PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29842871-10 2018 We found that the metabolism of fluorescent substrates by CYP2B6, CYP2C19, CYP2E1, and CYP1A1 in the presence of serum obtained from DSS-treated mice was activated by 42%, 37%, 37%, and 23%, respectively, relative to that associated with sera from control mice. 3-(trimethylsilyl)propanesulfonic acid 133-136 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 58-64 29842871-10 2018 We found that the metabolism of fluorescent substrates by CYP2B6, CYP2C19, CYP2E1, and CYP1A1 in the presence of serum obtained from DSS-treated mice was activated by 42%, 37%, 37%, and 23%, respectively, relative to that associated with sera from control mice. 3-(trimethylsilyl)propanesulfonic acid 133-136 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 66-73 29842871-10 2018 We found that the metabolism of fluorescent substrates by CYP2B6, CYP2C19, CYP2E1, and CYP1A1 in the presence of serum obtained from DSS-treated mice was activated by 42%, 37%, 37%, and 23%, respectively, relative to that associated with sera from control mice. 3-(trimethylsilyl)propanesulfonic acid 133-136 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 75-81 29842871-10 2018 We found that the metabolism of fluorescent substrates by CYP2B6, CYP2C19, CYP2E1, and CYP1A1 in the presence of serum obtained from DSS-treated mice was activated by 42%, 37%, 37%, and 23%, respectively, relative to that associated with sera from control mice. 3-(trimethylsilyl)propanesulfonic acid 133-136 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 87-93 19127062-6 2008 Furthermore, X-ALD lymphoblasts produced higher levels of nitric oxide (NO) and cytokines (tumor necrosis factor-alpha and interleukin 1 beta), and treatment with NaPA or lovastatin decreased the synthesis of NO. Lovastatin 171-181 interleukin 1 beta Homo sapiens 123-141 18097565-0 2008 Ciglitazone, an agonist of peroxisome proliferator-activated receptor gamma, exerts potentiated cytostatic/cytotoxic effects against tumor cells when combined with lovastatin. Lovastatin 164-174 peroxisome proliferator activated receptor gamma Homo sapiens 27-75 18302447-4 2008 OBJECTIVE: To evaluate the incidence and clinical consequences of the use of lovastatin or simvastatin with concomitant CYP3A4 inhibitors and inducers, and with fibrates. Lovastatin 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 18302447-14 2008 CONCLUSION: Although the pharmacokinetic interactions between lovastatin or simvastatin and CYP3A4 inhibitors and inducers are substantial, their clinical relevance seems to be limited, at least with lower statin doses. Lovastatin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 17497701-11 2008 These data demonstrate that lovastatin protects MSCs from Hypoxia/SD-induced apoptosis via PI3K/Akt and MEK/ERK1/2 pathways, suggesting that it may prove a useful therapeutic adjunct for transplanting MSCs into damaged heart after myocardial infarction. Lovastatin 28-38 AKT serine/threonine kinase 1 Rattus norvegicus 96-99 17497701-11 2008 These data demonstrate that lovastatin protects MSCs from Hypoxia/SD-induced apoptosis via PI3K/Akt and MEK/ERK1/2 pathways, suggesting that it may prove a useful therapeutic adjunct for transplanting MSCs into damaged heart after myocardial infarction. Lovastatin 28-38 mitogen activated protein kinase 3 Rattus norvegicus 108-114 18034278-5 2008 Flow cytometry revealed significant increases in three of four lung cancer cell lines in apoptosis and necrosis after lovastatin treatment at 10 microM for 72 h. Lovastatin adversely affected lung cancer cell survival with increases in cell-cycle check-point inhibitors p21WAF and/or p27KIP and a decrease in cyclin D1. Lovastatin 118-128 cyclin D1 Homo sapiens 309-318 18034278-5 2008 Flow cytometry revealed significant increases in three of four lung cancer cell lines in apoptosis and necrosis after lovastatin treatment at 10 microM for 72 h. Lovastatin adversely affected lung cancer cell survival with increases in cell-cycle check-point inhibitors p21WAF and/or p27KIP and a decrease in cyclin D1. Lovastatin 162-172 cyclin D1 Homo sapiens 309-318 18034278-8 2008 Lovastatin induces apoptosis and necrosis in lung cancer cell lines by causing alterations in the cell cycle, reducing glutathione, and activating p53, Bax protein, and caspases while increasing cytochrome c in apoptosis pathways. Lovastatin 0-10 tumor protein p53 Homo sapiens 147-150 18034278-8 2008 Lovastatin induces apoptosis and necrosis in lung cancer cell lines by causing alterations in the cell cycle, reducing glutathione, and activating p53, Bax protein, and caspases while increasing cytochrome c in apoptosis pathways. Lovastatin 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 152-155 18034278-8 2008 Lovastatin induces apoptosis and necrosis in lung cancer cell lines by causing alterations in the cell cycle, reducing glutathione, and activating p53, Bax protein, and caspases while increasing cytochrome c in apoptosis pathways. Lovastatin 0-10 cytochrome c, somatic Homo sapiens 195-207 18078859-4 2008 Our data show that treatment with lovastatin results in a marked improvement in insulin sensitivity characterized by an increase in glucose disappearance rate during the insulin tolerance test. Lovastatin 34-44 insulin Homo sapiens 80-87 18078859-4 2008 Our data show that treatment with lovastatin results in a marked improvement in insulin sensitivity characterized by an increase in glucose disappearance rate during the insulin tolerance test. Lovastatin 34-44 insulin Homo sapiens 170-177 18078859-6 2008 Our data also show that lovastatin treatment was associated with an increase in insulin-stimulated insulin receptor substrate (IRS) 1/phosphatidylinositol 3-kinase/Akt pathway in the liver and muscle of HFD-fed rats in parallel with a decrease in the inflammatory pathway (c-jun N-terminal kinase and I kappa beta kinase (IKKbeta)/inhibitor of kappaB/nuclear factor kappaB) related to insulin resistance. Lovastatin 24-34 insulin Homo sapiens 80-87 18078859-6 2008 Our data also show that lovastatin treatment was associated with an increase in insulin-stimulated insulin receptor substrate (IRS) 1/phosphatidylinositol 3-kinase/Akt pathway in the liver and muscle of HFD-fed rats in parallel with a decrease in the inflammatory pathway (c-jun N-terminal kinase and I kappa beta kinase (IKKbeta)/inhibitor of kappaB/nuclear factor kappaB) related to insulin resistance. Lovastatin 24-34 insulin Homo sapiens 99-106 18078859-6 2008 Our data also show that lovastatin treatment was associated with an increase in insulin-stimulated insulin receptor substrate (IRS) 1/phosphatidylinositol 3-kinase/Akt pathway in the liver and muscle of HFD-fed rats in parallel with a decrease in the inflammatory pathway (c-jun N-terminal kinase and I kappa beta kinase (IKKbeta)/inhibitor of kappaB/nuclear factor kappaB) related to insulin resistance. Lovastatin 24-34 AKT serine/threonine kinase 1 Rattus norvegicus 164-167 18078859-6 2008 Our data also show that lovastatin treatment was associated with an increase in insulin-stimulated insulin receptor substrate (IRS) 1/phosphatidylinositol 3-kinase/Akt pathway in the liver and muscle of HFD-fed rats in parallel with a decrease in the inflammatory pathway (c-jun N-terminal kinase and I kappa beta kinase (IKKbeta)/inhibitor of kappaB/nuclear factor kappaB) related to insulin resistance. Lovastatin 24-34 inhibitor of nuclear factor kappa B kinase subunit beta Rattus norvegicus 322-329 18078859-6 2008 Our data also show that lovastatin treatment was associated with an increase in insulin-stimulated insulin receptor substrate (IRS) 1/phosphatidylinositol 3-kinase/Akt pathway in the liver and muscle of HFD-fed rats in parallel with a decrease in the inflammatory pathway (c-jun N-terminal kinase and I kappa beta kinase (IKKbeta)/inhibitor of kappaB/nuclear factor kappaB) related to insulin resistance. Lovastatin 24-34 insulin Homo sapiens 99-106 18504415-9 2008 Considering that both SNP and lovastatin can activate caspase-3, cells were treated with the caspase-3 inhibitor Ac-DEVD-CHO. Lovastatin 30-40 caspase 3 Homo sapiens 54-63 18504415-9 2008 Considering that both SNP and lovastatin can activate caspase-3, cells were treated with the caspase-3 inhibitor Ac-DEVD-CHO. Lovastatin 30-40 caspase 3 Homo sapiens 93-102 18188523-5 2008 The proportion of cells in G0/G1 phase, apoptosis and p21 protein expression increased after lovastatin alone or combined with 4-Gy irradiation in both cell lines. Lovastatin 93-103 cyclin dependent kinase inhibitor 1A Homo sapiens 54-57 18061125-0 2008 Lovastatin inhibits oxidized low-density lipoprotein-induced plasminogen activator inhibitor and transforming growth factor-beta1 expression via a decrease in Ras/extracellular signal-regulated kinase activity in mesangial cells. Lovastatin 0-10 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 123-129 18061125-0 2008 Lovastatin inhibits oxidized low-density lipoprotein-induced plasminogen activator inhibitor and transforming growth factor-beta1 expression via a decrease in Ras/extracellular signal-regulated kinase activity in mesangial cells. Lovastatin 0-10 mitogen-activated protein kinase 1 Homo sapiens 163-200 18061125-5 2008 Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity. Lovastatin 143-153 mitogen-activated protein kinase 3 Homo sapiens 210-216 18061125-5 2008 Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity. Lovastatin 143-153 SMAD family member 3 Homo sapiens 237-242 18061125-5 2008 Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity. Lovastatin 143-153 transforming growth factor beta 1 Homo sapiens 255-264 18061125-5 2008 Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity. Lovastatin 143-153 serpin family E member 1 Homo sapiens 269-274 18061125-5 2008 Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity. Lovastatin 143-153 serpin family E member 1 Homo sapiens 308-313 18061125-8 2008 These results indicate that lovastatin prevents the Ox-LDL-induced Ras/ERK activation that results in inhibition of Smad3 activation in mesangial cells with subsequent downregulation of TGF-beta target genes. Lovastatin 28-38 mitogen-activated protein kinase 1 Homo sapiens 71-74 18061125-8 2008 These results indicate that lovastatin prevents the Ox-LDL-induced Ras/ERK activation that results in inhibition of Smad3 activation in mesangial cells with subsequent downregulation of TGF-beta target genes. Lovastatin 28-38 SMAD family member 3 Homo sapiens 116-121 18061125-8 2008 These results indicate that lovastatin prevents the Ox-LDL-induced Ras/ERK activation that results in inhibition of Smad3 activation in mesangial cells with subsequent downregulation of TGF-beta target genes. Lovastatin 28-38 transforming growth factor beta 1 Homo sapiens 186-194 18034661-9 2007 Lovastatin similarly increased SOD, CAT and GSH by 32%, 29%, and 64% in the liver and by 17%, 26%, and 73% in the kidney of alloxan-treated rats. Lovastatin 0-10 catalase Rattus norvegicus 36-39 17497701-0 2008 Lovastatin protects mesenchymal stem cells against hypoxia- and serum deprivation-induced apoptosis by activation of PI3K/Akt and ERK1/2. Lovastatin 0-10 AKT serine/threonine kinase 1 Rattus norvegicus 122-125 17497701-0 2008 Lovastatin protects mesenchymal stem cells against hypoxia- and serum deprivation-induced apoptosis by activation of PI3K/Akt and ERK1/2. Lovastatin 0-10 mitogen activated protein kinase 3 Rattus norvegicus 130-136 17497701-6 2008 We demonstrated that lovastatin (0.01-1 microM) remarkably prevented MSCs from Hypoxia/SD-induced apoptosis through inhibition of the mitochondrial apoptotic pathway, leading to attenuation of caspase-3 activation. Lovastatin 21-31 caspase 3 Rattus norvegicus 193-202 17497701-8 2008 Furthermore, the antiapoptotic effect of lovastatin on mitochondrial apoptotic pathway was effectively abrogated by both PI3K inhibitor, LY294002 and ERK1/2 inhibitor, U0126. Lovastatin 41-51 mitogen activated protein kinase 3 Rattus norvegicus 150-156 17497701-9 2008 The phosphorylations of Akt/GSK3 beta and ERK1/2 stimulated by lovastatin were detected. Lovastatin 63-73 AKT serine/threonine kinase 1 Rattus norvegicus 24-27 17497701-9 2008 The phosphorylations of Akt/GSK3 beta and ERK1/2 stimulated by lovastatin were detected. Lovastatin 63-73 glycogen synthase kinase 3 beta Rattus norvegicus 28-37 17923246-12 2007 Furthermore, toxicity of the pgp substrate drug daunorubicin was enhanced following lovastatin preculture (p = 0.04). Lovastatin 84-94 ATP binding cassette subfamily B member 1 Homo sapiens 29-32 17497701-9 2008 The phosphorylations of Akt/GSK3 beta and ERK1/2 stimulated by lovastatin were detected. Lovastatin 63-73 mitogen activated protein kinase 3 Rattus norvegicus 42-48 17900611-9 2007 In contrast, a specific inhibitor of COX-2, NS398, significantly inhibited the lovastatin-induced expression of BK-2Rs. Lovastatin 79-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 17992259-3 2007 We report that lovastatin induced the expression of atrogin-1, a key gene involved in skeletal muscle atrophy, in humans with statin myopathy, in zebrafish embryos, and in vitro in murine skeletal muscle cells. Lovastatin 15-25 F-box protein 32 Homo sapiens 52-61 17992259-4 2007 In cultured mouse myotubes, atrogin-1 induction following lovastatin treatment was accompanied by distinct morphological changes, largely absent in atrogin-1 null cells. Lovastatin 58-68 F-box protein 32 Mus musculus 28-37 17992259-6 2007 Moreover, atrogin-1 knockdown in zebrafish embryos prevented lovastatin-induced muscle injury. Lovastatin 61-71 F-box protein 32 Danio rerio 10-19 17935545-7 2007 All treatments were well tolerated, and after 4 weeks the mean LDL-C, TC and TG levels in the group receiving 20 mg of lovastatin plus 10 g of psyllium fell by 30.88%, 26.88% and 26.21% from baseline, compared with 24.78%, 19.55% and 32.88% in the group receiving 20 mg of lovastatin and 3.58%, 2.90% and 10.95% in the group receiving 10 g of psyllium respectively. Lovastatin 119-129 component of oligomeric golgi complex 2 Homo sapiens 63-68 17900611-10 2007 Here