
33795785-6	2021	We identified c-jun as an essential PRMT5 transcription factor and a probable target for Quinacrine.	Quinacrine	89-99	protein arginine methyltransferase 5	Homo sapiens	36-41
33713017-8	2021	We report that quinacrine and niclosamide, like BMP2, significantly increased neurite length, as a readout of neurotrophic action, in SH-SY5Y cells and dopaminergic neurons in primary cultures of rat ventral mesencephalon.	Quinacrine	15-25	bone morphogenetic protein 2	Homo sapiens	48-52
33713017-0	2021	Quinacrine and Niclosamide Promote Neurite Growth in Midbrain Dopaminergic Neurons Through the Canonical BMP-Smad Pathway and Protect Against Neurotoxin and alpha-Synuclein-Induced Neurodegeneration.	Quinacrine	0-10	bone morphogenetic protein 1	Homo sapiens	105-108
33735393-0	2021	Sensitization of A-549 lung cancer cells to Cisplatin by Quinacrine-loaded lipidic nanoparticles via suppressing Nrf2 mediated defense mechanism.	Quinacrine	57-67	NFE2 like bZIP transcription factor 2	Homo sapiens	113-117
33735393-2	2021	By harnessing liposome as an advanced nanoparticles transporter, we formulated Quinacrine known as nrf2 inhibitor into nano-carrier, and sensitized A-549 lung tumor cells to Cisplatin.	Quinacrine	79-89	NFE2 like bZIP transcription factor 2	Homo sapiens	99-103
33735393-6	2021	Additionally, Quinacrine-loaded liposomes declined Nrf2 expression more than Quinacrine alone (p<0.05).	Quinacrine	14-24	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
33713017-0	2021	Quinacrine and Niclosamide Promote Neurite Growth in Midbrain Dopaminergic Neurons Through the Canonical BMP-Smad Pathway and Protect Against Neurotoxin and alpha-Synuclein-Induced Neurodegeneration.	Quinacrine	0-10	synuclein alpha	Homo sapiens	157-172
33713017-7	2021	In this study, we investigated the neurotrophic potential of two FDA-approved drugs, quinacrine and niclosamide, that are modulators of BMP2 signalling.	Quinacrine	85-95	bone morphogenetic protein 2	Homo sapiens	136-140
33713017-9	2021	We also show that these effects of quinacrine and niclosamide require the activation of BMP-Smad signalling.	Quinacrine	35-45	bone morphogenetic protein 1	Homo sapiens	88-91
33713017-10	2021	Finally, we demonstrate that quinacrine and niclosamide are neuroprotective against degeneration induced by the neurotoxins, MPP+ and 6-OHDA, and by viral-mediated overexpression of alpha-synuclein in vitro.	Quinacrine	29-39	synuclein alpha	Homo sapiens	182-197
31562955-3	2021	The anticancer potential of quinacrine was discovered in a screen for small molecule activators of p53, and was specifically shown to inhibit NFkappaB suppression of p53.	Quinacrine	28-38	tumor protein p53	Homo sapiens	99-102
33398369-0	2021	[Corrigendum] Anticancer effect of quinacrine on diffuse large B-cell lymphoma via inhibition of MSI2-NUMB signaling pathway.	Quinacrine	35-45	musashi RNA binding protein 2	Homo sapiens	97-101
33398369-0	2021	[Corrigendum] Anticancer effect of quinacrine on diffuse large B-cell lymphoma via inhibition of MSI2-NUMB signaling pathway.	Quinacrine	35-45	NUMB endocytic adaptor protein	Homo sapiens	102-106
33316543-10	2021	When injected into mice, chloroquine caused accumulation of LC3B-II in heart tissue, and quinacrine was effective at blocking LC3B-II degradation in male, but not female skeletal muscle.	Quinacrine	89-99	microtubule-associated protein 1 light chain 3 beta	Mus musculus	126-130
31562955-3	2021	The anticancer potential of quinacrine was discovered in a screen for small molecule activators of p53, and was specifically shown to inhibit NFkappaB suppression of p53.	Quinacrine	28-38	tumor protein p53	Homo sapiens	166-169
31562955-4	2021	However, quinacrine can cause cell death in cells that lack p53 or have p53 mutations, which is a common occurrence in many malignant tumors including high grade serous ovarian cancer.	Quinacrine	9-19	tumor protein p53	Homo sapiens	60-63
31562955-4	2021	However, quinacrine can cause cell death in cells that lack p53 or have p53 mutations, which is a common occurrence in many malignant tumors including high grade serous ovarian cancer.	Quinacrine	9-19	tumor protein p53	Homo sapiens	72-75
33247672-0	2020	Effects of Quinacrine on Expression of Hippo signaling Pathway Components (LATS1, LATS2, and YAP) in Human Breast Cancer Stem Cells.	Quinacrine	11-21	large tumor suppressor kinase 1	Homo sapiens	75-80
32871377-1	2020	A new HPLC method was developed for the enantio-separation and chiral recognition mechanism of quinolones (lomefloxacine, ofloxacine, primaquine and quinacrine) on Vancomycin CSP.	Quinacrine	149-159	DnaJ heat shock protein family (Hsp40) member C5	Homo sapiens	175-178
33245730-0	2020	Correction: Quinacrine inhibits GSTA1 activity and induces apoptosis through G1/S arrest and generation of ROS in human non-small cell lung cancer cell lines.	Quinacrine	12-22	glutathione S-transferase alpha 1	Homo sapiens	32-37
33247672-4	2020	In this study, we evaluated the effect of quinacrine on expression of LATS1, LATS2, and YAP genes of the Hippo signaling pathway and YAP level in human breast cancer stem cells (MDA-MB 231 cell line).	Quinacrine	42-52	large tumor suppressor kinase 1	Homo sapiens	70-75
33247672-4	2020	In this study, we evaluated the effect of quinacrine on expression of LATS1, LATS2, and YAP genes of the Hippo signaling pathway and YAP level in human breast cancer stem cells (MDA-MB 231 cell line).	Quinacrine	42-52	large tumor suppressor kinase 2	Homo sapiens	77-82
33247672-4	2020	In this study, we evaluated the effect of quinacrine on expression of LATS1, LATS2, and YAP genes of the Hippo signaling pathway and YAP level in human breast cancer stem cells (MDA-MB 231 cell line).	Quinacrine	42-52	Yes1 associated transcriptional regulator	Homo sapiens	88-91
32243572-9	2020	AGS7-derived iPSCs displayed altered viability when treated with low dose of mepacrine, and higher expression of cyclic GMP-AMP synthase (cGAS), which is the main target for mepacrine action.	Quinacrine	77-86	interferon induced with helicase C domain 1	Homo sapiens	0-4
32878257-8	2020	Annexin V real-time apoptosis study revealed significant apoptotic induction in MPM cells following QA treatment.	Quinacrine	100-102	annexin A5	Homo sapiens	0-9
32603697-0	2020	Nanoformulated quinacrine regulates NECTIN-4 domain specific functions in cervical cancer stem cells.	Quinacrine	15-25	nectin cell adhesion molecule 4	Homo sapiens	36-44
32603697-5	2020	were used to delineate the function of each domain of NECTIN-4 in cancer and their regulation by nano-formulated quinacrine (NQC).	Quinacrine	113-123	nectin cell adhesion molecule 4	Homo sapiens	54-62
32243572-9	2020	AGS7-derived iPSCs displayed altered viability when treated with low dose of mepacrine, and higher expression of cyclic GMP-AMP synthase (cGAS), which is the main target for mepacrine action.	Quinacrine	174-183	interferon induced with helicase C domain 1	Homo sapiens	0-4
32243572-9	2020	AGS7-derived iPSCs displayed altered viability when treated with low dose of mepacrine, and higher expression of cyclic GMP-AMP synthase (cGAS), which is the main target for mepacrine action.	Quinacrine	174-183	cyclic GMP-AMP synthase	Homo sapiens	113-136
32243572-9	2020	AGS7-derived iPSCs displayed altered viability when treated with low dose of mepacrine, and higher expression of cyclic GMP-AMP synthase (cGAS), which is the main target for mepacrine action.	Quinacrine	174-183	cyclic GMP-AMP synthase	Homo sapiens	138-142
31935471-0	2020	Development of inhalable quinacrine loaded bovine serum albumin modified cationic nanoparticles: Repurposing quinacrine for lung cancer therapeutics.	Quinacrine	25-35	albumin	Homo sapiens	50-63
32766144-0	2020	Repositioning Quinacrine Toward Treatment of Ovarian Cancer by Rational Combination With TRAIL.	Quinacrine	14-24	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	89-94
32766144-1	2020	Quinacrine has been identified as a potent DR5-inducing agent that sensitizes cancer cells to TRAIL-induced apoptosis.	Quinacrine	0-10	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	43-46
32766144-1	2020	Quinacrine has been identified as a potent DR5-inducing agent that sensitizes cancer cells to TRAIL-induced apoptosis.	Quinacrine	0-10	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	94-99