we show for the first time that lovastatin induces the expression of BK-2Rs in cultured human coronary artery endothelial cells through a novel cholesterol-independent pleiotropic mechanism that involves RhoA kinase inhibition and COX-2 activation. Lovastatin 37-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 236-241 17907956-7 2007 This is indicated by a reported ability of micromolar concentrations of lovastatin and simvastatin to strongly stimulate brain vascular endothelial cells to make this Abeta ejector. Lovastatin 72-82 amyloid beta precursor protein Homo sapiens 167-172 17932552-0 2007 Increased expression of CD14 in macrophages after inhibition of the cholesterol biosynthetic pathway by lovastatin. Lovastatin 104-114 CD14 molecule Homo sapiens 24-28 17932552-6 2007 Treatment of RAW 264.7 macrophages with lovastatin resulted in elevated mCD14 levels and decreased sCD14 levels after LPS stimulation. Lovastatin 40-50 CD14 antigen Mus musculus 72-77 17878231-5 2007 Conversely, cholesterol-lowering agents (fluvastatin and lovastatin) and cholesterol-depleting agents (beta-cyclodextrin and nystatin) enhance TGF-beta responsiveness by increasing non-lipid raft microdomain accumulation of TGF-beta receptors and facilitating TGF-beta-induced signaling. Lovastatin 57-67 transforming growth factor, beta 1 Mus musculus 143-151 17699156-6 2007 In this study, lovastatin treatment induced eIF2alpha phosphorylation and inhibited global protein translation. Lovastatin 15-25 eukaryotic translation initiation factor 2A Homo sapiens 44-53 17699156-8 2007 In CHOP(-/-) murine embryonic fibroblasts (MEFs), lovastatin-induced apoptosis was attenuated indicating a role for CHOP in this response. Lovastatin 50-60 DNA-damage inducible transcript 3 Mus musculus 3-7 17699156-8 2007 In CHOP(-/-) murine embryonic fibroblasts (MEFs), lovastatin-induced apoptosis was attenuated indicating a role for CHOP in this response. Lovastatin 50-60 DNA-damage inducible transcript 3 Mus musculus 116-120 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 48-58 eukaryotic translation initiation factor 2A Homo sapiens 17-26 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 48-58 eukaryotic translation initiation factor 2 alpha kinase 4 Homo sapiens 34-38 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 48-58 activating transcription factor 4 Homo sapiens 72-76 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 48-58 eukaryotic translation initiation factor 2 alpha kinase 4 Homo sapiens 133-137 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 81-91 eukaryotic translation initiation factor 2A Homo sapiens 17-26 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 81-91 eukaryotic translation initiation factor 2 alpha kinase 4 Homo sapiens 34-38 17699156-9 2007 Furthermore, the eIF2alpha kinase GCN2 mediates lovastatin induction of ATF4 and lovastatin-induced apoptosis was also attenuated in GCN2(-/-) MEFs. Lovastatin 81-91 eukaryotic translation initiation factor 2 alpha kinase 4 Homo sapiens 133-137 17655813-6 2007 Percent LDL-C reduction was significantly greater (p < 0.0001) with RSV (28.4%) compared to ATV (22.5%), SMV (20.1%), PRV (13.7%), FLV (15.8%), and LOV (17.3%). Lovastatin 151-154 component of oligomeric golgi complex 2 Homo sapiens 8-13 17919499-9 2007 The addition of the specific inhibitor of BMPs, noggin, completely prevents lovastatin-induced apoptosis in sensitive cells. Lovastatin 76-86 noggin Mus musculus 48-54 17555307-5 2007 In combination treatments, 1-3 microM 5b plus 1 microM lovastatin induced a significant inhibition of RhoB prenylation, and a combination of these drugs at 1 microM each also resulted in significant cell cycle arrest in G1. Lovastatin 55-65 ras homolog family member B Homo sapiens 102-106 17586475-0 2007 Lovastatin suppresses erythropoietin receptor surface expression through dual inhibition of glycosylation and geranylgeranylation. Lovastatin 0-10 erythropoietin receptor Homo sapiens 22-45 17586475-6 2007 Treatment of cells with lovastatin, a selective inhibitor of the rate-limiting enzyme in the mevalonate pathway leads to inhibition of cell surface EpoR that is induced by Epo starvation. Lovastatin 24-34 erythropoietin receptor Homo sapiens 148-152 17586475-6 2007 Treatment of cells with lovastatin, a selective inhibitor of the rate-limiting enzyme in the mevalonate pathway leads to inhibition of cell surface EpoR that is induced by Epo starvation. Lovastatin 24-34 erythropoietin Homo sapiens 148-151 17586475-8 2007 Adding back geranylgeranyl pyrophosphate to lovastatin-treated cells completely prevents the lovastatin effect on EpoR expression. Lovastatin 44-54 erythropoietin receptor Homo sapiens 114-118 17586475-8 2007 Adding back geranylgeranyl pyrophosphate to lovastatin-treated cells completely prevents the lovastatin effect on EpoR expression. Lovastatin 93-103 erythropoietin receptor Homo sapiens 114-118 17586475-12 2007 Finally, lovastatin inhibits Epo"s stimulatory effects on cell proliferation. Lovastatin 9-19 erythropoietin Homo sapiens 29-32 17612572-12 2007 Our results show that pre-administration of lovastatin improved functional outcomes and reduced extent of brain damage, with a concomitant decrease in tissue levels of TNF-alpha and IL-1beta mRNA and protein. Lovastatin 44-54 tumor necrosis factor Rattus norvegicus 168-177 17612572-12 2007 Our results show that pre-administration of lovastatin improved functional outcomes and reduced extent of brain damage, with a concomitant decrease in tissue levels of TNF-alpha and IL-1beta mRNA and protein. Lovastatin 44-54 interleukin 1 beta Rattus norvegicus 182-190 17392396-3 2007 In rat and human hepatic or gut S9 fractions and rat gut lumen, GFJ inhibited the hydrolysis of enalapril and lovastatin, which are known to be metabolized principally by esterases, lovastatin being metabolized also by CYP3A. Lovastatin 110-120 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 219-224 17452418-6 2007 In Caco-2 cells, demonstrated to contain minimal CYP3A activity, the permeability coefficient of the prodrugs lovastatin and enalapril was increased in the presence of the active flavonoids kaempferol and naringenin, consistent with inhibition of esterase activity. Lovastatin 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 17615423-12 2007 In patients requiring the concurrent use of statins and CYP3A4 inhibitors, pravastatin, fluvastatin, and rosuvastatin carry the lowest risk of drug interactions; atorvastatin carries moderate risk, whereas simvastatin and lovastatin have the highest risk and should be avoided in patients taking concomitant CYP3A4 inhibitors. Lovastatin 222-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 17412884-0 2007 Apomine enhances the antitumor effects of lovastatin on myeloma cells by down-regulating 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Lovastatin 42-52 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 89-136 17412884-7 2007 Accumulation of unprenylated Rap1A by lovastatin was enhanced in the presence of apomine. Lovastatin 38-48 RAP1A, member of RAS oncogene family Homo sapiens 29-34 17264303-2 2007 Exposure of U937 and U266 cells to minimally toxic concentrations of UCN-01 and various statins (eg, lovastatin, simvastatin, or fluvastatin) dramatically increased mitochondrial dysfunction, caspase activation, and apoptosis. Lovastatin 101-111 urocortin Homo sapiens 69-72 17472962-4 2007 The HRI lovastatin induced apoptosis in the human colon cancer cell line SW480 by blocking the cholesterol synthesis pathway. Lovastatin 8-18 eukaryotic translation initiation factor 2 alpha kinase 1 Homo sapiens 4-7 17472962-5 2007 Immunoblot analysis of antiapoptotic molecules, including survivin, XIAP, cIAP-1, cIAP-2, Bcl-2, and Bcl-X(L), revealed that only survivin expression was decreased by lovastatin. Lovastatin 167-177 BCL2 like 1 Homo sapiens 101-109 17472962-11 2007 In addition, lovastatin blocked Ras activation and Akt phosphorylation. Lovastatin 13-23 AKT serine/threonine kinase 1 Homo sapiens 51-54 17472962-12 2007 We conclude that survivin down-regulation is crucial in lovastatin-induced apoptosis in cancer cells and that lovastatin decreases survivin expression by inhibiting Ras-mediated PI3-kinase activation via the blocking of Ras isoprenylation. Lovastatin 110-120 peptidase inhibitor 3 Homo sapiens 178-181 17520029-2 2007 PRINCIPLE FINDINGS: Here we demonstrate that treatment of an enriched CD4(+) lymphocyte population with lovastatin (Lov), mevastatin (Mev) and simvastatin (activated and non-activated, Sim(A) and Sim(N), respectively) can reduce the cell surface expression of the CC-chemokine receptor CCR5 (P<0.01 for Sim(A) and Lov). Lovastatin 104-114 CD4 molecule Homo sapiens 70-73 17264303-4 2007 Potentiation of UCN-01 lethality by lovastatin was associated with disruption of Ras prenylation and activation. Lovastatin 36-46 urocortin Homo sapiens 16-19 17264303-7 2007 U266 cells ectopically expressing JNK1-APF, a dominant negative JNK1 mutant, displayed significantly reduced susceptibility to lovastatin/UCN-01-mediated lethality. Lovastatin 127-137 mitogen-activated protein kinase 8 Homo sapiens 34-38 17513950-9 2007 Treatment of endothelial cells with lovastatin increased CYP2C9 expression. Lovastatin 36-46 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 57-63 17513950-10 2007 After 96 hours of treatment, fluvastatin and lovastatin clearly increased CYP2C9 protein level. Lovastatin 45-55 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 74-80 17213228-4 2007 To identify such regulatory mechanisms, we isolated and characterized the Arabidopsis T-DNA insertion mutant lovastatin insensitive 1 (loi1), which is resistant to lovastatin and clomazone, inhibitors of the MVA and MEP pathways, respectively. Lovastatin 109-119 Pentatricopeptide repeat (PPR) superfamily protein Arabidopsis thaliana 135-139 17126835-10 2007 Lovastatin also reduced the accumulation of microglia and decreased the expression of TNF-alpha in the demyelinative lesions. Lovastatin 0-10 tumor necrosis factor Rattus norvegicus 86-95 17208229-18 2007 In the supernatants of lymph node cells stimulated with S-Ag peptide (5 microg/ml), 77 or 87% inhibition of IFN-gamma production was observed in rats treated with atorvastatin or lovastatin, respectively, compared with controls. Lovastatin 179-189 S-antigen visual arrestin Rattus norvegicus 56-60 17208229-18 2007 In the supernatants of lymph node cells stimulated with S-Ag peptide (5 microg/ml), 77 or 87% inhibition of IFN-gamma production was observed in rats treated with atorvastatin or lovastatin, respectively, compared with controls. Lovastatin 179-189 interferon gamma Rattus norvegicus 108-117 17142457-0 2007 Regulation of human cytochrome P450 4F2 expression by sterol regulatory element-binding protein and lovastatin. Lovastatin 100-110 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 20-39 17142457-2 2007 Real time PCR and immunoblots indicate that lovastatin treatment increases expression of the endogenous CYP4F2 gene in human primary hepatocytes and HepG2 cells. Lovastatin 44-54 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 104-110 17142457-4 2007 Immunoblots indicate that lovastatin-treated human hepatocytes display increased proteolytic processing of SREBP-2. Lovastatin 26-36 sterol regulatory element binding transcription factor 2 Homo sapiens 107-114 17142457-5 2007 In HepG2 cells, co-administration of a potent suppressor of SREBP-2 activation, 25-hydroxycholesterol, inhibits CYP4F2 mRNA induction by lovastatin. Lovastatin 137-147 sterol regulatory element binding transcription factor 2 Homo sapiens 60-67 17142457-5 2007 In HepG2 cells, co-administration of a potent suppressor of SREBP-2 activation, 25-hydroxycholesterol, inhibits CYP4F2 mRNA induction by lovastatin. Lovastatin 137-147 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 112-118 17142457-8 2007 Lovastatin-induced reporter expression is inhibited by overexpressed Insig-1, which prevents proteolytic activation of endogenous SREBPs. Lovastatin 0-10 insulin induced gene 1 Homo sapiens 69-76 17179158-1 2007 Lovastatin promotes osteoblast differentiation by increasing bone morphogenetic protein-2 (BMP-2) expression. Lovastatin 0-10 bone morphogenetic protein 2 Homo sapiens 61-89 17179158-1 2007 Lovastatin promotes osteoblast differentiation by increasing bone morphogenetic protein-2 (BMP-2) expression. Lovastatin 0-10 bone morphogenetic protein 2 Homo sapiens 91-96 17179158-2 2007 We demonstrate that lovastatin stimulates tyrosine phosphorylation of the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K), leading to an increase in its kinase activity in osteoblast cells. Lovastatin 20-30 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 100-129 17179158-4 2007 Expression of dominant-negative PI3K and PTEN, an inhibitor of PI3K signaling, significantly attenuated lovastatin-induced transcription of BMP-2. Lovastatin 104-114 phosphatase and tensin homolog Homo sapiens 41-45 17179158-4 2007 Expression of dominant-negative PI3K and PTEN, an inhibitor of PI3K signaling, significantly attenuated lovastatin-induced transcription of BMP-2. Lovastatin 104-114 bone morphogenetic protein 2 Homo sapiens 140-145 17179158-7 2007 Lovastatin-induced Erk1/2 activity contributed to BMP-2 transcription. Lovastatin 0-10 mitogen-activated protein kinase 3 Homo sapiens 19-25 17179158-7 2007 Lovastatin-induced Erk1/2 activity contributed to BMP-2 transcription. Lovastatin 0-10 bone morphogenetic protein 2 Homo sapiens 50-55 17179158-8 2007 Inhibition of PI3K abrogated Erk1/2 activity in response to lovastatin, indicating the presence of a signal relay between them. Lovastatin 60-70 mitogen-activated protein kinase 3 Homo sapiens 29-35 17179158-9 2007 We provide, as a mechanism of this cross-talk, the first evidence that lovastatin stimulates rapid activation of Ras, which associates with and activates PI3K in the plasma membrane, which in turn regulates Akt and Erk1/2 to induce BMP-2 expression for osteoblast differentiation. Lovastatin 71-81 AKT serine/threonine kinase 1 Homo sapiens 207-210 17179158-9 2007 We provide, as