32766144-2	2020	In the current study, we found that quinacrine increased DR5 mRNA levels significantly in ovarian cancer cell lines regardless of p53 status.	Quinacrine	36-46	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	57-60
32766144-3	2020	Further study showed the half-life of DR5 in quinacrine-treated cells was significantly prolonged, indicating that DR5 protein degradation was inhibited by quinacrine.	Quinacrine	45-55	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	38-41
32766144-3	2020	Further study showed the half-life of DR5 in quinacrine-treated cells was significantly prolonged, indicating that DR5 protein degradation was inhibited by quinacrine.	Quinacrine	45-55	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	115-118
32766144-3	2020	Further study showed the half-life of DR5 in quinacrine-treated cells was significantly prolonged, indicating that DR5 protein degradation was inhibited by quinacrine.	Quinacrine	156-166	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	38-41
32766144-3	2020	Further study showed the half-life of DR5 in quinacrine-treated cells was significantly prolonged, indicating that DR5 protein degradation was inhibited by quinacrine.	Quinacrine	156-166	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	115-118
32766144-5	2020	We found that quinacrine enhanced TRAIL sensitivity or reversed TRAIL resistance in all the ovarian cancer cell lines tested.	Quinacrine	14-24	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	34-39
32766144-5	2020	We found that quinacrine enhanced TRAIL sensitivity or reversed TRAIL resistance in all the ovarian cancer cell lines tested.	Quinacrine	14-24	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	64-69
32559203-3	2020	The purpose of this study was to determine whether pharmacological activation of p53 by Quinacrine affects RV remodeling and function in the pulmonary artery banding (PAB) model of compensated RVH in mice.	Quinacrine	88-98	transformation related protein 53, pseudogene	Mus musculus	81-84
32559203-8	2020	Quinacrine induced p53 accumulation did not further deteriorate RV function at day 7 after PAB.	Quinacrine	0-10	transformation related protein 53, pseudogene	Mus musculus	19-22
32405336-0	2020	Quinacrine inhibits GSTA1 activity and induces apoptosis through G1/S arrest and generation of ROS in human non-small cell lung cancer cell lines.	Quinacrine	0-10	glutathione S-transferase alpha 1	Homo sapiens	20-25
31935471-0	2020	Development of inhalable quinacrine loaded bovine serum albumin modified cationic nanoparticles: Repurposing quinacrine for lung cancer therapeutics.	Quinacrine	109-119	albumin	Homo sapiens	50-63
31935471-6	2020	These concerns were circumvented by coating nanoparticles with bovine serum albumin (BSA), which retained the cationic charge, reduced NP toxicity and modulated QA release.	Quinacrine	161-163	albumin	Homo sapiens	70-83
32098922-0	2020	Quinacrine causes apoptosis in human cancer cell lines through caspase-mediated pathway and regulation of small-GTPase.	Quinacrine	0-10	caspase 9	Homo sapiens	63-70
31877386-0	2020	Quinacrine and curcumin synergistically increased the breast cancer stem cells death by inhibiting ABCG2 and modulating DNA damage repair pathway.	Quinacrine	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	99-104
31491980-0	2019	Quinacrine-Mediated Inhibition of Nrf2 Reverses Hypoxia-Induced 5-Fluorouracil Resistance in Colorectal Cancer.	Quinacrine	0-10	nuclear factor, erythroid derived 2, like 2	Mus musculus	34-38
30463093-5	2019	Mepacrine uptake and release patterns were correlated with CD63 exposure, platelet ADP/ATP release and content, and the bleeding score ascertained by the ISTH-BAT.	Quinacrine	0-9	CD63 molecule	Homo sapiens	59-63
31352610-8	2019	Serotonin-induced contraction of the MetS vessels was significantly inhibited in the presence of the selective PLA2 inhibitor quinacrine (10-6 M), the COX inhibitor indomethacin (10-5 M), and the TP receptor antagonist SQ29548 (10-6 M), respectively (P &lt; 0.05).	Quinacrine	126-136	phospholipase A2, major isoenzyme	Sus scrofa	111-115
29545477-0	2018	Therapeutic Effect of Quinacrine, an Antiprotozoan Drug, by Selective Suppression of p-CHK1/2 in p53-Negative Malignant Cancers.	Quinacrine	22-32	checkpoint kinase 1	Homo sapiens	87-93
30603978-8	2019	The role of Nectin-4 in the sensitization of 5-FU resistant metastatic CC cells upon incubation with Nano-formulated Quinacrine (NQC) was investigated using multiple bioassays including MTT, FACS, ELISA, immunoflurescence, Western blotting, comet and in vivo plasmid-based short patch and long patch base excision repair assays.	Quinacrine	117-127	nectin cell adhesion molecule 4	Homo sapiens	12-20
31296070-0	2019	Quinacrine Depletes BCR-ABL and Suppresses Ph-Positive Leukemia Cells.	Quinacrine	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
31296070-2	2019	In this study, we demonstrate that quinacrine (QC) induces apoptosis in BCR-ABL positive CML and acute lymphoblastic leukemia (ALL) cells.	Quinacrine	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
30126780-8	2018	The p53 inhibitor and activator pifithrin-alpha and quinacrine, respectively, were used to modulate p53 activity in vivo after ischemia.	Quinacrine	52-62	transformation related protein 53, pseudogene	Mus musculus	100-103
29545477-0	2018	Therapeutic Effect of Quinacrine, an Antiprotozoan Drug, by Selective Suppression of p-CHK1/2 in p53-Negative Malignant Cancers.	Quinacrine	22-32	tumor protein p53	Homo sapiens	97-100
29545477-8	2018	Moreover, QNC treatment displayed antitumor effects in a Villin-Cre;p53+/LSL-R172H intestinal cancer mouse model system as well as HCT116 p53-/- xenografts.Implications: QNC has been used for the past over 70 years without obvious side effects, as such it is a plausible drug candidate for relapsed cancers, small-cell lung cancer, breast cancer as well as various p53-inactivated human malignancies.	Quinacrine	10-13	transformation related protein 53, pseudogene	Mus musculus	68-71
29545477-8	2018	Moreover, QNC treatment displayed antitumor effects in a Villin-Cre;p53+/LSL-R172H intestinal cancer mouse model system as well as HCT116 p53-/- xenografts.Implications: QNC has been used for the past over 70 years without obvious side effects, as such it is a plausible drug candidate for relapsed cancers, small-cell lung cancer, breast cancer as well as various p53-inactivated human malignancies.	Quinacrine	10-13	transformation related protein 53, pseudogene	Mus musculus	138-141
29545477-8	2018	Moreover, QNC treatment displayed antitumor effects in a Villin-Cre;p53+/LSL-R172H intestinal cancer mouse model system as well as HCT116 p53-/- xenografts.Implications: QNC has been used for the past over 70 years without obvious side effects, as such it is a plausible drug candidate for relapsed cancers, small-cell lung cancer, breast cancer as well as various p53-inactivated human malignancies.	Quinacrine	10-13	transformation related protein 53, pseudogene	Mus musculus	138-141
29386219-1	2018	Purpose: We aimed to investigate the therapeutic efficacy of single agent and the combination of quinacrine and suberoylanilide hydroxamic acid (SAHA) in wt- and mut-p53 upper gastrointestinal cancer (UGC) cell models.Experimental Design: ATP-Glo, clonogenic cell survival, Annexin V, comet, DNA double-strand breaks (DSBs), qPCR, and Western blot analysis assays were utilized.Results: Using clonogenic cell survival, ATP-Glo cell viability, Annexin V, and sub-G0 population analysis, we demonstrated that a combination of quinacrine and SAHA significantly decreased colony formation and increased cancer cell death (range, 4-20 fold) in six UGC cell models, as compared with single-agent treatments, irrespective of the p53 status (P < 0.01).	Quinacrine	97-107	tumor protein p53	Homo sapiens	166-169
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	18-28	tumor protein p53	Homo sapiens	64-67
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	96-106	tumor protein p53	Homo sapiens	162-165
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	96-106	tumor protein p53	Homo sapiens	174-177
29386219-6	2018	Tumor xenograft data confirmed that a combination of quinacrine and SAHA is more effective than a single-agent treatment in abrogating tumor growth in vivo (P < 0.01).Conclusions: Our novel findings show that the combination of quinacrine and SAHA promotes DNA damage and is effective in inducing cancer cell death, irrespective of p53 status and resistance to CDDP or gefitinib in UGC models.	Quinacrine	53-63	tumor protein p53	Homo sapiens	332-335