a mechanism of this cross-talk, the first evidence that lovastatin stimulates rapid activation of Ras, which associates with and activates PI3K in the plasma membrane, which in turn regulates Akt and Erk1/2 to induce BMP-2 expression for osteoblast differentiation. Lovastatin 71-81 mitogen-activated protein kinase 3 Homo sapiens 215-221 17179158-9 2007 We provide, as a mechanism of this cross-talk, the first evidence that lovastatin stimulates rapid activation of Ras, which associates with and activates PI3K in the plasma membrane, which in turn regulates Akt and Erk1/2 to induce BMP-2 expression for osteoblast differentiation. Lovastatin 71-81 bone morphogenetic protein 2 Homo sapiens 232-237 17245169-13 2007 At 24 hours, tPA mRNA levels in peritoneal tissue and tPA activity in peritoneal fluid from lovastatin-treated animals were increased by 57% and 379%, respectively (P < 0.05), while PAI-1 levels were unchanged. Lovastatin 92-102 serpin family E member 1 Homo sapiens 185-190 17245169-14 2007 HMC incubated with either lovastatin or atorvastatin showed concentration-dependent increases in tPA production and decreases in PAI-1 production (P < 0.05). Lovastatin 26-36 serpin family E member 1 Homo sapiens 129-134 17245169-15 2007 These lovastatin-induced changes in tPA and PAI-1 production were significantly reversed by the addition of MVA, GGPP, and FPP. Lovastatin 6-16 serpin family E member 1 Homo sapiens 44-49 17251057-3 2007 In this work, we investigated the role of JNK and p38 MAPK in neuroblast apoptosis induced by lovastatin. Lovastatin 94-104 mitogen-activated protein kinase 8 Rattus norvegicus 42-45 17251057-4 2007 We found that lovastatin induced the activation of JNK, but not p38 MAPK. Lovastatin 14-24 mitogen-activated protein kinase 8 Rattus norvegicus 51-54 17251057-7 2007 Pre-treatment with iJNK-I (a selective JNK inhibitor) prevented the effect of lovastatin on both neuroblast apoptosis and the activation of the JNK cascade. Lovastatin 78-88 mitogen-activated protein kinase 8 Rattus norvegicus 20-23 17251057-7 2007 Pre-treatment with iJNK-I (a selective JNK inhibitor) prevented the effect of lovastatin on both neuroblast apoptosis and the activation of the JNK cascade. Lovastatin 78-88 mitogen-activated protein kinase 8 Rattus norvegicus 39-42 17251057-8 2007 Furthermore, we found that the activation of the JNK signalling pathway triggered by lovastatin is accompanied by caspase-3 activation which is also inhibited by iJNK-I pre-treatment. Lovastatin 85-95 mitogen-activated protein kinase 8 Rattus norvegicus 49-52 17251057-8 2007 Furthermore, we found that the activation of the JNK signalling pathway triggered by lovastatin is accompanied by caspase-3 activation which is also inhibited by iJNK-I pre-treatment. Lovastatin 85-95 caspase 3 Rattus norvegicus 114-123 17251057-10 2007 Taken together, our data suggest that the activation of the JNK/c-Jun/BimEL signalling pathway plays a crucial role in lovastatin-induced neuroblast apoptosis. Lovastatin 119-129 mitogen-activated protein kinase 8 Rattus norvegicus 60-63 17179181-1 2007 We examined the change in the subcellular distribution of a lysosomal enzyme, beta-glucuronidase (beta-G), caused by decreased cholesterol levels in mouse melanoma cells using an HMG-CoA reductase inhibitor, lovastatin and lipoprotein-deficient serum (LDS). Lovastatin 208-218 glucuronidase, beta Mus musculus 78-96 17179181-1 2007 We examined the change in the subcellular distribution of a lysosomal enzyme, beta-glucuronidase (beta-G), caused by decreased cholesterol levels in mouse melanoma cells using an HMG-CoA reductase inhibitor, lovastatin and lipoprotein-deficient serum (LDS). Lovastatin 208-218 glucuronidase, beta Mus musculus 98-104 17179181-3 2007 Furthermore, another lysosomal enzyme, cathepsin H, was found to be released in the medium from cells treated with lovastatin. Lovastatin 115-125 cathepsin H Mus musculus 39-50 17179181-5 2007 Next, when cells were treated with LDS without lovastatin, concomitantly with the decrease in the levels of cholesterol and beta-G activity in the cells, beta-G activity in the medium increased. Lovastatin 47-57 glucuronidase, beta Mus musculus 124-130 17179181-5 2007 Next, when cells were treated with LDS without lovastatin, concomitantly with the decrease in the levels of cholesterol and beta-G activity in the cells, beta-G activity in the medium increased. Lovastatin 47-57 glucuronidase, beta Mus musculus 154-160 17179181-6 2007 Also, the ratio of beta-G (3.2-fold) released in the medium from cells treated with Dulbecco"s modified Eagle medium (D-MEM) containing lovastatin and LDS was higher than that (2.3-fold) on treatment with D-MEM containing LDS without lovastatin. Lovastatin 136-146 glucuronidase, beta Mus musculus 19-25 17179181-6 2007 Also, the ratio of beta-G (3.2-fold) released in the medium from cells treated with Dulbecco"s modified Eagle medium (D-MEM) containing lovastatin and LDS was higher than that (2.3-fold) on treatment with D-MEM containing LDS without lovastatin. Lovastatin 234-244 glucuronidase, beta Mus musculus 19-25 17090659-6 2007 Upregulation of LDLR by lipoprotein-deficient serum/lovastatin in wild-type cells resulted in a 7-fold increase of LPL-mediated LDL uptake. Lovastatin 52-62 low density lipoprotein receptor Mus musculus 16-20 17090659-6 2007 Upregulation of LDLR by lipoprotein-deficient serum/lovastatin in wild-type cells resulted in a 7-fold increase of LPL-mediated LDL uptake. Lovastatin 52-62 lipoprotein lipase Mus musculus 115-118 17213228-5 2007 The accumulation of the major products of these pathways, i.e. sterols and chlorophyll, was less affected by lovastatin and clomazone, respectively, in loi1 than in the wild type. Lovastatin 109-119 Pentatricopeptide repeat (PPR) superfamily protein Arabidopsis thaliana 152-156 17213228-6 2007 Furthermore, the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity analysis showed higher activity of HMGR in loi1-1 treated with lovastatin than that in the WT. Lovastatin 144-154 Pentatricopeptide repeat (PPR) superfamily protein Arabidopsis thaliana 124-130 17213228-7 2007 We consider that the lovastatin-resistant phenotype of loi1-1 was derived from this post-transcriptional up-regulation of HMGR. Lovastatin 21-31 Pentatricopeptide repeat (PPR) superfamily protein Arabidopsis thaliana 55-61 17158337-4 2007 Lovastatin specifically recruits the forkhead box FoxO3a transcription factor to the p21 promoter, mediating transcriptional transactivation of the p21 gene as analyzed in isolated primary cardiomyocytes. Lovastatin 0-10 forkhead box O3 Homo sapiens 50-56 17158337-4 2007 Lovastatin specifically recruits the forkhead box FoxO3a transcription factor to the p21 promoter, mediating transcriptional transactivation of the p21 gene as analyzed in isolated primary cardiomyocytes. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 85-88 17158337-4 2007 Lovastatin specifically recruits the forkhead box FoxO3a transcription factor to the p21 promoter, mediating transcriptional transactivation of the p21 gene as analyzed in isolated primary cardiomyocytes. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 148-151 17158337-5 2007 Lovastatin also stimulates protein kinase B/Akt kinase activity, and Akt-dependent phosphorylation forces p21 in the cytoplasm, where it inhibits Rho-kinases contributing to the suppression of cardiomyocyte hypertrophy. Lovastatin 0-10 AKT serine/threonine kinase 1 Homo sapiens 44-47 17158337-5 2007 Lovastatin also stimulates protein kinase B/Akt kinase activity, and Akt-dependent phosphorylation forces p21 in the cytoplasm, where it inhibits Rho-kinases contributing to the suppression of cardiomyocyte hypertrophy. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 106-109 17158337-6 2007 Loss of p21 or FoxO3a by RNA interference causes a general inhibition of lovastatin signal transduction. Lovastatin 73-83 cyclin dependent kinase inhibitor 1A Homo sapiens 8-11 17158337-6 2007 Loss of p21 or FoxO3a by RNA interference causes a general inhibition of lovastatin signal transduction. Lovastatin 73-83 forkhead box O3 Homo sapiens 15-21 17008555-3 2007 We demonstrated that human NPC1L1 mRNA expression was significantly decreased by 25-hydroxycholesterol but increased in response to cellular cholesterol depletion achieved by incubation with Mevinolin (an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase) in human intestinal Caco-2 cells. Lovastatin 191-200 NPC1 like intracellular cholesterol transporter 1 Homo sapiens 27-33 16952276-3 2007 We showed that lovastatin efficiently inhibited Ras activation, which was associated with a significant decrease in ERK1/2 (extracellular-signal-regulated kinase 1/2) phosphorylation. Lovastatin 15-25 mitogen activated protein kinase 3 Rattus norvegicus 116-122 16952276-3 2007 We showed that lovastatin efficiently inhibited Ras activation, which was associated with a significant decrease in ERK1/2 (extracellular-signal-regulated kinase 1/2) phosphorylation. Lovastatin 15-25 mitogen activated protein kinase 3 Rattus norvegicus 124-165 16952276-4 2007 Lovastatin also decreased CREB phosphorylation and CREB-mediated gene expression. Lovastatin 0-10 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 16952276-4 2007 Lovastatin also decreased CREB phosphorylation and CREB-mediated gene expression. Lovastatin 0-10 cAMP responsive element binding protein 1 Rattus norvegicus 51-55 16952276-5 2007 The effects of lovastatin on the Ras/ERK1/2/CREB pathway were time- and concentration-dependent and fully prevented by mevalonate. Lovastatin 15-25 mitogen activated protein kinase 3 Rattus norvegicus 37-43 16952276-5 2007 The effects of lovastatin on the Ras/ERK1/2/CREB pathway were time- and concentration-dependent and fully prevented by mevalonate. Lovastatin 15-25 cAMP responsive element binding protein 1 Rattus norvegicus 44-48 16952276-9 2007 Our results suggest that lovastatin triggers neuroblast apoptosis by regulating several signalling pathways, including the Ras/ERK1/2 pathway. Lovastatin 25-35 mitogen activated protein kinase 3 Rattus norvegicus 127-133 17103090-8 2007 GJIC was also upregulated in MCF-7 cells, with transfer of LY Fluorescence reaching 4 to 5 rows of cells from the scraped line after treatment with 16 micromol/L Lovastatin for 72 h. Finally, downregulation of ERK1 and p38(MAPK) phosphorylation were found in Lovastatin-treated MCF-7 cells. Lovastatin 162-172 mitogen-activated protein kinase 3 Homo sapiens 210-214 17103090-8 2007 GJIC was also upregulated in MCF-7 cells, with transfer of LY Fluorescence reaching 4 to 5 rows of cells from the scraped line after treatment with 16 micromol/L Lovastatin for 72 h. Finally, downregulation of ERK1 and p38(MAPK) phosphorylation were found in Lovastatin-treated MCF-7 cells. Lovastatin 162-172 mitogen-activated protein kinase 14 Homo sapiens 219-222 17705568-7 2007 In the FATS study, the severity of stenosis after 2.5 years in recipients of lovastatin plus colestipol was reduced by 2.8% compared with placebo, while the frequency of lesion progression was halved and the frequency of lesion regression was tripled. Lovastatin 77-87 chromosome 10 open reading frame 90 Homo sapiens 7-11 17050804-7 2007 Inhibition of phosphatidylinositol 3-kinase, expression of dominant-negative AKT, or treatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG. Lovastatin 132-142 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 104-121 17050804-7 2007 Inhibition of phosphatidylinositol 3-kinase, expression of dominant-negative AKT, or treatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG. Lovastatin 132-142 AKT serine/threonine kinase 1 Homo sapiens 154-157 17050804-7 2007 Inhibition of phosphatidylinositol 3-kinase, expression of dominant-negative AKT, or treatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG. Lovastatin 132-142 chorionic gonadotropin subunit beta 5 Homo sapiens 212-215 17050804-9 2007 Treatment with hCG and lovastatin decreased expression of BCL-(XL) and XIAP, and increased expression of IkappaB. Lovastatin 23-33 BCL2 like 1 Homo sapiens 58-66 17050804-9 2007 Treatment with hCG and lovastatin decreased expression of BCL-(XL) and XIAP, and increased expression of IkappaB. Lovastatin 23-33 X-linked inhibitor of apoptosis Homo sapiens 71-75 17050804-12 2007 The promotion of hCG lethality by lovastatin was abolished by overexpression of BCL-(XL), and was dependent upon activation of caspase-9. Lovastatin 34-44 chorionic gonadotropin subunit beta 5 Homo sapiens 17-20 17050804-12 2007 The promotion of hCG lethality by lovastatin was abolished by overexpression of BCL-(XL), and was dependent upon activation of caspase-9. Lovastatin 34-44 BCL2 like 1 Homo sapiens 80-87 17050804-12 2007 The promotion of hCG lethality by lovastatin was abolished by overexpression of BCL-(XL), and was dependent upon activation of caspase-9. Lovastatin 34-44 caspase 9 Homo sapiens 127-136 17178259-4 2006 Simvastatin, lovastatin, and atorvastatin are metabolized by cytochrome P450 (CYP) 3A4 (simvastatin acid is also metabolized by CYP2C8); their plasma concentrations and risk of myotoxicity are greatly increased by strong inhibitors of CYP3A4 (eg, itraconazole and ritonavir). Lovastatin 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-86 17005160-0 2006 Elevated K-ras activity with cholestyramine and lovastatin, but not konjac mannan or niacin in lung--importance of mouse strain. Lovastatin 48-58 Kirsten rat sarcoma viral oncogene homolog Mus musculus 9-14 17088865-7 2006 Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK). Lovastatin 0-10 tumor protein p53 Homo sapiens 58-61 17088865-7 2006 Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK). Lovastatin 0-10 checkpoint kinase 1 Homo sapiens 106-111 17234346-0 2007 Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling. Lovastatin 0-10 amyloid beta precursor protein Homo sapiens 42-47 17234346-0 2007 Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling. Lovastatin 0-10 catenin beta 1 Homo sapiens 90-102 17234346-0 2007 Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling. Lovastatin 0-10 hepatocyte nuclear factor 4 alpha Homo sapiens 103-106 17234346-5 2007 Lovastatin has been shown to decrease the production of Abeta and to promote neuronal survival. Lovastatin 0-10 amyloid beta precursor protein Homo sapiens 56-61 17234346-7 2007 We propose that the neuroprotective effect of lovastatin may be due to inactivation of GSK-3beta activity, resulting in induction of Wnt signaling. Lovastatin 46-56 glycogen synthase kinase 3 beta Homo sapiens 87-96 17234346-8 2007 Here, we report that lovastatin prevented Abeta-induced apoptosis in human SK-NSH cells. Lovastatin 21-31 amyloid beta precursor protein Homo sapiens 42-47 17234346-10 2007 Lovastatin treatment induced an increase in TCF/LEF-chloramphenicol acetyl transferase (CAT) gene reporter activity. Lovastatin 0-10 hepatocyte nuclear factor 4 alpha Homo sapiens 44-47 17234346-11 2007 More importantly, beta-catenin and TCF were required for the neuroprotective function of lovastatin. Lovastatin 89-99 catenin beta 1 Homo sapiens 18-30 17234346-11 2007 More importantly, beta-catenin and TCF were required for the neuroprotective function of lovastatin. Lovastatin 89-99 hepatocyte nuclear factor 4 alpha Homo sapiens 35-38 17234346-12 2007 Our results suggest that lovastatin protects neuronal cells from Abeta-induced apoptosis and causes reduction in GSK-3beta activity, resulting in activation of Wnt signaling. Lovastatin 25-35 amyloid beta precursor protein Homo sapiens 65-70 17234346-12 2007 Our results suggest that lovastatin protects neuronal cells from Abeta-induced apoptosis and causes reduction in GSK-3beta activity, resulting in activation of Wnt signaling. Lovastatin 25-35 glycogen synthase kinase 3 beta Homo sapiens 113-122 17184503-0 2006 Regulation of hepatic cholesterol metabolism in CETP/LDLr mice by cholesterol feeding and by drugs (cholestyramine and lovastatin) that lower plasma cholesterol. Lovastatin 119-129 cholesteryl ester transfer protein Homo sapiens 48-52 17184503-0 2006 Regulation of hepatic cholesterol metabolism in CETP/LDLr mice by cholesterol feeding and by drugs (cholestyramine and lovastatin) that lower plasma cholesterol. Lovastatin 119-129 low density lipoprotein receptor Mus musculus 53-57 17178259-4 2006 Simvastatin, lovastatin, and atorvastatin are metabolized by cytochrome P450 (CYP) 3A4 (simvastatin acid is also metabolized by CYP2C8); their plasma concentrations and risk of myotoxicity are greatly increased by strong inhibitors of CYP3A4 (eg, itraconazole and ritonavir). Lovastatin 13-23 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 128-134 17178259-4 2006 Simvastatin, lovastatin, and atorvastatin are metabolized by cytochrome P450 (CYP) 3A4 (simvastatin acid is also metabolized by CYP2C8); their plasma concentrations and risk of myotoxicity are greatly increased by strong inhibitors of CYP3A4 (eg, itraconazole and ritonavir). Lovastatin 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 16868926-6 2006 Correspondingly, specific inhibition of cholesterol synthesis in periovulatory human granulosa cells using HMG-CoA reductase inhibitors (lovastatin or simvastatin) increased apoptosis, measured as caspase-3/7 activity. Lovastatin 137-147 caspase 3 Homo sapiens 197-206 17233196-4 2006 Phenytoin induces the CYP3A4 isoform of the CYP450 system and can reduce the bioavailability, and thus the efficacy of the statins metabolized by this enzyme, including atorvastatin and lovastatin. Lovastatin 186-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 17184503-14 2006 That is, different to unabsorbed cholestyramine, lovastatin, as an absorbed plasma cholesterol-lowering drug, may have modified the activity of other unknown genes that play roles in the interaction of CETP with the metabolism of hepatic cholesterol. Lovastatin 49-59 cholesteryl ester transfer protein Homo sapiens 202-206 16968805-13 2006 Lovastatin significantly decreased Rho kinase and nuclear factor-kappaB activity, significantly increased Akt activity, and resulted in decreased monocyte IL-6 levels; these effects were reversed with mevalonate and geranylgeranyl pyrophosphate, indicating direct effects of statins on protein prenylation. Lovastatin 0-10 AKT serine/threonine kinase 1 Homo sapiens 106-109 16968805-13 2006 Lovastatin significantly decreased Rho kinase and nuclear factor-kappaB activity, significantly increased Akt activity, and resulted in decreased monocyte IL-6 levels; these effects were reversed with mevalonate and geranylgeranyl pyrophosphate, indicating direct effects of statins on protein prenylation. Lovastatin 0-10 interleukin 6 Homo sapiens 155-159 16947002-10 2006 In addition, the lovastatin-treated glands also showed a decreased expression of phosphorylated ERK1/2 and a number of PCNA-positive cells. Lovastatin 17-27 mitogen activated protein kinase 3 Rattus norvegicus 96-102 16947002-10 2006 In addition, the lovastatin-treated glands also showed a decreased expression of phosphorylated ERK1/2 and a number of PCNA-positive cells. Lovastatin 17-27 proliferating cell nuclear antigen Rattus norvegicus 119-123 16714062-6 2006 Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9. Lovastatin 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-98 16675062-0 2006 Influence of cholesterol and lovastatin on alpha-form of secreted amyloid precursor protein and expression of alpha7 nicotinic receptor on astrocytes. Lovastatin 29-39 amyloid beta precursor protein Homo sapiens 66-91 16675062-1 2006 The influence of cholesterol and the lovastatin (cholesterol-lowering drug) on secretion of alpha-secretase cleavage product of amyloid precursor protein (APP) and expression of nicotinic acetylcholine receptors (nAChRs) was investigated in human HTB-15 astrocytes. Lovastatin 37-47 amyloid beta precursor protein Homo sapiens 128-153 16714062-6 2006 Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9. Lovastatin 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 16910707-8 2006 Furthermore, glutathione S-transferase P 1 and cytoskeleton-8, -18, and -19 revealed a down-regulation in a dose-dependent manner in exposure of Caco-2 cells to monacolin K. Lovastatin 161-172 glutathione S-transferase pi 1 Homo sapiens 13-42 16936274-1 2006 Combination therapy with multiple sclerosis (MS) therapeutics is gaining momentum over monotherapy for improving MS. Lovastatin, an HMG-CoA reductase inhibitor (statin), was immunomodulatory in an experimental autoimmune encephalomyelitis (EAE) model of MS. Lovastatin biases the immune response from Th1 to a protective Th2 response in EAE by a different mechanism than 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside, an immunomodulating agent that activates AMP-activated protein kinase. Lovastatin 117-127 negative elongation factor complex member C/D Homo sapiens 301-304 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Lovastatin 19-29 cyclin dependent kinase 2 Homo sapiens 80-84 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Lovastatin 19-29 cyclin dependent kinase 2 Homo sapiens 244-248 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Lovastatin 19-29 H3 histone pseudogene 16 Homo sapiens 289-292 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Lovastatin 19-29 dynactin subunit 6 Homo sapiens 297-300 16857822-3 2006 Lovastatin is a specific and potent inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 49-89 16857822-4 2006 Targeting 3-hydroxy-3-methylglutaryl CoA reductase using lovastatin induces a potent tumor-specific apoptotic response in a variety of tumor types at therapeutically achievable levels of this drug. Lovastatin 57-67 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 10-50 16857822-6 2006 Lovastatin treatment inhibited EGF-induced EGFR autophosphorylation and its downstream signaling cascades by 24 hours. Lovastatin 0-10 epidermal growth factor receptor Homo sapiens 43-47 16857822-10 2006 The use of lovastatin, which is metabolized by CYP3A4, is contraindicated with drugs, such as gefitinib and erlotinib, which are also metabolized by CYP3A4 due to greatly enhanced toxicity. Lovastatin 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 16857822-10 2006 The use of lovastatin, which is metabolized by CYP3A4, is contraindicated with drugs, such as gefitinib and erlotinib, which are also metabolized by CYP3A4 due to greatly enhanced toxicity. Lovastatin 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 16784888-6 2006 TM7SF2 mRNA and C14SR protein expression in HepG2 cells grown in delipidated serum (LPDS) plus lovastatin (sterol starvation) were 4- and 8-fold higher, respectively, than in LPDS plus 25-hydroxycholesterol (sterol feeding), resulting in 4-fold higher 3beta-hydroxysterol Delta(14)-reductase activity. Lovastatin 95-105 transmembrane 7 superfamily member 2 Homo sapiens 0-6 16729291-3 2006 RESULTS: We demonstrate that lovastatin and simvastatin induce a 50 to 60% reduction in the diffusion rates of bovine serum albumin and [(14)C]-sucrose across human BBB-ECs in vitro through abrogation of isoprenylation processes, but independent of the expression of the tight junction molecules occludin, VE-cadherin, JAM-1, zonula occluden-1, and zonula occluden-2. Lovastatin 29-39 occludin Homo sapiens 296-304 16729291-3 2006 RESULTS: We demonstrate that lovastatin and simvastatin induce a 50 to 60% reduction in the diffusion rates of bovine serum albumin and [(14)C]-sucrose across human BBB-ECs in vitro through abrogation of isoprenylation processes, but independent of the expression of the tight junction molecules occludin, VE-cadherin, JAM-1, zonula occluden-1, and zonula occluden-2. Lovastatin 29-39 cadherin 5 Homo sapiens 306-317 16729291-3 2006 RESULTS: We demonstrate that lovastatin and simvastatin induce a 50 to 60% reduction in the diffusion rates of bovine serum albumin and [(14)C]-sucrose across human BBB-ECs in vitro through abrogation of isoprenylation processes, but independent of the expression of the tight junction molecules occludin, VE-cadherin, JAM-1, zonula occluden-1, and zonula occluden-2. Lovastatin 29-39 F11 receptor Homo sapiens 319-324 16729291-5 2006 We further demonstrate that lovastatin and simvastatin treatment of BBB-ECs significantly restricts the migration of clinically isolated syndrome-derived and MS-derived monocytes and lymphocytes across the human BBB in vitro, through a specific reduction in the secretion of the chemokines monocyte chemotactic protein-1/CCL2 and interferon-gamma-inducible protein-10/CXCL10 by BBB-ECs. Lovastatin 28-38 C-C motif chemokine ligand 2 Homo sapiens 290-320 16729291-5 2006 We further demonstrate that lovastatin and simvastatin treatment of BBB-ECs significantly restricts the migration of clinically isolated syndrome-derived and MS-derived monocytes and lymphocytes across the human BBB in vitro, through a specific reduction in the secretion of the chemokines monocyte chemotactic protein-1/CCL2 and interferon-gamma-inducible protein-10/CXCL10 by BBB-ECs. Lovastatin 28-38 C-C motif chemokine ligand 2 Homo sapiens 321-325 16729291-5 2006 We further demonstrate that lovastatin and simvastatin treatment of BBB-ECs significantly restricts the migration of clinically isolated syndrome-derived and MS-derived monocytes and lymphocytes across the human BBB in vitro, through a specific reduction in the secretion of the chemokines monocyte chemotactic protein-1/CCL2 and interferon-gamma-inducible protein-10/CXCL10 by BBB-ECs. Lovastatin 28-38 C-X-C motif chemokine ligand 10 Homo sapiens 330-367 16729291-5 2006 We further demonstrate that lovastatin and simvastatin treatment of BBB-ECs significantly restricts the migration of clinically isolated syndrome-derived and MS-derived monocytes and lymphocytes across the human BBB in vitro, through a specific reduction in the secretion of the chemokines monocyte chemotactic protein-1/CCL2 and interferon-gamma-inducible protein-10/CXCL10 by BBB-ECs. Lovastatin 28-38 C-X-C motif chemokine ligand 10 Homo sapiens 368-374 16785563-0 2006 Lovastatin-induced apoptosis in macrophages through the Rac1/Cdc42/JNK pathway. Lovastatin 0-10 Rac family small GTPase 1 Homo sapiens 56-60 16785563-0 2006 Lovastatin-induced apoptosis in macrophages through the Rac1/Cdc42/JNK pathway. Lovastatin 0-10 cell division cycle 42 Homo sapiens 61-66 16785563-0 2006 Lovastatin-induced apoptosis in macrophages through the Rac1/Cdc42/JNK pathway. Lovastatin 0-10 mitogen-activated protein kinase 8 Homo sapiens 67-70 16785563-7 2006 Further investigation of the molecular mechanism has revealed that Rac1 and Cdc42, the small GTPase family members, may play an important role in lovastatin-induced macrophage apoptosis. Lovastatin 146-156 Rac family small GTPase 1 Homo sapiens 67-71 16785563-7 2006 Further investigation of the molecular mechanism has revealed that Rac1 and Cdc42, the small GTPase family members, may play an important role in lovastatin-induced macrophage apoptosis. Lovastatin 146-156 cell division cycle 42 Homo sapiens 76-81 16678134-3 2006 The HMG-CoA reductase inhibitor lovastatin suppressed cholesterol synthesis from [2-(14)C]acetate and [1-(14)C]C8:0 but not from [1-(14)C]C24:0, implicating a peroxisomal, lovastatin-resistant HMG-CoA reductase. Lovastatin 32-42 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-21 16678134-3 2006 The HMG-CoA reductase inhibitor lovastatin suppressed cholesterol synthesis from [2-(14)C]acetate and [1-(14)C]C8:0 but not from [1-(14)C]C24:0, implicating a peroxisomal, lovastatin-resistant HMG-CoA reductase. Lovastatin 32-42 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 193-210 16702307-10 2006 Inhibition of VEGF release by flavonoids, tocopherols, and lovastatin in these models of neoplastic cells suggests a novel mechanism for mammary cancer prevention. Lovastatin 59-69 vascular endothelial growth factor A Homo sapiens 14-18 16751413-4 2006 In this study, we show that lovastatin increased efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent manner. Lovastatin 28-38 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 78-136 16751413-6 2006 Lovastatin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decreased membrane localization of RhoA, to a greater extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer of RhoA. Lovastatin 0-10 ras homolog family member A Homo sapiens 80-84 16751413-6 2006 Lovastatin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decreased membrane localization of RhoA, to a greater extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer of RhoA. Lovastatin 0-10 ras homolog family member A Homo sapiens 135-139 16751413-6 2006 Lovastatin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decreased membrane localization of RhoA, to a greater extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer of RhoA. Lovastatin 0-10 Rac family small GTPase 1 Homo sapiens 166-178 16751413-6 2006 Lovastatin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decreased membrane localization of RhoA, to a greater extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer of RhoA. Lovastatin 0-10 ras homolog family member A Homo sapiens 135-139 16425225-8 2006 To support this, we show, using reporter assays including dominant-negative constructs of PPARgamma, that both Lovastatin and Rosiglitazone specifically mediate PPARgamma activation. Lovastatin 111-121 peroxisome proliferator activated receptor gamma Homo sapiens 90-99 16425225-8 2006 To support this, we show, using reporter assays including dominant-negative constructs of PPARgamma, that both Lovastatin and Rosiglitazone specifically mediate PPARgamma activation. Lovastatin 111-121 peroxisome proliferator activated receptor gamma Homo sapiens 161-170 16425225-0 2006 Increased PTEN expression due to transcriptional activation of PPARgamma by Lovastatin and Rosiglitazone. Lovastatin 76-86 phosphatase and tensin homolog Homo sapiens 10-14 16425225-10 2006 These data are the first to demonstrate that Lovastatin can signal through PPARgamma and directly demonstrate that PPARgamma can upregulate PTEN at the transcriptional level. Lovastatin 45-55 peroxisome proliferator activated receptor gamma Homo sapiens 75-84 16425225-0 2006 Increased PTEN expression due to transcriptional activation of PPARgamma by Lovastatin and Rosiglitazone. Lovastatin 76-86 peroxisome proliferator activated receptor gamma Homo sapiens 63-72 16425225-4 2006 We show here that the PPARgamma agonist Rosiglitazone, along with Lovastatin, induce PTEN in a dose- and time-dependent manner. Lovastatin 66-76 peroxisome proliferator activated receptor gamma Homo sapiens 22-31 16425225-10 2006 These data are the first to demonstrate that Lovastatin can signal through PPARgamma and directly demonstrate that PPARgamma can upregulate PTEN at the transcriptional level. Lovastatin 45-55 peroxisome proliferator activated receptor gamma Homo sapiens 115-124 16425225-4 2006 We show here that the PPARgamma agonist Rosiglitazone, along with Lovastatin, induce PTEN in a dose- and time-dependent manner. Lovastatin 66-76 phosphatase and tensin homolog Homo sapiens 85-89 16425225-10 2006 These data are the first to demonstrate that Lovastatin can signal through PPARgamma and directly demonstrate that PPARgamma can upregulate PTEN at the transcriptional level. Lovastatin 45-55 phosphatase and tensin homolog Homo sapiens 140-144 16425225-5 2006 Lovastatin- or Rosiglitazone-induced PTEN expression was accompanied by a decrease in phosphorylated-AKT and phosphorylated-MAPK and an increase in G1 arrest. Lovastatin 0-10 phosphatase and tensin homolog Homo sapiens 37-41 16425225-11 2006 Since PTEN is constitutively active, our data indicates it may be worthwhile to examine Rosiglitazone and Lovastatin stimulation as mechanisms to increase PTEN expression for therapeutic and preventative strategies including cancer, diabetes mellitus and cardiovascular disease. Lovastatin 106-116 phosphatase and tensin homolog Homo sapiens 6-10 16425225-6 2006 We demonstrate that the mechanism of Lovastatin- and Rosiglitazone-associated PTEN expression was a result of an increase in PTEN mRNA, suggesting that this increase was transcriptionally-mediated. Lovastatin 37-47 phosphatase and tensin homolog Homo sapiens 78-82 16425225-11 2006 Since PTEN is constitutively active, our data indicates it may be worthwhile to examine Rosiglitazone and Lovastatin stimulation as mechanisms to increase PTEN expression for therapeutic and preventative strategies including cancer, diabetes mellitus and cardiovascular disease. Lovastatin 106-116 phosphatase and tensin homolog Homo sapiens 155-159 16425225-6 2006 We demonstrate that the mechanism of Lovastatin- and Rosiglitazone-associated PTEN expression was a result of an increase in PTEN mRNA, suggesting that this increase was transcriptionally-mediated. Lovastatin 37-47 phosphatase and tensin homolog Homo sapiens 125-129 16523333-14 2006 In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone. Lovastatin 94-104 BCL2 apoptosis regulator Homo sapiens 22-27 16581329-6 2006 In persons taking simvastatin, lovastatin, or atorvastatin, 60% of cases involved drugs known to inhibit CYP3A4 (especially erythromycin and azole antifungals), and 19% involved fibrates, principally gemfibrozil. Lovastatin 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 16523333-14 2006 In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone. Lovastatin 94-104 BCL2 associated X, apoptosis regulator Homo sapiens 28-31 16427097-8 2006 Specifically, we demonstrate that 3 statins, simvastatin, lovastatin, and mevastatin induce dose-dependent apoptosis in the TR-PCT1 pericyte cell line, that simvastatin (empirically shown to be the most potent of the 3 statins) induces similar levels of apoptosis in freshly isolated pericytes, and that simvastatin-induced apoptosis in pericytes is cholesterol, caspase-3, and caspase-7 mediated. Lovastatin 58-68 caspase 3 Rattus norvegicus 363-372 16581325-4 2006 Drug metabolism studies show simvastatin and lovastatin to be especially sensitive to the inhibiting effects of other drugs on the cytochrome P-450 3A4 (CYP3A4) isoenzyme. Lovastatin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-151 16581325-4 2006 Drug metabolism studies show simvastatin and lovastatin to be especially sensitive to the inhibiting effects of other drugs on the cytochrome P-450 3A4 (CYP3A4) isoenzyme. Lovastatin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 16581329-5 2006 Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). Lovastatin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 16581329-5 2006 Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). Lovastatin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 16581329-5 2006 Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). Lovastatin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 244-250 16436135-8 2006 Moreover, both statins, and to a lesser degree lovastatin, were found to inhibit the SCF-induced differentiation of MCs from their progenitors. Lovastatin 47-57 KIT ligand Homo sapiens 85-88 16427097-8 2006 Specifically, we demonstrate that 3 statins, simvastatin, lovastatin, and mevastatin induce dose-dependent apoptosis in the TR-PCT1 pericyte cell line, that simvastatin (empirically shown to be the most potent of the 3 statins) induces similar levels of apoptosis in freshly isolated pericytes, and that simvastatin-induced apoptosis in pericytes is cholesterol, caspase-3, and caspase-7 mediated. Lovastatin 58-68 caspase 7 Rattus norvegicus 378-387 16472124-0 2006 Lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF-alpha in cerebral vascular endothelial cells. Lovastatin 0-10 CD40 molecule Homo sapiens 51-55 16343726-6 2006 In experiments in vitro, lovastatin-induced MPT in a dose-dependent manner (10-80 microM) by a mechanism sensitive to cyclosporin A (cyclophilin sequestrant), dithiothreitol (reducing agent), adenine nucleotide carrier inhibitor (ADP), catalase (H2O2 reductant) and EGTA (calcium chelator). Lovastatin 25-35 catalase Homo sapiens 236-244 16467108-10 2006 Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation. Lovastatin 0-10 tumor protein p53 Homo sapiens 96-99 16467108-10 2006 Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 100-103 16467108-10 2006 Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation. Lovastatin 0-10 checkpoint kinase 1 Homo sapiens 172-177 16472124-0 2006 Lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF-alpha in cerebral vascular endothelial cells. Lovastatin 0-10 tumor necrosis factor Homo sapiens 78-87 16472124-5 2006 Preincubation with lovastatin (10(-7), 10(-6) and 10(-5) mol/l) for 24 hours (h) protected CVECs from TNF-alpha-induced decrease of cellular viability. Lovastatin 19-29 tumor necrosis factor Homo sapiens 102-111 16472124-6 2006 Further, lovastatin inhibited the TNF-alpha-induced increases of NO level, NOS activity, apoptotic cells and CD40 expression in a dose-dependent manner, and anti-CD40 antibody also inhibited the cellular apoptosis induced by TNF-alpha. Lovastatin 9-19 tumor necrosis factor Homo sapiens 34-43 16472124-6 2006 Further, lovastatin inhibited the TNF-alpha-induced increases of NO level, NOS activity, apoptotic cells and CD40 expression in a dose-dependent manner, and anti-CD40 antibody also inhibited the cellular apoptosis induced by TNF-alpha. Lovastatin 9-19 CD40 molecule Homo sapiens 109-113 16472124-6 2006 Further, lovastatin inhibited the TNF-alpha-induced increases of NO level, NOS activity, apoptotic cells and CD40 expression in a dose-dependent manner, and anti-CD40 antibody also inhibited the cellular apoptosis induced by TNF-alpha. Lovastatin 9-19 tumor necrosis factor Homo sapiens 225-234 16955753-1 2006 Cardiovascular drugs such as lovastatin, simvastatin, amlodipine besylate, nifedipine, and hydralazine hydrochloride inhibit cholesterol esterase (CEase) in vitro. Lovastatin 29-39 carboxyl ester lipase Homo sapiens 125-145 16955753-1 2006 Cardiovascular drugs such as lovastatin, simvastatin, amlodipine besylate, nifedipine, and hydralazine hydrochloride inhibit cholesterol esterase (CEase) in vitro. Lovastatin 29-39 carboxyl ester lipase Homo sapiens 147-152 16094629-6 2006 This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. Lovastatin 149-159 E2F transcription factor 1 Homo sapiens 68-73 16316623-0 2006 Lovastatin-induced RhoA modulation and its effect on senescence in prostate cancer cells. Lovastatin 0-10 ras homolog family member A Homo sapiens 19-23 16094629-6 2006 This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. Lovastatin 149-159 interferon alpha inducible protein 27 Homo sapiens 78-81 16094629-6 2006 This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. Lovastatin 149-159 cyclin dependent kinase inhibitor 1B Homo sapiens 82-86 16094629-6 2006 This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. Lovastatin 149-159 cyclin dependent kinase 2 Homo sapiens 241-245 16094629-6 2006 This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. Lovastatin 149-159 cyclin A2 Homo sapiens 247-255 16316623-5 2006 We found that constitutively active RhoA (caRhoA) reversed lovastatin-induced senescence in caRhoA-transfected PC-3 cells. Lovastatin 59-69 ras homolog family member A Homo sapiens 36-40 16424040-7 2006 Cells devoid of p21 were refractory to the growth-inhibitory activity of lovastatin, FTI-277, and GGTI-298. Lovastatin 73-83 cyclin dependent kinase inhibitor 1A Homo sapiens 16-19 16817619-6 2006 Morphologically, the cells treated with various doses of Mevinolin expressed similar structural changes to those observed using PTH. Lovastatin 57-66 parathyroid hormone Homo sapiens 128-131 16214041-4 2006 In this study, we showed that lovastatin, fluvastatin, atorvastatin, simvastatin, mevastatin and pravastatin are able to upregulate the mRNA expression of HO-1 gene. Lovastatin 30-40 heme oxygenase 1 Mus musculus 155-159 16454747-6 2006 We found that lovastatin induced apoptosis in myeloma and lymphoma cells by inhibition of geranylgeranylation and subsequent down regulation of Mcl-1, probably the most important anti-apoptotic protein in myeloma. Lovastatin 14-24 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 144-149 16367743-0 2006 Cleavage of focal adhesion proteins and PKCdelta during lovastatin-induced apoptosis in spontaneously immortalized rat brain neuroblasts. Lovastatin 56-66 protein kinase C, delta Rattus norvegicus 40-48 16367743-3 2006 We found that lovastatin exposure induced focal adhesion kinase, Crk-associated substrate (p130(Cas)), PKCdelta cleavage and caspase-3 activation in a concentration-dependent manner. Lovastatin 14-24 BCAR1 scaffold protein, Cas family member Rattus norvegicus 65-101 16367743-3 2006 We found that lovastatin exposure induced focal adhesion kinase, Crk-associated substrate (p130(Cas)), PKCdelta cleavage and caspase-3 activation in a concentration-dependent manner. Lovastatin 14-24 protein kinase C, delta Rattus norvegicus 103-111 16367743-3 2006 We found that lovastatin exposure induced focal adhesion kinase, Crk-associated substrate (p130(Cas)), PKCdelta cleavage and caspase-3 activation in a concentration-dependent manner. Lovastatin 14-24 caspase 3 Rattus norvegicus 125-134 16367743-6 2006 In contrast, the lovastatin-induced cleavage of PKCdelta was only blocked by z-VAD-fmk suggesting that PKCdelta cleavage is caspase-dependent but caspase-3-independent. Lovastatin 17-27 protein kinase C, delta Rattus norvegicus 48-56 16367743-6 2006 In contrast, the lovastatin-induced cleavage of PKCdelta was only blocked by z-VAD-fmk suggesting that PKCdelta cleavage is caspase-dependent but caspase-3-independent. Lovastatin 17-27 protein kinase C, delta Rattus norvegicus 103-111 16367743-6 2006 In contrast, the lovastatin-induced cleavage of PKCdelta was only blocked by z-VAD-fmk suggesting that PKCdelta cleavage is caspase-dependent but caspase-3-independent. Lovastatin 17-27 caspase 3 Rattus norvegicus 146-155 16367743-9 2006 These findings may suggest that the caspase-dependent component leading to the neuroblast cell death is likely to involve the cleavage of focal adhesion proteins and PKCdelta, which may be partially responsible for some biochemical features of neuroblast apoptosis induced by lovastatin. Lovastatin 276-286 protein kinase C, delta Rattus norvegicus 166-174 16203826-5 2006 Using two different Epo-responsive cell lines, we found that depletion of