29386219-6	2018	Tumor xenograft data confirmed that a combination of quinacrine and SAHA is more effective than a single-agent treatment in abrogating tumor growth in vivo (P < 0.01).Conclusions: Our novel findings show that the combination of quinacrine and SAHA promotes DNA damage and is effective in inducing cancer cell death, irrespective of p53 status and resistance to CDDP or gefitinib in UGC models.	Quinacrine	228-238	tumor protein p53	Homo sapiens	332-335
29366881-0	2018	Metallic gold and bioactive quinacrine hybrid nanoparticles inhibit oral cancer stem cell and angiogenesis by deregulating inflammatory cytokines in p53 dependent manner.	Quinacrine	28-38	transformation related protein 53, pseudogene	Mus musculus	149-152
29623929-6	2018	Flow cytometry, atomic force microscopy and western blot assays revealed that irradiated cells pretreated with quinacrine showed markedly less apoptosis, necrosis, and membrane damage, and greater expression of heat shock protein 70, than cells exposed to microwave irradiation alone.	Quinacrine	111-121	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	211-232
29623929-7	2018	These results suggest that quinacrine stabilizes the neuronal membrane structure by upregulating the expression of heat shock protein 70, thus reducing neuronal injury caused by microwave radiation.	Quinacrine	27-37	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	115-136
29207489-5	2017	In contrast, a chromatin immunoprecipitation assay showed that quinacrine prevented the binding of p65 to the ICAM-1 promoter following TNF-alpha stimulation.	Quinacrine	63-73	RELA proto-oncogene, NF-kB subunit	Homo sapiens	99-102
28872299-4	2017	The aggregation kinetics of alpha-Syn using ThT fluorescence and conformational transition by circular dichroism (CD) in the presence and absence of these four compounds suggest that, except Quin, the remaining three molecules inhibit alpha-Syn aggregation in a concentration dependent manner.	Quinacrine	191-195	synuclein alpha	Homo sapiens	28-37
29207489-0	2017	Quinacrine Inhibits ICAM-1 Transcription by Blocking DNA Binding of the NF-kappaB Subunit p65 and Sensitizes Human Lung Adenocarcinoma A549 Cells to TNF-alpha and the Fas Ligand.	Quinacrine	0-10	intercellular adhesion molecule 1	Homo sapiens	20-26
29207489-0	2017	Quinacrine Inhibits ICAM-1 Transcription by Blocking DNA Binding of the NF-kappaB Subunit p65 and Sensitizes Human Lung Adenocarcinoma A549 Cells to TNF-alpha and the Fas Ligand.	Quinacrine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	72-81
29207489-0	2017	Quinacrine Inhibits ICAM-1 Transcription by Blocking DNA Binding of the NF-kappaB Subunit p65 and Sensitizes Human Lung Adenocarcinoma A549 Cells to TNF-alpha and the Fas Ligand.	Quinacrine	0-10	RELA proto-oncogene, NF-kB subunit	Homo sapiens	90-93
29207489-0	2017	Quinacrine Inhibits ICAM-1 Transcription by Blocking DNA Binding of the NF-kappaB Subunit p65 and Sensitizes Human Lung Adenocarcinoma A549 Cells to TNF-alpha and the Fas Ligand.	Quinacrine	0-10	tumor necrosis factor	Homo sapiens	149-158
29207489-0	2017	Quinacrine Inhibits ICAM-1 Transcription by Blocking DNA Binding of the NF-kappaB Subunit p65 and Sensitizes Human Lung Adenocarcinoma A549 Cells to TNF-alpha and the Fas Ligand.	Quinacrine	0-10	Fas ligand	Homo sapiens	167-177
29207489-2	2017	In the present study, we demonstrated that quinacrine decreased the expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) alpha in human lung adenocarcinoma A549 cells.	Quinacrine	43-53	intercellular adhesion molecule 1	Homo sapiens	82-115
29207489-2	2017	In the present study, we demonstrated that quinacrine decreased the expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) alpha in human lung adenocarcinoma A549 cells.	Quinacrine	43-53	intercellular adhesion molecule 1	Homo sapiens	117-123
29207489-2	2017	In the present study, we demonstrated that quinacrine decreased the expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) alpha in human lung adenocarcinoma A549 cells.	Quinacrine	43-53	tumor necrosis factor	Homo sapiens	136-169
29207489-2	2017	In the present study, we demonstrated that quinacrine decreased the expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) alpha in human lung adenocarcinoma A549 cells.	Quinacrine	43-53	interleukin 1 alpha	Homo sapiens	174-187
29207489-2	2017	In the present study, we demonstrated that quinacrine decreased the expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) alpha in human lung adenocarcinoma A549 cells.	Quinacrine	43-53	interleukin 1 alpha	Homo sapiens	189-200
29207489-3	2017	Quinacrine inhibited ICAM-1 mRNA expression and nuclear factor kappaB (NF-kappaB)-responsive luciferase reporter activity following a treatment with TNF-alpha and IL-1alpha.	Quinacrine	0-10	intercellular adhesion molecule 1	Homo sapiens	21-27
29207489-3	2017	Quinacrine inhibited ICAM-1 mRNA expression and nuclear factor kappaB (NF-kappaB)-responsive luciferase reporter activity following a treatment with TNF-alpha and IL-1alpha.	Quinacrine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	71-80
29207489-3	2017	Quinacrine inhibited ICAM-1 mRNA expression and nuclear factor kappaB (NF-kappaB)-responsive luciferase reporter activity following a treatment with TNF-alpha and IL-1alpha.	Quinacrine	0-10	tumor necrosis factor	Homo sapiens	149-158
29207489-3	2017	Quinacrine inhibited ICAM-1 mRNA expression and nuclear factor kappaB (NF-kappaB)-responsive luciferase reporter activity following a treatment with TNF-alpha and IL-1alpha.	Quinacrine	0-10	interleukin 1 alpha	Homo sapiens	163-172
29410485-0	2018	Quinacrine upregulates p21/p27 independent of p53 through autophagy-mediated downregulation of p62-Skp2 axis in ovarian cancer.	Quinacrine	0-10	H3 histone pseudogene 16	Homo sapiens	23-26
29410485-0	2018	Quinacrine upregulates p21/p27 independent of p53 through autophagy-mediated downregulation of p62-Skp2 axis in ovarian cancer.	Quinacrine	0-10	interferon alpha inducible protein 27	Homo sapiens	27-30
29410485-0	2018	Quinacrine upregulates p21/p27 independent of p53 through autophagy-mediated downregulation of p62-Skp2 axis in ovarian cancer.	Quinacrine	0-10	sequestosome 1	Homo sapiens	95-98
29410485-0	2018	Quinacrine upregulates p21/p27 independent of p53 through autophagy-mediated downregulation of p62-Skp2 axis in ovarian cancer.	Quinacrine	0-10	S-phase kinase associated protein 2	Homo sapiens	99-103
29115587-0	2018	Anticancer effect of quinacrine on diffuse large B-cell lymphoma via inhibition of MSI2-NUMB signaling pathway.	Quinacrine	21-31	musashi RNA binding protein 2	Homo sapiens	83-87
29115587-0	2018	Anticancer effect of quinacrine on diffuse large B-cell lymphoma via inhibition of MSI2-NUMB signaling pathway.	Quinacrine	21-31	NUMB endocytic adaptor protein	Homo sapiens	88-92
29207489-5	2017	In contrast, a chromatin immunoprecipitation assay showed that quinacrine prevented the binding of p65 to the ICAM-1 promoter following TNF-alpha stimulation.	Quinacrine	63-73	intercellular adhesion molecule 1	Homo sapiens	110-116
29207489-5	2017	In contrast, a chromatin immunoprecipitation assay showed that quinacrine prevented the binding of p65 to the ICAM-1 promoter following TNF-alpha stimulation.	Quinacrine	63-73	tumor necrosis factor	Homo sapiens	136-145
29207489-6	2017	Moreover, TNF-alpha and the Fas ligand effectively reduced the viability of A549 cells in the presence of quinacrine only.	Quinacrine	106-116	tumor necrosis factor	Homo sapiens	10-19
29207489-6	2017	Moreover, TNF-alpha and the Fas ligand effectively reduced the viability of A549 cells in the presence of quinacrine only.	Quinacrine	106-116	Fas ligand	Homo sapiens	28-38
29207489-7	2017	Quinacrine down-regulated the constitutive and TNF-alpha-induced expression of c-FLIP and Mcl-1 in A549 cells.	Quinacrine	0-10	tumor necrosis factor	Homo sapiens	47-56
29207489-7	2017	Quinacrine down-regulated the constitutive and TNF-alpha-induced expression of c-FLIP and Mcl-1 in A549 cells.	Quinacrine	0-10	CASP8 and FADD like apoptosis regulator	Homo sapiens	79-85
29207489-7	2017	Quinacrine down-regulated the constitutive and TNF-alpha-induced expression of c-FLIP and Mcl-1 in A549 cells.	Quinacrine	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	90-95