mevalonate and its isoprenoid derivatives using the 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor lovastatin impairs Epo signaling as assessed by phosphorylation of cellular substrates and inhibition of apoptosis. Lovastatin 183-193 erythropoietin Mus musculus 20-23 16203826-5 2006 Using two different Epo-responsive cell lines, we found that depletion of mevalonate and its isoprenoid derivatives using the 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor lovastatin impairs Epo signaling as assessed by phosphorylation of cellular substrates and inhibition of apoptosis. Lovastatin 183-193 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 126-172 16316623-6 2006 Thus, we postulate that modulation of RhoA may be critical in lovastatin-induced senescence in PC-3 cells. Lovastatin 62-72 ras homolog family member A Homo sapiens 38-42 16400415-0 2005 Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results. Lovastatin 0-10 carbonic anhydrase 1 Rattus norvegicus 54-57 16400415-9 2005 The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 +/- 17.88) was statically significant increased when compared with animals that just presented SE. Lovastatin 86-96 carbonic anhydrase 1 Rattus norvegicus 36-39 16273297-0 2005 Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells. Lovastatin 0-10 TNF receptor superfamily member 1B Homo sapiens 22-25 16273297-0 2005 Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells. Lovastatin 0-10 TNF receptor superfamily member 1B Homo sapiens 40-45 16273297-3 2005 We investigated the effect of lovastatin on the expression level of TNF receptors (TNFR) in primary human endothelial cells (HUVEC). Lovastatin 30-40 TNF receptor superfamily member 1A Homo sapiens 68-81 16273297-3 2005 We investigated the effect of lovastatin on the expression level of TNF receptors (TNFR) in primary human endothelial cells (HUVEC). Lovastatin 30-40 TNF receptor superfamily member 1A Homo sapiens 83-87 16273297-4 2005 ELISA, FACS and immunocytochemical analyses show that lovastatin selectively increases the cell surface expression of TNFR2 without affecting the expression level of TNFR1. Lovastatin 54-64 TNF receptor superfamily member 1B Homo sapiens 118-123 16273297-5 2005 This effect of lovastatin is independent from inhibition of cell-cycle progression since cells both in G1- and G2-phase showed elevated levels of TNFR2 after lovastatin treatment. Lovastatin 15-25 TNF receptor superfamily member 1B Homo sapiens 146-151 16273297-5 2005 This effect of lovastatin is independent from inhibition of cell-cycle progression since cells both in G1- and G2-phase showed elevated levels of TNFR2 after lovastatin treatment. Lovastatin 158-168 TNF receptor superfamily member 1B Homo sapiens 146-151 16273297-6 2005 To analyze the physiological relevance of lovastatin-mediated upregulation of TNFR2, we investigated the expression of the cell adhesion molecule E-selectin, which is inducible by TNFalpha. Lovastatin 42-52 TNF receptor superfamily member 1B Homo sapiens 78-83 16273297-7 2005 While lovastatin on its own did not change the number of HUVEC expressing E-selectin protein, it promoted the TNFalpha-stimulated increase in the percentage of E-selectin expressing endothelial cells in a dose-dependent manner. Lovastatin 6-16 tumor necrosis factor Homo sapiens 110-118 16273297-7 2005 While lovastatin on its own did not change the number of HUVEC expressing E-selectin protein, it promoted the TNFalpha-stimulated increase in the percentage of E-selectin expressing endothelial cells in a dose-dependent manner. Lovastatin 6-16 selectin E Homo sapiens 160-170 16273297-8 2005 This indicates that lovastatin sensitizes HUVEC towards TNFalpha-induced signaling by upregulation of TNFR2 expression. Lovastatin 20-30 tumor necrosis factor Homo sapiens 56-64 16273297-8 2005 This indicates that lovastatin sensitizes HUVEC towards TNFalpha-induced signaling by upregulation of TNFR2 expression. Lovastatin 20-30 TNF receptor superfamily member 1B Homo sapiens 102-107 16271875-0 2005 The HMG-CoA reductase inhibitor lovastatin reverses the learning and attention deficits in a mouse model of neurofibromatosis type 1. Lovastatin 32-42 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 4-21 16192990-6 2005 The Abeta blockade of the nitrergic vasodilation and inward currents, but not that of calcium influx, was prevented by acute pretreatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors mevastatin and lovastatin. Lovastatin 227-237 succinate-CoA ligase ADP-forming subunit beta Homo sapiens 4-9 16192990-6 2005 The Abeta blockade of the nitrergic vasodilation and inward currents, but not that of calcium influx, was prevented by acute pretreatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors mevastatin and lovastatin. Lovastatin 227-237 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 143-200 16271875-0 2005 The HMG-CoA reductase inhibitor lovastatin reverses the learning and attention deficits in a mouse model of neurofibromatosis type 1. Lovastatin 32-42 neurofibromin 1 Mus musculus 108-132 16271875-4 2005 Here, we identify lovastatin as a potent inhibitor of p21Ras/Mitogen Activated Protein Kinase (MAPK) activity in the brain. Lovastatin 18-28 Harvey rat sarcoma virus oncogene Mus musculus 54-93 16271875-5 2005 Lovastatin is a specific inhibitor of three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used commonly for the treatment of hypercholesterolemia. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 81-99 16271875-6 2005 We report that lovastatin decreased the enhanced brain p21Ras-MAPK activity of the nf1+/- mice, rescued their LTP deficits, and reversed their spatial learning and attention impairments. Lovastatin 15-25 Harvey rat sarcoma virus oncogene Mus musculus 55-61 16271875-6 2005 We report that lovastatin decreased the enhanced brain p21Ras-MAPK activity of the nf1+/- mice, rescued their LTP deficits, and reversed their spatial learning and attention impairments. Lovastatin 15-25 neurofibromin 1 Mus musculus 83-86 16271875-7 2005 Therefore, these results demonstrate that lovastatin may prove useful in the treatment of Neurofibromatosis Type 1. Lovastatin 42-52 neurofibromin 1 Mus musculus 90-114 16125679-7 2005 Inhibition of isoprenylation in cells in culture with lovastatin resulted in decreased binding of CaM to Ral. Lovastatin 54-64 calmodulin 1 Homo sapiens 98-101 16125679-7 2005 Inhibition of isoprenylation in cells in culture with lovastatin resulted in decreased binding of CaM to Ral. Lovastatin 54-64 RAS like proto-oncogene A Homo sapiens 105-108 16234849-0 2005 The association between RhoB and caspase-2: changes with lovastatin-induced apoptosis. Lovastatin 57-67 ras homolog family member B Mus musculus 24-28 16234849-0 2005 The association between RhoB and caspase-2: changes with lovastatin-induced apoptosis. Lovastatin 57-67 caspase 2 Mus musculus 33-42 16234849-3 2005 Although the RhoB-caspase-2 complex was constitutively present, the link between RhoB and caspase-2 may be operative in apoptosis because the HMG-CoA reductase inhibitor lovastatin increased the RhoB-caspase complex, especially in the nuclear fraction of the cell, with a peak occurrence 2 h after treatment. Lovastatin 170-180 ras homolog family member B Mus musculus 13-17 16234849-3 2005 Although the RhoB-caspase-2 complex was constitutively present, the link between RhoB and caspase-2 may be operative in apoptosis because the HMG-CoA reductase inhibitor lovastatin increased the RhoB-caspase complex, especially in the nuclear fraction of the cell, with a peak occurrence 2 h after treatment. Lovastatin 170-180 caspase 2 Mus musculus 18-27 16234849-3 2005 Although the RhoB-caspase-2 complex was constitutively present, the link between RhoB and caspase-2 may be operative in apoptosis because the HMG-CoA reductase inhibitor lovastatin increased the RhoB-caspase complex, especially in the nuclear fraction of the cell, with a peak occurrence 2 h after treatment. Lovastatin 170-180 ras homolog family member B Mus musculus 81-85 16234849-3 2005 Although the RhoB-caspase-2 complex was constitutively present, the link between RhoB and caspase-2 may be operative in apoptosis because the HMG-CoA reductase inhibitor lovastatin increased the RhoB-caspase complex, especially in the nuclear fraction of the cell, with a peak occurrence 2 h after treatment. Lovastatin 170-180 caspase 2 Mus musculus 90-99 16234849-3 2005 Although the RhoB-caspase-2 complex was constitutively present, the link between RhoB and caspase-2 may be operative in apoptosis because the HMG-CoA reductase inhibitor lovastatin increased the RhoB-caspase complex, especially in the nuclear fraction of the cell, with a peak occurrence 2 h after treatment. Lovastatin 170-180 ras homolog family member B Mus musculus 81-85 16234849-5 2005 Lovastatin produced apoptosis that was accompanied by an activation of caspase-2, as demonstrated by its immunohistochemistry and by the fact that the caspase-2 inhibitor zVDVAD reduced lovastatin-induced apoptosis. Lovastatin 0-10 caspase 2 Mus musculus 71-80 16234849-5 2005 Lovastatin produced apoptosis that was accompanied by an activation of caspase-2, as demonstrated by its immunohistochemistry and by the fact that the caspase-2 inhibitor zVDVAD reduced lovastatin-induced apoptosis. Lovastatin 0-10 caspase 2 Mus musculus 151-160 16234849-5 2005 Lovastatin produced apoptosis that was accompanied by an activation of caspase-2, as demonstrated by its immunohistochemistry and by the fact that the caspase-2 inhibitor zVDVAD reduced lovastatin-induced apoptosis. Lovastatin 186-196 caspase 2 Mus musculus 71-80 16234849-5 2005 Lovastatin produced apoptosis that was accompanied by an activation of caspase-2, as demonstrated by its immunohistochemistry and by the fact that the caspase-2 inhibitor zVDVAD reduced lovastatin-induced apoptosis. Lovastatin 186-196 caspase 2 Mus musculus 151-160 16234849-8 2005 Caspase-2 inhibition with zVDVAD reduced lovastatin-induced alteration in cytoskeletal F-actin. Lovastatin 41-51 caspase 2 Mus musculus 0-9 15980231-6 2005 RESULTS: PTM and PCB cells treated with lovastatin or compactin exhibited dramatic changes in cell shape and cytoskeletal organization within 24 hours, consisting of cell rounding, actin depolymerization, and decreased focal adhesions. Lovastatin 40-50 pyruvate carboxylase Homo sapiens 17-20 16159044-9 2005 The mean LDL-C was lowered from 110.9 to 108.4 mg/dL (P < .001) following the conversion to lovastatin. Lovastatin 95-105 component of oligomeric golgi complex 2 Homo sapiens 9-14 16141529-0 2005 Lovastatin reduces nuclear factor kappaB activation induced by C-reactive protein in human vascular endothelial cells. Lovastatin 0-10 C-reactive protein Homo sapiens 63-81 16141529-6 2005 By using an electrophoretic mobility shift assays (EMSA), we found that CRP (50 microg/ml) increased activation of NF-kappaB and degradation of inhibitory kappa B (IkappaB) in HUVECs, reaching a maximal effect after the incubation with CRP for 1 h. Lovastatin (10(-5) mol/l) diminished NF-kappaB activation induced by CRP. Lovastatin 249-259 C-reactive protein Homo sapiens 72-75 16141529-7 2005 Furthermore, lovastatin may block NF-kappaB activation by causing a stabilization of the IkappaB-alpha in cellular cytoplasm with western blotting analysis. Lovastatin 13-23 NFKB inhibitor alpha Homo sapiens 89-102 16156861-5 2005 However, combinations of FTI and GGTI or lovastatin were found to synergistically inhibit MM cell proliferation, migration, K- and N-RAS processing, RAS-to-mitogen-activated protein kinase signalling and to induce apoptosis. Lovastatin 41-51 KRAS proto-oncogene, GTPase Homo sapiens 124-136 16172195-0 2005 Lovastatin suppresses invasiveness of anaplastic thyroid cancer cells by inhibiting Rho geranylgeranylation and RhoA/ROCK signaling. Lovastatin 0-10 ras homolog family member A Homo sapiens 112-116 16172195-2 2005 Previously, we have reported that lovastatin treatment induced the occurrence of apoptosis and differentiation in ARO anaplastic thyroid cancer cells. Lovastatin 34-44 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 114-117 16172195-3 2005 Here, we demonstrated that lovastatin inhibited the ARO cell invasiveness and delineated the underlying molecular mechanism. Lovastatin 27-37 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 52-55 16172195-5 2005 Lovastatin also reduced EGF-induced increases in the levels of phosphorylated p125(FAK) and paxillin. Lovastatin 0-10 SEC23 interacting protein Homo sapiens 78-82 16172195-5 2005 Lovastatin also reduced EGF-induced increases in the levels of phosphorylated p125(FAK) and paxillin. Lovastatin 0-10 protein tyrosine kinase 2 Homo sapiens 83-86 16172195-8 2005 Western blot analysis showed that lovastatin inhibited membrane translocation of Rho (e.g. RhoA and Rac1) through decreasing post-translational geranylgeranyl modification of Rho. Lovastatin 34-44 ras homolog family member A Homo sapiens 91-95 16172195-8 2005 Western blot analysis showed that lovastatin inhibited membrane translocation of Rho (e.g. RhoA and Rac1) through decreasing post-translational geranylgeranyl modification of Rho. Lovastatin 34-44 Rac family small GTPase 1 Homo sapiens 100-104 16172195-10 2005 Taken together, our results suggested that lovastatin suppressed EGF-induced ARO cell invasiveness through the reduction of Rho geranylgeranylation, which in turn suppressed the membrane translocation, and subsequent suppression of Rho/ROCK and FAK/paxillin signaling. Lovastatin 43-53 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 77-80 16172195-10 2005 Taken together, our results suggested that lovastatin suppressed EGF-induced ARO cell invasiveness through the reduction of Rho geranylgeranylation, which in turn suppressed the membrane translocation, and subsequent suppression of Rho/ROCK and FAK/paxillin signaling. Lovastatin 43-53 protein tyrosine kinase 2 Homo sapiens 245-248 16126908-2 2005 Here, we have demonstrated the potential of lovastatin, a HMG-CoA reductase inhibitor, for the restoration of impaired remyelination mediated through enhanced survival and differentiation of OPs