29207489-8	2017	These results revealed that quinacrine inhibits ICAM-1 transcription by blocking the DNA binding of p65 and sensitizes A549 cells to TNF-alpha and the Fas ligand.	Quinacrine	28-38	intercellular adhesion molecule 1	Homo sapiens	48-54
29207489-8	2017	These results revealed that quinacrine inhibits ICAM-1 transcription by blocking the DNA binding of p65 and sensitizes A549 cells to TNF-alpha and the Fas ligand.	Quinacrine	28-38	RELA proto-oncogene, NF-kB subunit	Homo sapiens	100-103
29207489-8	2017	These results revealed that quinacrine inhibits ICAM-1 transcription by blocking the DNA binding of p65 and sensitizes A549 cells to TNF-alpha and the Fas ligand.	Quinacrine	28-38	tumor necrosis factor	Homo sapiens	133-142
29207489-8	2017	These results revealed that quinacrine inhibits ICAM-1 transcription by blocking the DNA binding of p65 and sensitizes A549 cells to TNF-alpha and the Fas ligand.	Quinacrine	28-38	Fas ligand	Homo sapiens	151-161
28702823-2	2017	Recently, we reported the molecular level details for the modulation of TRAIL-DR5 axis by quinacrine (QC) in breast cancer cells.	Quinacrine	90-100	TNF superfamily member 10	Homo sapiens	72-77
28936683-0	2017	TRAIL enhances quinacrine-mediated apoptosis in breast cancer cells through induction of autophagy via modulation of p21 and DR5 interactions.	Quinacrine	15-25	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	0-5
28936683-0	2017	TRAIL enhances quinacrine-mediated apoptosis in breast cancer cells through induction of autophagy via modulation of p21 and DR5 interactions.	Quinacrine	15-25	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	117-120
28936683-0	2017	TRAIL enhances quinacrine-mediated apoptosis in breast cancer cells through induction of autophagy via modulation of p21 and DR5 interactions.	Quinacrine	15-25	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	125-128
28936683-1	2017	PURPOSE: Previously, we reported that quinacrine (QC) may cause apoptosis in breast and colon cancer cells by activating the death receptor 5 (DR5), resulting in autophagic cell death through p21 modulation.	Quinacrine	38-48	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	125-141
28936683-1	2017	PURPOSE: Previously, we reported that quinacrine (QC) may cause apoptosis in breast and colon cancer cells by activating the death receptor 5 (DR5), resulting in autophagic cell death through p21 modulation.	Quinacrine	38-48	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	143-146
28936683-1	2017	PURPOSE: Previously, we reported that quinacrine (QC) may cause apoptosis in breast and colon cancer cells by activating the death receptor 5 (DR5), resulting in autophagic cell death through p21 modulation.	Quinacrine	38-48	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	192-195
29100024-7	2017	Taken together, the repositioning potential of quinacrine for treatment of AML is reinforced by demonstrating significant in vivo activity and promising synergies when quinacrine is combined with different agents, including cytarabine, the hypomethylating agent azacitidine and HSP-90 inhibitor geldanamycin.	Quinacrine	47-57	heat shock protein 86, pseudogene 1	Mus musculus	278-284
29404393-0	2018	Dimeric quinacrines as chemical tools to identify PPT1, a new regulator of autophagy in cancer cells.	Quinacrine	8-19	palmitoyl-protein thioesterase 1	Mus musculus	50-54
29404393-1	2018	DQ661 is a novel dimeric quinacrine that affects multiple lysosomal functions (autophagy and macropinocytosis) and mTORC1 (mechanistic target of rapamycin) activity by specifically targeting protein-palmitoyl thioesterase 1 (PPT1).	Quinacrine	25-35	CREB regulated transcription coactivator 1	Mus musculus	115-121
29404393-1	2018	DQ661 is a novel dimeric quinacrine that affects multiple lysosomal functions (autophagy and macropinocytosis) and mTORC1 (mechanistic target of rapamycin) activity by specifically targeting protein-palmitoyl thioesterase 1 (PPT1).	Quinacrine	25-35	palmitoyl-protein thioesterase 1	Mus musculus	191-223
29404393-1	2018	DQ661 is a novel dimeric quinacrine that affects multiple lysosomal functions (autophagy and macropinocytosis) and mTORC1 (mechanistic target of rapamycin) activity by specifically targeting protein-palmitoyl thioesterase 1 (PPT1).	Quinacrine	25-35	palmitoyl-protein thioesterase 1	Mus musculus	225-229
28899863-4	2017	We report a screen of novel dimeric antimalarials that identifies dimeric quinacrines (DQ) as potent anticancer compounds, which concurrently inhibit mTOR and autophagy.	Quinacrine	74-85	mechanistic target of rapamycin kinase	Mus musculus	150-154
28867437-0	2017	Quinacrine induces the apoptosis of human leukemia U937 cells through FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	0-10	forkhead box P3	Homo sapiens	70-75
28867437-0	2017	Quinacrine induces the apoptosis of human leukemia U937 cells through FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	0-10	microRNA 183	Homo sapiens	76-83
28867437-0	2017	Quinacrine induces the apoptosis of human leukemia U937 cells through FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	0-10	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	84-93
28867437-0	2017	Quinacrine induces the apoptosis of human leukemia U937 cells through FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	0-10	BCL2 associated X, apoptosis regulator	Homo sapiens	112-115
28867437-4	2017	Quinacrine-induced apoptosis of U937 cells was accompanied with ROS generation, mitochondrial depolarization, and BAX upregulation.	Quinacrine	0-10	BCL2 associated X, apoptosis regulator	Homo sapiens	114-117
28867437-5	2017	Quinacrine-treated U937 cells showed ROS-mediated p38 MAPK activation and ERK inactivation, which in turn upregulated FOXP3 transcription.	Quinacrine	0-10	mitogen-activated protein kinase 14	Homo sapiens	50-53
28867437-5	2017	Quinacrine-treated U937 cells showed ROS-mediated p38 MAPK activation and ERK inactivation, which in turn upregulated FOXP3 transcription.	Quinacrine	0-10	mitogen-activated protein kinase 1	Homo sapiens	54-58
28867437-5	2017	Quinacrine-treated U937 cells showed ROS-mediated p38 MAPK activation and ERK inactivation, which in turn upregulated FOXP3 transcription.	Quinacrine	0-10	mitogen-activated protein kinase 1	Homo sapiens	74-77
28867437-5	2017	Quinacrine-treated U937 cells showed ROS-mediated p38 MAPK activation and ERK inactivation, which in turn upregulated FOXP3 transcription.	Quinacrine	0-10	forkhead box P3	Homo sapiens	118-123
28867437-8	2017	BAX knock-down attenuated quinacrine-induced mitochondrial depolarization and increased the viability of quinacrine-treated cells.	Quinacrine	26-36	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
28867437-8	2017	BAX knock-down attenuated quinacrine-induced mitochondrial depolarization and increased the viability of quinacrine-treated cells.	Quinacrine	105-115	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
28867437-9	2017	Together, our data indicate that quinacrine-induced apoptosis of U937 cells is mediated by mitochondrial alterations triggered by FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	33-43	forkhead box P3	Homo sapiens	130-135
28867437-9	2017	Together, our data indicate that quinacrine-induced apoptosis of U937 cells is mediated by mitochondrial alterations triggered by FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	33-43	microRNA 183	Homo sapiens	136-143
28867437-9	2017	Together, our data indicate that quinacrine-induced apoptosis of U937 cells is mediated by mitochondrial alterations triggered by FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	33-43	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	144-153
28867437-9	2017	Together, our data indicate that quinacrine-induced apoptosis of U937 cells is mediated by mitochondrial alterations triggered by FOXP3/miR-183/beta-TrCP/SP1 axis-mediated BAX upregulation.	Quinacrine	33-43	BCL2 associated X, apoptosis regulator	Homo sapiens	172-175
28702823-2	2017	Recently, we reported the molecular level details for the modulation of TRAIL-DR5 axis by quinacrine (QC) in breast cancer cells.	Quinacrine	90-100	TNF receptor superfamily member 10b	Homo sapiens	78-81
28936487-5	2017	By contrast, in murine fetal liver- and human CD34+ cell-derived MKs and the megakaryocytoid cell lines, MEG-01 and differentiated G1ME2, labeling by mepacrine overlapped nearly completely with labeling by LysoTracker and partially with labeling by DQ  BSA.	Quinacrine	150-159	CD34 molecule	Homo sapiens	46-50
28941496-0	2017	Quinacrine Suppresses Tumor Necrosis Factor-alpha and IFN-alpha in Dermatomyositis and Cutaneous Lupus Erythematosus.	Quinacrine	0-10	tumor necrosis factor	Homo sapiens	22-49
28941496-0	2017	Quinacrine Suppresses Tumor Necrosis Factor-alpha and IFN-alpha in Dermatomyositis and Cutaneous Lupus Erythematosus.	Quinacrine	0-10	interferon alpha 1	Homo sapiens	54-63
28586716-0	2017	Design, synthesis and characterization of novel quinacrine analogs that preferentially kill cancer over non-cancer cells through the down-regulation of Bcl-2 and up-regulation of Bax and Bad.	Quinacrine	48-58	BCL2 apoptosis regulator	Homo sapiens	152-157
28586716-0	2017	Design, synthesis and characterization of novel quinacrine analogs that preferentially kill cancer over non-cancer cells through the down-regulation of Bcl-2 and up-regulation of Bax and Bad.	Quinacrine	48-58	BCL2 associated X, apoptosis regulator	Homo sapiens	179-182
28720477-5	2017	Here, we have shown that a nano-formulated bioactive small molecule inhibitor Quinacrine (NQC) caused apoptosis in oral cancer stem cells (OCSCs; isolated from different oral cancer cells and oral cancer patient derived primary cells) by down regulating WNT-beta catenin and HH-GLI components through activation of GSK3beta.	Quinacrine	78-88	catenin beta 1	Homo sapiens	258-270
28720477-5	2017	Here, we have shown that a nano-formulated bioactive small molecule inhibitor Quinacrine (NQC) caused apoptosis in oral cancer stem cells (OCSCs; isolated from different oral cancer cells and oral cancer patient derived primary cells) by down regulating WNT-beta catenin and HH-GLI components through activation of GSK3beta.	Quinacrine	78-88	glycogen synthase kinase 3 beta	Homo sapiens	315-323
28288868-0	2017	Inhibition of Kir4.1 potassium channels by quinacrine.	Quinacrine	43-53	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	14-20
28320710-8	2017	Furthermore, augmentation of p53 activity using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even after establishment of thrombosis.	Quinacrine	84-94	transformation related protein 53, pseudogene	Mus musculus	29-32
28320710-8	2017	Furthermore, augmentation of p53 activity using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even after establishment of thrombosis.	Quinacrine	84-94	transformation related protein 53, pseudogene	Mus musculus	79-82
28320710-8	2017	Furthermore, augmentation of p53 activity using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even after establishment of thrombosis.	Quinacrine	84-94	transformation related protein 53, pseudogene	Mus musculus	79-82
28255014-4	2017	The FLI1 variant carriers" platelets exhibited a defect in aggregation induced by low-dose adenosine diphosphate (ADP), collagen and thrombin receptor-activating peptide (TRAP), a defect in adenosine triphosphate (ATP) secretion, a reduced mepacrine uptake and release and a reduced CD63 expression upon TRAP stimulation.	Quinacrine	240-249	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	4-8
28255014-4	2017	The FLI1 variant carriers" platelets exhibited a defect in aggregation induced by low-dose adenosine diphosphate (ADP), collagen and thrombin receptor-activating peptide (TRAP), a defect in adenosine triphosphate (ATP) secretion, a reduced mepacrine uptake and release and a reduced CD63 expression upon TRAP stimulation.	Quinacrine	240-249	TRAP	Homo sapiens	171-175
28288868-3	2017	In this work, we examined the effects of the cationic amphiphilic drug quinacrine on Kir4.1 channels heterologously expressed in HEK293 cells, employing the patch clamp technique.	Quinacrine	71-81	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	85-91
28288868-4	2017	Quinacrine inhibited the currents of Kir4.1 channels in a concentration and voltage dependent manner.	Quinacrine	0-10	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	37-43
28288868-5	2017	In inside-out patches, quinacrine inhibited Kir4.1 channels with an IC50 value of 1.8+-0.3muM and with extremely slow blocking and unblocking kinetics.	Quinacrine	23-33	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	44-50
28288868-6	2017	Molecular modeling combined with mutagenesis studies suggested that quinacrine blocks Kir4.1 by plugging the central cavity of the channels, stabilized by the residues E158 and T128.	Quinacrine	68-78	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	86-92
28288868-7	2017	Overall, this study shows that quinacrine blocks Kir4.1 channels, which would be expected to impact the potassium transport in several tissues.	Quinacrine	31-41	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	49-55
28075530-15	2017	RUNX1 downregulation resulted in impaired handling of mepacrine and mislocalization of the DG marker CD63 in HEL cells, indicating impaired DG formation, recapitulating findings on PLDN downregulation.	Quinacrine	54-63	RUNX family transcription factor 1	Homo sapiens	0-5
27917594-0	2017	A novel two-nucleotide deletion in HPS6 affects mepacrine uptake and platelet dense granule secretion in a family with Hermansky-Pudlak syndrome.	Quinacrine	48-57	HPS6 biogenesis of lysosomal organelles complex 2 subunit 3	Homo sapiens	35-39
28129740-3	2017	In the present study an attempt was made to investigate the effect of quinacrine, a phospholipase A2 inhibitor against glycerol induced AKI in rats.	Quinacrine	70-80	phospholipase A2 group IB	Rattus norvegicus	84-100
27762493-0	2017	Quinacrine Mediated Sensitization of Glioblastoma (GBM) Cells to TRAIL through MMP-Sensitive PEG Hydrogel Carriers.	Quinacrine	0-10	TNF superfamily member 10	Homo sapiens	65-70
27762493-5	2017	Quinacrine (QC), a recently discovered TRAIL sensitizer drug, is loaded into the hydrogel carriers and the influence of this system on the apoptosis of a malignant type of brain cancer, glioblastoma multiforme (GBM), has been investigated in detail.	Quinacrine	0-10	TNF superfamily member 10	Homo sapiens	39-44
28129740-12	2017	CONCLUSION: The reversal of glycerol induced AKI by quinacrine points towards a role of phospholipase A2 (PLA2) in the pathogenesis of renal injury.	Quinacrine	52-62	phospholipase A2 group IB	Rattus norvegicus	88-104
28129740-12	2017	CONCLUSION: The reversal of glycerol induced AKI by quinacrine points towards a role of phospholipase A2 (PLA2) in the pathogenesis of renal injury.	Quinacrine	52-62	phospholipase A2 group IB	Rattus norvegicus	106-110
26434592-2	2016	By comparing the treatment effects of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demonstrate that inhibition of the oxidative arm of the pentose phosphate pathway (oxPPP) is required for antimalarial induced apoptosis.	Quinacrine	77-87	KRAS proto-oncogene, GTPase	Homo sapiens	95-99
27542249-0	2017	Quinacrine induces apoptosis in cancer cells by forming a functional bridge between TRAIL-DR5 complex and modulating the mitochondrial intrinsic cascade.	Quinacrine	0-10	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	84-89
27542249-0	2017	Quinacrine induces apoptosis in cancer cells by forming a functional bridge between TRAIL-DR5 complex and modulating the mitochondrial intrinsic cascade.	Quinacrine	0-10	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	90-93
27542249-4	2017	Literature suggest that quinacrine (QC) acts as a DR5 agonistic ligand.	Quinacrine	24-34	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	50-53
27307592-0	2016	Sorafenib and Quinacrine Target Anti-Apoptotic Protein MCL1: A Poor Prognostic Marker in Anaplastic Thyroid Cancer (ATC).	Quinacrine	14-24	myeloid cell leukemia sequence 1	Mus musculus	55-59
27307592-4	2016	We aimed to assess the activity of the antimalaria drug quinacrine known to target NFkappaB signaling in combination with the clinically relevant kinase inhibitor sorafenib in ATC cells.	Quinacrine	56-66	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-91
27307592-6	2016	We assessed the responses of a panel of human ATC cell lines to quinacrine and sorafenib in vitro and in vivo RESULTS: We detected increased expression of NFkappaB-p65/RELA and MCL1 in the nucleus of a subset of ATC compared with non-neoplastic thyroid.	Quinacrine	64-74	RELA proto-oncogene, NF-kB subunit	Homo sapiens	155-167