in the spinal cord of treated EAE animals. Lovastatin 44-54 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 58-75 15955822-9 2005 When LFA-1 was shifted into the low affinity state by lovastatin, both monomeric and dimeric ICAM-1 dissociated in less than 1 s, and the dissociation rates were within 50% of each other. Lovastatin 54-64 integrin subunit alpha L Homo sapiens 5-10 15955822-9 2005 When LFA-1 was shifted into the low affinity state by lovastatin, both monomeric and dimeric ICAM-1 dissociated in less than 1 s, and the dissociation rates were within 50% of each other. Lovastatin 54-64 intercellular adhesion molecule 1 Homo sapiens 93-99 15998357-3 2005 Simvastatin, lovastatin, atorvastatin and fluvastatin were the most potent inhibitors of CYP2C8 activity with K(i) (IC(50)) values of 7.1 (9.6) muM, 8.4 (15) microM, 16 (38) microM and 19 (37) microM, respectively. Lovastatin 13-23 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 89-95 16079481-0 2005 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, lovastatin (statin) ameliorates CCK-induced acute pancreatitis in rats. Lovastatin 73-83 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 4-61 16079481-0 2005 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, lovastatin (statin) ameliorates CCK-induced acute pancreatitis in rats. Lovastatin 73-83 cholecystokinin Rattus norvegicus 105-108 16079481-2 2005 The aim of this study was to investigate the effect of Lovastatin (statin) on the cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. Lovastatin 55-65 cholecystokinin Rattus norvegicus 82-109 16079481-2 2005 The aim of this study was to investigate the effect of Lovastatin (statin) on the cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. Lovastatin 55-65 cholecystokinin Rattus norvegicus 111-114 19956523-5 2005 RESULTS: RhoA significantly enhanced the resistance to lovastatin, 5-FU, taxol and vincristine, but did not affect the sensitivity to cisplatin or etoposide in SNU638. Lovastatin 55-65 ras homolog family member A Homo sapiens 9-13 16101671-6 2005 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor that abrogates the prenylation of Ggamma, shifted the subcellular localization of enhanced green fluorescence protein-fused Ggamma2 and Gbeta2 from the cytoplasm/plasma membrane to the nucleus and further suppressed glucocorticoid receptor-induced transcriptional activity. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-71 16101671-6 2005 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor that abrogates the prenylation of Ggamma, shifted the subcellular localization of enhanced green fluorescence protein-fused Ggamma2 and Gbeta2 from the cytoplasm/plasma membrane to the nucleus and further suppressed glucocorticoid receptor-induced transcriptional activity. Lovastatin 0-10 nuclear receptor subfamily 3 group C member 1 Homo sapiens 298-321 15951198-0 2005 Lovastatin-induced PC-12 cell differentiation is associated with RhoA/RhoA kinase pathway inactivation. Lovastatin 0-10 ras homolog family member A Rattus norvegicus 65-69 15951198-0 2005 Lovastatin-induced PC-12 cell differentiation is associated with RhoA/RhoA kinase pathway inactivation. Lovastatin 0-10 ras homolog family member A Rattus norvegicus 70-74 15951198-5 2005 Furthermore, we show that lovastatin inhibits both RhoA activation and Cofilin phosphorylation, while geranylgeraniol reverses these effects. Lovastatin 26-36 ras homolog family member A Rattus norvegicus 51-55 17319473-15 2006 A fixed dose combination of lovastatin and niacin(ER) significantly improved cholesterol lipoprotein lipids as well as lp(a) and apoA1/apoB levels in Asian Indian dyslipidemic patients. Lovastatin 28-38 apolipoprotein A1 Homo sapiens 129-134 17319473-15 2006 A fixed dose combination of lovastatin and niacin(ER) significantly improved cholesterol lipoprotein lipids as well as lp(a) and apoA1/apoB levels in Asian Indian dyslipidemic patients. Lovastatin 28-38 apolipoprotein B Homo sapiens 135-139 16051523-2 2005 Lovastatin and simvastatin increased the production of IL-1beta in a dose dependent manner and reduced secretion of IL-1ra at high concentration. Lovastatin 0-10 interleukin 1 beta Homo sapiens 55-63 16051523-2 2005 Lovastatin and simvastatin increased the production of IL-1beta in a dose dependent manner and reduced secretion of IL-1ra at high concentration. Lovastatin 0-10 interleukin 1 receptor antagonist Homo sapiens 116-122 16245407-8 2005 Reverse transcription-polymerase chain reaction and Western blot analysis showed that Cx40 and Cx43 mRNA and protein expression was elevated after injury (P < .001 for both proteins and both assays), and these elevations were suppressed by lovastatin and fluvastatin to a similar degree (P < .05 for both drugs and both assays). Lovastatin 243-253 gap junction alpha-1 protein Oryctolagus cuniculus 95-99 16245407-12 2005 Lovastatin and fluvastatin suppress upregulated Cx40 and Cx43 expression and reduce neointimal proliferation, suggesting that Cx40 and Cx43 may play a role in statin-induced antiproliferative effect. Lovastatin 0-10 gap junction alpha-1 protein Oryctolagus cuniculus 57-61 16245407-12 2005 Lovastatin and fluvastatin suppress upregulated Cx40 and Cx43 expression and reduce neointimal proliferation, suggesting that Cx40 and Cx43 may play a role in statin-induced antiproliferative effect. Lovastatin 0-10 gap junction alpha-1 protein Oryctolagus cuniculus 135-139 16111478-5 2005 Lovastatin decreases protein kinase B (PKB)/Akt phosphorylation, and its downstream effectors, p70S6K and the eukaryotic initiation factor 4E (eIF4E) regulatory protein 1, 4E-BP1, in a concentration-dependent manner, and reduces p70S6K expression. Lovastatin 0-10 ribosomal protein S6 kinase B1 Rattus norvegicus 95-101 16111478-5 2005 Lovastatin decreases protein kinase B (PKB)/Akt phosphorylation, and its downstream effectors, p70S6K and the eukaryotic initiation factor 4E (eIF4E) regulatory protein 1, 4E-BP1, in a concentration-dependent manner, and reduces p70S6K expression. Lovastatin 0-10 eukaryotic translation initiation factor 4E Rattus norvegicus 110-141 16111478-5 2005 Lovastatin decreases protein kinase B (PKB)/Akt phosphorylation, and its downstream effectors, p70S6K and the eukaryotic initiation factor 4E (eIF4E) regulatory protein 1, 4E-BP1, in a concentration-dependent manner, and reduces p70S6K expression. Lovastatin 0-10 eukaryotic translation initiation factor 4E Rattus norvegicus 143-148 16111478-5 2005 Lovastatin decreases protein kinase B (PKB)/Akt phosphorylation, and its downstream effectors, p70S6K and the eukaryotic initiation factor 4E (eIF4E) regulatory protein 1, 4E-BP1, in a concentration-dependent manner, and reduces p70S6K expression. Lovastatin 0-10 eukaryotic translation initiation factor 4E binding protein 1 Rattus norvegicus 172-178 16111478-5 2005 Lovastatin decreases protein kinase B (PKB)/Akt phosphorylation, and its downstream effectors, p70S6K and the eukaryotic initiation factor 4E (eIF4E) regulatory protein 1, 4E-BP1, in a concentration-dependent manner, and reduces p70S6K expression. Lovastatin 0-10 ribosomal protein S6 kinase B1 Rattus norvegicus 229-235 15980231-8 2005 Both lovastatin and compactin decreased MLC phosphorylation in PTM and PCB cells. Lovastatin 5-15 modulator of VRAC current 1 Homo sapiens 40-43 15980231-8 2005 Both lovastatin and compactin decreased MLC phosphorylation in PTM and PCB cells. Lovastatin 5-15 pyruvate carboxylase Homo sapiens 71-74 15980231-11 2005 CONCLUSIONS: This study demonstrates that the statin drugs lovastatin and compactin induce changes in cell shape and actin cytoskeletal organization and decrease MLC phosphorylation in PTM and PCB cells, all of which are events that are likely to lead to cellular and tissue relaxation. Lovastatin 59-69 modulator of VRAC current 1 Homo sapiens 162-165 15980231-11 2005 CONCLUSIONS: This study demonstrates that the statin drugs lovastatin and compactin induce changes in cell shape and actin cytoskeletal organization and decrease MLC phosphorylation in PTM and PCB cells, all of which are events that are likely to lead to cellular and tissue relaxation. Lovastatin 59-69 pyruvate carboxylase Homo sapiens 193-196 15585148-0 2004 [Effects of lovastatin on renal function and expression of phosphorylating-p38 mitogen-activated protein kinase in experimental diabetic nephropathy in rats]. Lovastatin 12-22 mitogen activated protein kinase 14 Rattus norvegicus 75-78 15788691-5 2005 EXPERIMENTAL DESIGN: In this study, we evaluated the effect of lovastatin on EGFR function and on gefitinib activity. Lovastatin 63-73 epidermal growth factor receptor Homo sapiens 77-81 15788691-8 2005 RESULTS: Lovastatin treatment inhibited EGF-induced EGFR autophosphorylation by 24 hours that was reversed by the coadministration of mevalonate. Lovastatin 9-19 epidermal growth factor receptor Homo sapiens 52-56 15788691-9 2005 Combining lovastatin and gefitinib treatments showed enhanced inhibition of AKT activation by EGF in SCC9 cells. Lovastatin 10-20 AKT serine/threonine kinase 1 Homo sapiens 76-79 15699169-2 2005 In an acute mouse model of autoimmune retinal disease, we demonstrate that treatment with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, lovastatin, suppresses clinical ocular pathology, retinal vascular leakage, and leukocytic infiltration into the retina. Lovastatin 153-163 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 94-141 15710425-4 2005 In lovastatin-treated resting human umbilical vein endothelial cells (HUVECs), increased levels of mRNA and protein of PECAM-1 as well as its bio-synthesis (all approximately 2-fold) were observed by real-time PCR, Western blotting and 35S-labeled methionine incorporation assay, respectively. Lovastatin 3-13 platelet and endothelial cell adhesion molecule 1 Homo sapiens 119-126 15710425-5 2005 Moreover, in lovastatin treated resting cells as well as TNF-alpha activated endothelial cells, unanimously decreased Triton X-100 insoluble and soluble PECAM-1 ratio was observed. Lovastatin 13-23 platelet and endothelial cell adhesion molecule 1 Homo sapiens 153-160 15710425-10 2005 We speculate that lovastatin regulates PECAM-1 expression in HUVECs through the mevalonate-GGPP pathway by inhibiting of Rho small GTPase. Lovastatin 18-28 platelet and endothelial cell adhesion molecule 1 Homo sapiens 39-46 15679472-3 2005 Some statins (atorvastatin, lovastatin and simvastatin) also requires metabolism by the cytochrome P450 3A4 system. Lovastatin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 15544924-3 2004 In cultured endothelial cells derived from human umbilical vein, simvastatin and lovastatin increased HO-1 mRNA levels in a concentration- and time-dependent fashion. Lovastatin 81-91 heme oxygenase 1 Homo sapiens 102-106 15342687-7 2004 ABCG5 and ABCG8 mRNA levels were decreased by stanol esters and cholestyramine/lovastatin. Lovastatin 79-89 ATP binding cassette subfamily G member 5 Homo sapiens 0-5 15342687-7 2004 ABCG5 and ABCG8 mRNA levels were decreased by stanol esters and cholestyramine/lovastatin. Lovastatin 79-89 ATP binding cassette subfamily G member 8 Homo sapiens 10-15 15605420-1 2005 The statins (including mevastatin and lovastatin) are a widely prescribed class of serum-cholesterol lowering drugs that function by inhibiting 3-hydroxymethylglutaryl coenzyme A (HMG CoA) reductase activity and cellular sterol synthesis. Lovastatin 38-48 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 144-198 15953363-0 2005 Inhibition of phosphoinositide 3 kinase-Akt (protein kinase B)-nuclear factor-kappa B pathway by lovastatin limits endothelial-monocyte cell interaction. Lovastatin 97-107 AKT serine/threonine kinase 1 Homo sapiens 40-43 15953363-0 2005 Inhibition of phosphoinositide 3 kinase-Akt (protein kinase B)-nuclear factor-kappa B pathway by lovastatin limits endothelial-monocyte cell interaction. Lovastatin 97-107 protein tyrosine kinase 2 beta Homo sapiens 45-61 15953363-4 2005 Here, using an in vitro system, we report that lovastatin inhibits endothelial-monocyte cell interaction by down-regulating the expression of vascular cell adhesion molecule-1 and E-selectin by inhibiting the phosphoinositide 3 kinase (PI3-kinase)/protein kinase B (Akt)/nuclear factor-kappa B (NF-kappaB) pathway in endothelial cells. Lovastatin 47-57 vascular cell adhesion molecule 1 Homo sapiens 142-175 15953363-4 2005 Here, using an in vitro system, we report that lovastatin inhibits endothelial-monocyte cell interaction by down-regulating the expression of vascular cell adhesion molecule-1 and E-selectin by inhibiting the phosphoinositide 3 kinase (PI3-kinase)/protein kinase B (Akt)/nuclear factor-kappa B (NF-kappaB) pathway in endothelial cells. Lovastatin 47-57 selectin E Homo sapiens 180-190 15953363-4 2005 Here, using an in vitro system, we report that lovastatin inhibits endothelial-monocyte cell interaction by down-regulating the expression of vascular cell adhesion molecule-1 and E-selectin by inhibiting the phosphoinositide 3 kinase (PI3-kinase)/protein kinase B (Akt)/nuclear factor-kappa B (NF-kappaB) pathway in endothelial cells. Lovastatin 47-57 protein tyrosine kinase 2 beta Homo sapiens 248-264 15953363-4 2005 Here, using an in vitro system, we report that lovastatin inhibits endothelial-monocyte cell interaction by down-regulating the expression of vascular cell adhesion molecule-1 and E-selectin by inhibiting the phosphoinositide 3 kinase (PI3-kinase)/protein kinase B (Akt)/nuclear factor-kappa B (NF-kappaB) pathway in endothelial cells. Lovastatin 47-57 AKT serine/threonine kinase 1 Homo sapiens 266-269 15953363-4 2005 Here, using an in vitro system, we report that lovastatin inhibits endothelial-monocyte cell interaction by down-regulating the expression of vascular cell adhesion molecule-1 and E-selectin by inhibiting the phosphoinositide 3 kinase (PI3-kinase)/protein kinase B (Akt)/nuclear factor-kappa B (NF-kappaB) pathway in endothelial cells. Lovastatin 47-57 nuclear factor kappa B subunit 1 Homo sapiens 295-304 15953363-6 2005 Co-transfection of constitutively active forms of PI3-kinase and Akt reversed the lovastatin-mediated