27307592-6	2016	We assessed the responses of a panel of human ATC cell lines to quinacrine and sorafenib in vitro and in vivo RESULTS: We detected increased expression of NFkappaB-p65/RELA and MCL1 in the nucleus of a subset of ATC compared with non-neoplastic thyroid.	Quinacrine	64-74	RELA proto-oncogene, NF-kB subunit	Homo sapiens	168-172
27307592-6	2016	We assessed the responses of a panel of human ATC cell lines to quinacrine and sorafenib in vitro and in vivo RESULTS: We detected increased expression of NFkappaB-p65/RELA and MCL1 in the nucleus of a subset of ATC compared with non-neoplastic thyroid.	Quinacrine	64-74	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	177-181
27307592-9	2016	At the molecular level, quinacrine and sorafenib inhibited expression of prosurvival MCL1, pSTAT3, and dampened NFkappaB signaling.	Quinacrine	24-34	myeloid cell leukemia sequence 1	Mus musculus	85-89
27307592-9	2016	At the molecular level, quinacrine and sorafenib inhibited expression of prosurvival MCL1, pSTAT3, and dampened NFkappaB signaling.	Quinacrine	24-34	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-120
27334689-3	2016	Here, we present preclinical effects of Quinacrine (QC) with ABT-888, a PARP inhibitor, on highly metastatic breast cancer stem cells (mBCSCs).	Quinacrine	40-50	poly(ADP-ribose) polymerase 1	Homo sapiens	72-76
26850987-0	2016	Chk1 inhibitor synergizes quinacrine mediated apoptosis in breast cancer cells by compromising the base excision repair cascade.	Quinacrine	26-36	checkpoint kinase 1	Homo sapiens	0-4
26864824-6	2016	Quinacrine-stained granules within marginal cells were labeled with LysoTracker, a lysosome tracer, and lysosomal-associated membrane protein 1(LAMP1), but not labeled with the mitochondrial tracer MitoTracker.	Quinacrine	0-10	lysosomal-associated membrane protein 1	Rattus norvegicus	104-143
26864824-6	2016	Quinacrine-stained granules within marginal cells were labeled with LysoTracker, a lysosome tracer, and lysosomal-associated membrane protein 1(LAMP1), but not labeled with the mitochondrial tracer MitoTracker.	Quinacrine	0-10	lysosomal-associated membrane protein 1	Rattus norvegicus	144-149
26295137-6	2015	The results showed that the targeting epirubicin plus quinacrine liposomes could enhance the accumulation and uptake of the drugs in cancer tissues, kill cancer cells directly, activate apoptotic enzymes, destroy the VM channels and downregulate the VM channel-forming marker molecules (EphA2, FAK, PI3K, MMP 9, MMP 14, VE-Cad and HIF-alpha), thereby exhibiting a strong overall anticancer efficacy.	Quinacrine	54-64	protein tyrosine kinase 2	Homo sapiens	294-297
26601776-8	2016	The quinacrine staining in DH was increased and co-localized with LAMP1 immunoreactivity after nerve injury.	Quinacrine	4-14	lysosomal-associated membrane protein 1	Rattus norvegicus	66-71
26500823-8	2015	Ancillary experiments did not support that low micromolar concentrations of quinacrine are substrates for organic cation transporters-1 to -3 or P-glycoprotein.	Quinacrine	76-86	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	106-141
26500823-9	2015	The secondary autophagy induced by quinacrine in cells may derive from the accumulation of incompetent autophagolysosomes, as judged from the accumulation of p62/SQSTM1 and LC3 II (immunoblots).	Quinacrine	35-45	sequestosome 1	Mus musculus	158-161
26500823-9	2015	The secondary autophagy induced by quinacrine in cells may derive from the accumulation of incompetent autophagolysosomes, as judged from the accumulation of p62/SQSTM1 and LC3 II (immunoblots).	Quinacrine	35-45	sequestosome 1	Mus musculus	162-168
26500823-10	2015	Accordingly, protracted lysosomogenesis is evidenced by increased expression of LAMP1 and LAMP2 in quinacrine-treated fibroblasts (48 h, immunoblots), a response that follows the nuclear translocation of the lysosomal genesis transcription factor TFEB and upregulation of LAMP1 and -2 mRNAs (24 h).	Quinacrine	99-109	lysosomal-associated membrane protein 1	Mus musculus	80-85
26500823-10	2015	Accordingly, protracted lysosomogenesis is evidenced by increased expression of LAMP1 and LAMP2 in quinacrine-treated fibroblasts (48 h, immunoblots), a response that follows the nuclear translocation of the lysosomal genesis transcription factor TFEB and upregulation of LAMP1 and -2 mRNAs (24 h).	Quinacrine	99-109	lysosomal-associated membrane protein 2	Mus musculus	90-95
26500823-10	2015	Accordingly, protracted lysosomogenesis is evidenced by increased expression of LAMP1 and LAMP2 in quinacrine-treated fibroblasts (48 h, immunoblots), a response that follows the nuclear translocation of the lysosomal genesis transcription factor TFEB and upregulation of LAMP1 and -2 mRNAs (24 h).	Quinacrine	99-109	transcription factor EB	Mus musculus	247-251
26500823-10	2015	Accordingly, protracted lysosomogenesis is evidenced by increased expression of LAMP1 and LAMP2 in quinacrine-treated fibroblasts (48 h, immunoblots), a response that follows the nuclear translocation of the lysosomal genesis transcription factor TFEB and upregulation of LAMP1 and -2 mRNAs (24 h).	Quinacrine	99-109	lysosomal-associated membrane protein 1	Mus musculus	272-284
25644209-1	2015	This study determined the effects of the estrogen receptor agonist ethinylestradiol (EE2) and the phospholipase A2 inhibitor quinacrine (QUIN) on the pathways controlling follicular development, steroidogenesis, oocyte maturation, ovulation and spawning success in adult zebrafish.	Quinacrine	125-135	phospholipase A2, group IB (pancreas)	Danio rerio	98-114
25644209-1	2015	This study determined the effects of the estrogen receptor agonist ethinylestradiol (EE2) and the phospholipase A2 inhibitor quinacrine (QUIN) on the pathways controlling follicular development, steroidogenesis, oocyte maturation, ovulation and spawning success in adult zebrafish.	Quinacrine	137-141	phospholipase A2, group IB (pancreas)	Danio rerio	98-114
26295137-6	2015	The results showed that the targeting epirubicin plus quinacrine liposomes could enhance the accumulation and uptake of the drugs in cancer tissues, kill cancer cells directly, activate apoptotic enzymes, destroy the VM channels and downregulate the VM channel-forming marker molecules (EphA2, FAK, PI3K, MMP 9, MMP 14, VE-Cad and HIF-alpha), thereby exhibiting a strong overall anticancer efficacy.	Quinacrine	54-64	EPH receptor A2	Homo sapiens	287-292
26295137-6	2015	The results showed that the targeting epirubicin plus quinacrine liposomes could enhance the accumulation and uptake of the drugs in cancer tissues, kill cancer cells directly, activate apoptotic enzymes, destroy the VM channels and downregulate the VM channel-forming marker molecules (EphA2, FAK, PI3K, MMP 9, MMP 14, VE-Cad and HIF-alpha), thereby exhibiting a strong overall anticancer efficacy.	Quinacrine	54-64	matrix metallopeptidase 9	Homo sapiens	305-310
26295137-6	2015	The results showed that the targeting epirubicin plus quinacrine liposomes could enhance the accumulation and uptake of the drugs in cancer tissues, kill cancer cells directly, activate apoptotic enzymes, destroy the VM channels and downregulate the VM channel-forming marker molecules (EphA2, FAK, PI3K, MMP 9, MMP 14, VE-Cad and HIF-alpha), thereby exhibiting a strong overall anticancer efficacy.	Quinacrine	54-64	matrix metallopeptidase 14	Homo sapiens	312-318
25956988-4	2015	ATP was assayed by luciferin-luciferase and visualised by quinacrine labeling.	Quinacrine	58-68	ATPase phospholipid transporting 8A2	Homo sapiens	0-3
25637864-1	2015	As part of its research program on nonsurgical permanent contraception, FHI 360, a nonprofit human development organization, created a stakeholder advisory committee to help address the controversy surrounding quinacrine.	Quinacrine	210-220	cytochrome P450 family 11 subfamily B member 1	Homo sapiens	72-75
25956988-10	2015	Quinacrine-ATP fluorescent loci in the perinuclear space, were diminished by hypoxia and monensin, whereas brefeldin A increased fluorescence intensity, consistent with inhibition of anterograde transport.	Quinacrine	0-10	ATPase phospholipid transporting 8A2	Homo sapiens	11-14
26076928-6	2015	In L-NAME-treated hearts, 5-HT-induced coronary flow increases were blocked by the phospholipase A2 inhibitor quinacrine and the cytochrome P450 inhibitor SKF525A, but were not inhibited by the cyclooxygenase inhibitor indomethacin.	Quinacrine	110-120	phospholipase A2 group IB	Rattus norvegicus	83-99
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	BCL2 apoptosis regulator	Homo sapiens	80-84
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	mitogen-activated protein kinase 1	Homo sapiens	120-123
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	mitogen-activated protein kinase 14	Homo sapiens	62-65
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	mitogen-activated protein kinase 1	Homo sapiens	66-70
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-129
25684043-0	2015	Quinacrine induces apoptosis in human leukemia K562 cells via p38 MAPK-elicited BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	0-10	BCL2 like 1	Homo sapiens	139-145
25684043-3	2015	Quinacrine induced K562 cell apoptosis accompanied with ROS generation, mitochondrial depolarization, and down-regulation of BCL2L1 and BCL2.	Quinacrine	0-10	BCL2 like 1	Homo sapiens	125-131
25684043-3	2015	Quinacrine induced K562 cell apoptosis accompanied with ROS generation, mitochondrial depolarization, and down-regulation of BCL2L1 and BCL2.	Quinacrine	0-10	BCL2 apoptosis regulator	Homo sapiens	125-129
25684043-4	2015	Upon exposure to quinacrine, ROS-mediated p38 MAPK activation and ERK inactivation were observed in K562 cells.	Quinacrine	17-27	mitogen-activated protein kinase 14	Homo sapiens	42-45
25684043-4	2015	Upon exposure to quinacrine, ROS-mediated p38 MAPK activation and ERK inactivation were observed in K562 cells.	Quinacrine	17-27	mitogen-activated protein kinase 1	Homo sapiens	46-50
25684043-4	2015	Upon exposure to quinacrine, ROS-mediated p38 MAPK activation and ERK inactivation were observed in K562 cells.	Quinacrine	17-27	mitogen-activated protein kinase 1	Homo sapiens	66-69
25684043-5	2015	Quinacrine-induced cell death and mitochondrial depolarization were suppressed by the p38MAPK inhibitor SB202190 and constitutively active MEK1 over-expression.	Quinacrine	0-10	mitogen-activated protein kinase kinase 1	Homo sapiens	139-143
25684043-8	2015	Over-expression of BCL2L1 and BCL2 attenuated quinacrine-evoked mitochondrial depolarization and rescued the viability of quinacrine-treated cells.	Quinacrine	46-56	BCL2 like 1	Homo sapiens	19-25
25684043-8	2015	Over-expression of BCL2L1 and BCL2 attenuated quinacrine-evoked mitochondrial depolarization and rescued the viability of quinacrine-treated cells.	Quinacrine	46-56	BCL2 apoptosis regulator	Homo sapiens	19-23
25684043-8	2015	Over-expression of BCL2L1 and BCL2 attenuated quinacrine-evoked mitochondrial depolarization and rescued the viability of quinacrine-treated cells.	Quinacrine	122-132	BCL2 like 1	Homo sapiens	19-25
25684043-8	2015	Over-expression of BCL2L1 and BCL2 attenuated quinacrine-evoked mitochondrial depolarization and rescued the viability of quinacrine-treated cells.	Quinacrine	122-132	BCL2 apoptosis regulator	Homo sapiens	19-23
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	mitogen-activated protein kinase 14	Homo sapiens	137-140
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	mitogen-activated protein kinase 1	Homo sapiens	141-145
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	BCL2 apoptosis regulator	Homo sapiens	155-159
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	mitogen-activated protein kinase 1	Homo sapiens	195-198
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	199-204
25684043-9	2015	Taken together, our data indicate that quinacrine-induced K562 cell apoptosis is mediated through mitochondrial alterations triggered by p38 MAPK-mediated BCL2 down-regulation and suppression of ERK/c-Jun-mediated BCL2L1 expression.	Quinacrine	39-49	BCL2 like 1	Homo sapiens	214-220
24998594-2	2015	However, recent studies show that quinacrine can suppress nuclear factor-kappaB (NF-kappaB), and activate p53 signaling.	Quinacrine	34-44	transformation related protein 53, pseudogene	Mus musculus	106-109
26316080-9	2015	The effect of clofazimine on annexin-V-binding was significantly blunted, but not fully abolished by removal of extracellular Ca(2+), and by phospholipase A2 inhibitor quinacrine (25 microM).	Quinacrine	168-178	annexin A5	Homo sapiens	29-38
25738356-5	2015	Moreover, blocking autophagy using pharmacological inhibitors LY294002, chloroquine (CQ) and quinacrine (QN) enhanced asparaginase-induced cell death and apoptosis, indicating the cytoprotective role of autophagy in asparaginase-treated K562 and KU812 cells.	Quinacrine	93-103	asparaginase	Homo sapiens	216-228
25738356-5	2015	Moreover, blocking autophagy using pharmacological inhibitors LY294002, chloroquine (CQ) and quinacrine (QN) enhanced asparaginase-induced cell death and apoptosis, indicating the cytoprotective role of autophagy in asparaginase-treated K562 and KU812 cells.	Quinacrine	105-107	asparaginase	Homo sapiens	118-130
25738356-5	2015	Moreover, blocking autophagy using pharmacological inhibitors LY294002, chloroquine (CQ) and quinacrine (QN) enhanced asparaginase-induced cell death and apoptosis, indicating the cytoprotective role of autophagy in asparaginase-treated K562 and KU812 cells.	Quinacrine	105-107	asparaginase	Homo sapiens	216-228
25738356-5	2015	Moreover, blocking autophagy using pharmacological inhibitors LY294002, chloroquine (CQ) and quinacrine (QN) enhanced asparaginase-induced cell death and apoptosis, indicating the cytoprotective role of autophagy in asparaginase-treated K562 and KU812 cells.	Quinacrine	93-103	asparaginase	Homo sapiens	118-130
26316080-9	2015	The effect of clofazimine on annexin-V-binding was significantly blunted, but not fully abolished by removal of extracellular Ca(2+), and by phospholipase A2 inhibitor quinacrine (25 microM).	Quinacrine	168-178	phospholipase A2 group IB	Homo sapiens	141-157
26316080-11	2015	The clofazimine induced annexin-V-binding was, however, completely abrogated by combined Ca(2+) removal and addition of quinacrine.	Quinacrine	120-130	annexin A5	Homo sapiens	24-33
25490024-6	2014	Autophagic vacuole biomarker LC3-II increased robustly in response to cediranib, quinacrine, or hypoxia.	Quinacrine	81-91	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	29-32
25490024-7	2014	Combined cediranib/quinacrine increased LC3-II further, with the largest increases occurring with combined cediranib/quinacrine/hypoxia.	Quinacrine	19-29	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	40-43
25490024-8	2014	Early stage autophagy inhibitor 3-MA prevented LC3-II accumulation with combined cediranib/quinacrine/hypoxia and substantially attenuated the associated reduction in cell viability.	Quinacrine	91-101	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	47-50
25490024-11	2014	Cediranib and quinacrine each strongly inhibited Akt phosphoryation, while bafilomycin A1 had no effect.	Quinacrine	14-24	thymoma viral proto-oncogene 1	Mus musculus	49-52
25490024-13	2014	Such accumulation is likely related to stimulation of autophagosome induction by hypoxia, which is prevalent in the glioma tumor microenvironment, as well as Akt signaling inhibition from both cediranib and quinacrine.	Quinacrine	207-217	thymoma viral proto-oncogene 1	Mus musculus	158-161
25490024-14	2014	Quinacrine"s unique ability to inhibit both Akt and autophagic vacuole degradation may enhance its ability to drive cytotoxic autophagic vacuole accumulation.	Quinacrine	0-10	thymoma viral proto-oncogene 1	Mus musculus	44-47
25187658-3	2014	Using high-throughput screening, we identified certain statins and antimalarial agents including chloroquine, hydroxychloroquine, and quinacrine as strong ERK5 activators.	Quinacrine	134-144	mitogen-activated protein kinase 7	Mus musculus	155-159
25028470-6	2014	Quinacrine decreased the level of active FACT subunit SSRP1 and suppressed NF-kappaB-dependent luciferase activity.	Quinacrine	0-10	structure specific recognition protein 1	Homo sapiens	54-59
25028470-8	2014	Moreover, transcriptomic profiling showed that quinacrine or combination treatment significantly affected cell-cycle-related genes that contain binding sites for transcription factors that regulate SSRP1 target genes.	Quinacrine	47-57	structure specific recognition protein 1	Homo sapiens	198-203
23603060-5	2013	However, the vacuolar (V)-ATPase inhibitor bafilomycin A1 prevented quinacrine transport or initiated its release in either cell type.	Quinacrine	68-78	dynein axonemal heavy chain 8	Homo sapiens	13-32
23603060-8	2013	Lymphocytes contained more LAMP1 than PMNLs, suggesting that the mass of lysosomes and late endosomes is a determinant of quinacrine uptake Vmax.	Quinacrine	122-132	lysosomal associated membrane protein 1	Homo sapiens	27-32
23344363-0	2013	Synthesis and biological evaluation of radioiodinated quinacrine-based derivatives for SPECT imaging of Abeta plaques.	Quinacrine	54-64	histocompatibility 2, class II antigen A, beta 1	Mus musculus	104-109
23344363-1	2013	The aim of the present study was to characterize the binding property of quinacrine-based acridine derivatives for Abeta plaques and to evaluate this series of compounds as Abeta imaging probes.	Quinacrine	73-83	histocompatibility 2, class II antigen A, beta 1	Mus musculus	115-120
23344363-1	2013	The aim of the present study was to characterize the binding property of quinacrine-based acridine derivatives for Abeta plaques and to evaluate this series of compounds as Abeta imaging probes.	Quinacrine	73-83	histocompatibility 2, class II antigen A, beta 1	Mus musculus	173-178
23344363-2	2013	Quinacrine clearly stained Abeta plaques in the brain sections of Abeta deposition model transgenic mice (Tg2576 mice).	Quinacrine	0-10	histocompatibility 2, class II antigen A, beta 1	Mus musculus	27-32
23344363-3	2013	Similarly, the quinacrine analog, 2-methoxy-9-(4-(dimethyl-1-methyl) -N-butyl) amino-6-iodo acridine (5), labeled Abeta plaques in the brain slices of Tg2576 mice.	Quinacrine	15-25	histocompatibility 2, class II antigen A, beta 1	Mus musculus	114-119
23344363-7	2013	Similar to quinacrine and 5, these compounds could detect Abeta plaques in the brain sections of Tg2576 mice.	Quinacrine	11-21	histocompatibility 2, class II antigen A, beta 1	Mus musculus	58-63
22305389-5	2012	From the amperometric current-time curves, the response time of the sensor to 20 muM quinacrine was obtained about 20s, and the detection limit of the quinacrine was found to be 10 muM estimated to a signal-to-noise ratio of 3.0.	Quinacrine	85-95	latexin	Homo sapiens	81-84
22305389-5	2012	From the amperometric current-time curves, the response time of the sensor to 20 muM quinacrine was obtained about 20s, and the detection limit of the quinacrine was found to be 10 muM estimated to a signal-to-noise ratio of 3.0.	Quinacrine	85-95	latexin	Homo sapiens	181-184
22305389-5	2012	From the amperometric current-time curves, the response time of the sensor to 20 muM quinacrine was obtained about 20s, and the detection limit of the quinacrine was found to be 10 muM estimated to a signal-to-noise ratio of 3.0.	Quinacrine	151-161	latexin	Homo sapiens	81-84
22305389-5	2012	From the amperometric current-time curves, the response time of the sensor to 20 muM quinacrine was obtained about 20s, and the detection limit of the quinacrine was found to be 10 muM estimated to a signal-to-noise ratio of 3.0.	Quinacrine	151-161	latexin	Homo sapiens	181-184
24653512-0	2012	Quinacrine Inhibits Cell Growth and Induces Apoptosis in Human Gastric Cancer Cell Line SGC-7901.	Quinacrine	0-10	sarcoglycan beta	Homo sapiens	88-91
23193914-0	2012	Quinacrine-mediated autophagy and apoptosis in colon cancer cells is through a p53- and p21-dependent mechanism.	Quinacrine	0-10	tumor protein p53	Homo sapiens	79-82
23193914-0	2012	Quinacrine-mediated autophagy and apoptosis in colon cancer cells is through a p53- and p21-dependent mechanism.	Quinacrine	0-10	H3 histone pseudogene 16	Homo sapiens	88-91
23193914-1	2012	We previously showed that quinacrine (QC), a small molecule antimalarial agent, also presented anticancer activity in breast cancer cells through activation of p53, p21, and inhibition of topoisomerase activity.	Quinacrine	26-36	tumor protein p53	Homo sapiens	160-163
23193914-1	2012	We previously showed that quinacrine (QC), a small molecule antimalarial agent, also presented anticancer activity in breast cancer cells through activation of p53, p21, and inhibition of topoisomerase activity.	Quinacrine	26-36	H3 histone pseudogene 16	Homo sapiens	165-168
25224579-9	2014	SP600125, rauwolscine, quinacrine dihydrochloride, nordihydroguaiaretic acid, AA-861, phenidone and GF 109203X attenuated dexmedetomidine-induced JNK phosphorylation.	Quinacrine	23-49	mitogen-activated protein kinase 8	Rattus norvegicus	146-149
25195052-11	2014	In quinacrine group, increase in the SOD1 expression levels was only statistically significant (p &lt; 0.05).	Quinacrine	3-13	superoxide dismutase 1	Rattus norvegicus	37-41
24704528-10	2014	Mepacrine or ibuprofen pretreatments almost completely blocked the pressor and bradycardic responses to CDP-choline while neomycine or furegrelate partially attenuated the drug-induced cardiovascular effects.	Quinacrine	0-9	cut-like homeobox 1	Rattus norvegicus	104-107
24469074-5	2014	Muscle fibres were stimulated in the absence and presence of the phospholipase A2 inhibitor quinacrine.	Quinacrine	92-102	phospholipase A2 group IB	Homo sapiens	65-81
23129580-0	2013	Lycopene synergistically enhances quinacrine action to inhibit Wnt-TCF signaling in breast cancer cells through APC.	Quinacrine	34-44	hepatocyte nuclear factor 4 alpha	Homo sapiens	67-70
23129580-0	2013	Lycopene synergistically enhances quinacrine action to inhibit Wnt-TCF signaling in breast cancer cells through APC.	Quinacrine	34-44	APC regulator of WNT signaling pathway	Homo sapiens	112-115
22820307-4	2012	We demonstrate that when mepacrine labeled whole blood is perfused at a shear rate of 100 s -1 over substrates patterned with micron-sized wide lines of fibrinogen, platelets selectively adhere to the areas of patterned fibrinogen.	Quinacrine	25-34	fibrinogen beta chain	Homo sapiens	153-163
22820307-4	2012	We demonstrate that when mepacrine labeled whole blood is perfused at a shear rate of 100 s -1 over substrates patterned with micron-sized wide lines of fibrinogen, platelets selectively adhere to the areas of patterned fibrinogen.	Quinacrine	25-34	fibrinogen beta chain	Homo sapiens	220-230
22207084-12	2012	U73122, quinacrine, and AACOCF3 inhibited DHT-induced activation of PKC.	Quinacrine	8-18	protein kinase C, gamma	Rattus norvegicus	68-71
22504301-4	2012	PA-induced phosphorylation of ERK1/2 was attenuated by a PLA(2) inhibitor (mepacrine) and, a G(i) protein inhibitor (pertussis toxin, PTX).	Quinacrine	75-84	mitogen-activated protein kinase 3	Homo sapiens	30-36
22504301-4	2012	PA-induced phosphorylation of ERK1/2 was attenuated by a PLA(2) inhibitor (mepacrine) and, a G(i) protein inhibitor (pertussis toxin, PTX).	Quinacrine	75-84	phospholipase A2 group IB	Homo sapiens	57-63
21544805-1	2012	The small molecule Quinacrine (QC, a derivative of 9-aminoacridine), an anti-malaria drug, displays activity against cancer cell lines and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Quinacrine	19-29	tumor protein p53	Homo sapiens	214-217
22768295-0	2012	Pharmacokinetics of quinacrine efflux from mouse brain via the P-glycoprotein efflux transporter.	Quinacrine	20-30	phosphoglycolate phosphatase	Mus musculus	63-77
22768295-4	2012	As a substrate of the P-glycoprotein (P-gp) efflux transporter, quinacrine is actively exported from the brain, preventing its accumulation to levels that may show efficacy in some disease models.	Quinacrine	64-74	phosphoglycolate phosphatase	Mus musculus	22-36
22768295-4	2012	As a substrate of the P-glycoprotein (P-gp) efflux transporter, quinacrine is actively exported from the brain, preventing its accumulation to levels that may show efficacy in some disease models.	Quinacrine	64-74	phosphoglycolate phosphatase	Mus musculus	38-42
22768295-5	2012	In the brains of P-gp-deficient Mdr1(0/0) mice, we found quinacrine reached concentrations of ~80 microM without any signs of acute toxicity.	Quinacrine	57-67	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	32-36
22768295-6	2012	Additionally, we examined the distribution and metabolism of quinacrine in the wild-type and Mdr1(0/0) brains.	Quinacrine	61-71	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	93-97
22768295-7	2012	In wild-type mice, the co-administration of cyclosporin A, a known P-gp inhibitor, resulted in a 6-fold increase in the accumulation of quinacrine in the brain.	Quinacrine	136-146	phosphoglycolate phosphatase	Mus musculus	67-71
22768295-8	2012	Our findings argue that the inhibition of the P-gp efflux transporter should improve the poor pharmacokinetic properties of quinacrine in the CNS.	Quinacrine	124-134	phosphoglycolate phosphatase	Mus musculus	46-50