inhibition of TNFalpha-induced adhesion, as well as activation of NF-kappaB, indicating the involvement of the PI3-kinase/Akt pathway in the interaction of adhesion molecules and the process of adhesion. Lovastatin 82-92 AKT serine/threonine kinase 1 Homo sapiens 65-68 15953363-6 2005 Co-transfection of constitutively active forms of PI3-kinase and Akt reversed the lovastatin-mediated inhibition of TNFalpha-induced adhesion, as well as activation of NF-kappaB, indicating the involvement of the PI3-kinase/Akt pathway in the interaction of adhesion molecules and the process of adhesion. Lovastatin 82-92 tumor necrosis factor Homo sapiens 116-124 15953363-6 2005 Co-transfection of constitutively active forms of PI3-kinase and Akt reversed the lovastatin-mediated inhibition of TNFalpha-induced adhesion, as well as activation of NF-kappaB, indicating the involvement of the PI3-kinase/Akt pathway in the interaction of adhesion molecules and the process of adhesion. Lovastatin 82-92 nuclear factor kappa B subunit 1 Homo sapiens 168-177 15953363-6 2005 Co-transfection of constitutively active forms of PI3-kinase and Akt reversed the lovastatin-mediated inhibition of TNFalpha-induced adhesion, as well as activation of NF-kappaB, indicating the involvement of the PI3-kinase/Akt pathway in the interaction of adhesion molecules and the process of adhesion. Lovastatin 82-92 AKT serine/threonine kinase 1 Homo sapiens 224-227 15772423-7 2005 Organophosphates are hydrolyzed almost exclusively by PON1, whereas bulky drug substrates such as lovastatin and spironolactone are hydrolyzed only by PON3. Lovastatin 98-108 paraoxonase 3 Homo sapiens 151-155 15755505-1 2005 Lovastatin, a competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase (HMGR), is used therapeutically to lower plasma cholesterol levels and has garnered attention for its cytotoxic effects in leukemia cells. Lovastatin 0-10 high mobility group AT-hook 1 Homo sapiens 83-87 15755505-5 2005 Our results show that in vivo lovastatin, at up to 200 mg/dose, induces an increased activity of leukemia cell HMGR and alters leukemia cell proliferation without discernibly altering Ras processing. Lovastatin 30-40 high mobility group AT-hook 1 Homo sapiens 111-115 15846140-7 2005 For human melanoma cells, lovastatin precipitated cell rounding, increased the percentage of apoptotic cells detected by ethidium bromide and acridine orange staining and by the Annexin V apoptosis detection kit, and resulted in a 50-fold increase in active caspase 3, corroborating that lovastatin induced apoptosis. Lovastatin 26-36 annexin A5 Homo sapiens 178-187 15846140-7 2005 For human melanoma cells, lovastatin precipitated cell rounding, increased the percentage of apoptotic cells detected by ethidium bromide and acridine orange staining and by the Annexin V apoptosis detection kit, and resulted in a 50-fold increase in active caspase 3, corroborating that lovastatin induced apoptosis. Lovastatin 26-36 caspase 3 Homo sapiens 258-267 15694950-0 2005 Lovastatin compromises C-reactive protein induced endothelial dysfunction including altered expression of cell adhesion molecules and increased monocyte recruitment. Lovastatin 0-10 C-reactive protein Homo sapiens 23-41 15862029-12 2005 CONCLUSION: Inhibition of glomerular cAMP-responsive element binding protein 1 may be responsible for the Lovastatin protective function that allevate the renal proliferation and hypertrophy in diabetic rats. Lovastatin 106-116 cAMP responsive element binding protein 1 Rattus norvegicus 37-78 15769392-6 2005 These effects of simvastatin and lovastatin on eNOS mRNA expression correlated with changes in nitric oxide production. Lovastatin 33-43 nitric oxide synthase 3 Homo sapiens 47-51 15530865-2 2004 In this study, we found in murine RAW264.7 macrophages, statins within 1-30 microM stimulated COX-2 gene transcription and PGE(2) formation, displaying potencies as lovastatin > fluvastatin > atorvastatin >> pravastatin. Lovastatin 165-175 cytochrome c oxidase II, mitochondrial Mus musculus 94-99 15585148-1 2004 OBJECTIVE: To investigate the effects of lovastatin on renal function, activity and expression of the p38 mitogen-activated protein kinase (MAPK) and cAMP responsive element-binding protein (CREB) in experimental diabetic nephropathy in rats. Lovastatin 41-51 mitogen activated protein kinase 14 Rattus norvegicus 102-138 15585148-1 2004 OBJECTIVE: To investigate the effects of lovastatin on renal function, activity and expression of the p38 mitogen-activated protein kinase (MAPK) and cAMP responsive element-binding protein (CREB) in experimental diabetic nephropathy in rats. Lovastatin 41-51 cAMP responsive element binding protein 1 Rattus norvegicus 150-189 15585148-1 2004 OBJECTIVE: To investigate the effects of lovastatin on renal function, activity and expression of the p38 mitogen-activated protein kinase (MAPK) and cAMP responsive element-binding protein (CREB) in experimental diabetic nephropathy in rats. Lovastatin 41-51 cAMP responsive element binding protein 1 Rattus norvegicus 191-195 15585148-8 2004 After lovastatin treatment, expression of P-p38 MAPK, P-CREB and TGF-beta(1), FN, LN were markedly decreased compared with diabetic group(all P<0.01). Lovastatin 6-16 mitogen activated protein kinase 14 Rattus norvegicus 44-47 15585148-8 2004 After lovastatin treatment, expression of P-p38 MAPK, P-CREB and TGF-beta(1), FN, LN were markedly decreased compared with diabetic group(all P<0.01). Lovastatin 6-16 cAMP responsive element binding protein 1 Rattus norvegicus 56-60 15585148-8 2004 After lovastatin treatment, expression of P-p38 MAPK, P-CREB and TGF-beta(1), FN, LN were markedly decreased compared with diabetic group(all P<0.01). Lovastatin 6-16 transforming growth factor, beta 1 Rattus norvegicus 65-76 15585148-9 2004 CONCLUSION: Inhibition of glomerular p38 MAPK signal transduction pathway may be responsible for the decrement of extracellular matrix accumulation and renal protective effects of lovastatin in uninephrectomized rats. Lovastatin 180-190 mitogen activated protein kinase 14 Rattus norvegicus 37-40 15304496-2 2004 LFA-1 is inhibited by the cholesterol-lowering drug lovastatin, which binds to an allosteric site of the alphaL I domain termed the lovastatin site (L-site). Lovastatin 52-62 integrin subunit alpha L Homo sapiens 0-5 15304496-2 2004 LFA-1 is inhibited by the cholesterol-lowering drug lovastatin, which binds to an allosteric site of the alphaL I domain termed the lovastatin site (L-site). Lovastatin 132-142 integrin subunit alpha L Homo sapiens 0-5 15304496-3 2004 Here we report for the first time the x-ray structures of the LFA-1 I domain complexed with derivatives of lovastatin optimized for LFA-1 inhibition. Lovastatin 107-117 integrin subunit alpha L Homo sapiens 62-67 15485695-0 2004 Synergistic upregulation of low-density lipoprotein receptor activity by tamoxifen and lovastatin. Lovastatin 87-97 low density lipoprotein receptor Homo sapiens 28-60 15345508-9 2004 In addition, the effect of lovastatin on phagocytosis is a function of cell activation because treatment of cells with tumor necrosis factor-alpha or lipopolysaccharide prevented inhibition of phagocytosis by lovastatin. Lovastatin 27-37 tumor necrosis factor Homo sapiens 119-146 15345508-9 2004 In addition, the effect of lovastatin on phagocytosis is a function of cell activation because treatment of cells with tumor necrosis factor-alpha or lipopolysaccharide prevented inhibition of phagocytosis by lovastatin. Lovastatin 209-219 tumor necrosis factor Homo sapiens 119-146 15485695-6 2004 When studied in combination, especially at relatively high LDL concentrations in the medium, tamoxifen and lovastatin stimulated LDL receptor activity synergistically, which is attributed to the different mechanism of action these drugs exhibit. Lovastatin 107-117 low density lipoprotein receptor Homo sapiens 129-141 15304496-3 2004 Here we report for the first time the x-ray structures of the LFA-1 I domain complexed with derivatives of lovastatin optimized for LFA-1 inhibition. Lovastatin 107-117 integrin subunit alpha L Homo sapiens 132-137 15304496-7 2004 Moreover, we demonstrate that the novel lovastatin-derived LFA-1 inhibitor LFA878 exhibits potent anti-inflammatory effects in carrageenan-induced rat paw edema. Lovastatin 40-50 integrin subunit alpha L Rattus norvegicus 59-64 15380892-8 2004 CONCLUSION: It would appear that both naringin and lovastatin contributed to hypocholesterolemic action via down-regulated ACAT activity and higher excretion of fecal sterols in response to high-cholesterol feeding. Lovastatin 51-61 sterol O-acyltransferase 1 Oryctolagus cuniculus 123-127 15378516-0 2004 Lovastatin modulation of microglial activation via suppression of functional CD40 expression. Lovastatin 0-10 CD40 molecule Homo sapiens 77-81 15378516-3 2004 Interestingly, lovastatin (one of the most commonly used anticholesterol drugs) treatment of vascular-derived cells has been reported to antagonize activation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, and it is well known that the JAK/STAT pathway plays a central role in interferon-gamma (IFN-gamma)-induced microglial CD40 expression. Lovastatin 15-25 interferon gamma Homo sapiens 331-358 15378516-3 2004 Interestingly, lovastatin (one of the most commonly used anticholesterol drugs) treatment of vascular-derived cells has been reported to antagonize activation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, and it is well known that the JAK/STAT pathway plays a central role in interferon-gamma (IFN-gamma)-induced microglial CD40 expression. Lovastatin 15-25 CD40 molecule Homo sapiens 379-383 15378516-6 2004 In this study, we examined the putative role of lovastatin in modulation of CD40 expression and its signaling in cultured microglia. Lovastatin 48-58 CD40 molecule Homo sapiens 76-80 15378516-7 2004 RT-PCR, Western immunoblotting, and flow cytometry data show that lovastatin suppresses IFN-gamma-induced CD40 expression. Lovastatin 66-76 interferon gamma Homo sapiens 88-97 15378516-7 2004 RT-PCR, Western immunoblotting, and flow cytometry data show that lovastatin suppresses IFN-gamma-induced CD40 expression. Lovastatin 66-76 CD40 molecule Homo sapiens 106-110 15378516-8 2004 Additionally, lovastatin markedly inhibits IFN-gamma-induced phosphorylation of JAK/STAT1. Lovastatin 14-24 interferon gamma Homo sapiens 43-52 15378516-8 2004 Additionally, lovastatin markedly inhibits IFN-gamma-induced phosphorylation of JAK/STAT1. Lovastatin 14-24 signal transducer and activator of transcription 1 Homo sapiens 84-89 15378516-9 2004 Furthermore, lovastatin is able to suppress microglial tumor necrosis factor-alpha, interleukin (IL)-beta1 and IL-6 production promoted either by IFN-gamma or by Abeta peptide challenge in the presence of CD40 cross-linking. Lovastatin 13-23 tumor necrosis factor Homo sapiens 55-82 15378516-9 2004 Furthermore, lovastatin is able to suppress microglial tumor necrosis factor-alpha, interleukin (IL)-beta1 and IL-6 production promoted either by IFN-gamma or by Abeta peptide challenge in the presence of CD40 cross-linking. Lovastatin 13-23 interleukin 6 Homo sapiens 111-115 15378516-9 2004 Furthermore, lovastatin is able to suppress microglial tumor necrosis factor-alpha, interleukin (IL)-beta1 and IL-6 production promoted either by IFN-gamma or by Abeta peptide challenge in the presence of CD40 cross-linking. Lovastatin 13-23 interferon gamma Homo sapiens 146-155 15378516-9 2004 Furthermore, lovastatin is able to suppress microglial tumor necrosis factor-alpha, interleukin (IL)-beta1 and IL-6 production promoted either by IFN-gamma or by Abeta peptide challenge in the presence of CD40 cross-linking. Lovastatin 13-23 CD40 molecule Homo sapiens 205-209 15378516-11 2004 Data reveal that lovastatin markedly attenuates CD40-mediated inhibition of microglial phagocytosis of Abeta. Lovastatin 17-27 CD40 molecule Homo sapiens 48-52 15180944-0 2004 Lovastatin inhibits tumor growth and lung metastasis in mouse mammary carcinoma model: a p53-independent mitochondrial-mediated apoptotic mechanism. Lovastatin 0-10 transformation related protein 53, pseudogene Mus musculus 89-92 15180944-8 2004 Consistent with initiation of apoptosis, cellular caspase-8, caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. Lovastatin 113-123 caspase 8 Mus musculus 50-59 15180944-8 2004 Consistent with initiation of apoptosis, cellular caspase-8, caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. Lovastatin 113-123 caspase 9 Mus musculus 61-70 15180944-8 2004 Consistent with initiation of apoptosis, cellular caspase-8, caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. Lovastatin 113-123 caspase 3 Mus musculus 75-84 15180944-9 2004 The mitochondrial membrane potential was also decreased, with subsequent release of cytochrome c. However, lovastatin-induced cell death was significantly reduced by the broad spectrum caspase inhibitor z-VAD-fmk, as well as the caspase-9 inhibitor z-LEHD-fmk and the caspase-3 inhibitor z-DEVD-fmk, but not by the specific caspase-8 inhibitor z-IETD-fmk. Lovastatin 107-117 caspase 9 Mus musculus 229-238 15180944-9 2004 The mitochondrial membrane potential was also decreased, with subsequent release of cytochrome c. However, lovastatin-induced cell death was significantly reduced by the broad spectrum caspase inhibitor z-VAD-fmk, as well as the caspase-9 inhibitor z-LEHD-fmk and the caspase-3 inhibitor z-DEVD-fmk, but not by the specific caspase-8 inhibitor z-IETD-fmk. Lovastatin 107-117 caspase 3 Mus musculus 268-277 15180944-9 2004 The mitochondrial membrane potential was also decreased, with subsequent release of cytochrome c. However, lovastatin-induced cell death was significantly reduced by the broad spectrum caspase inhibitor z-VAD-fmk, as well as the caspase-9 inhibitor z-LEHD-fmk and the caspase-3 inhibitor z-DEVD-fmk, but not by the specific caspase-8 inhibitor z-IETD-fmk. Lovastatin 107-117 caspase 8 Mus musculus 324-333 15180944-10 2004 Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release. Lovastatin 83-93 BCL2-associated X protein Mus musculus 56-59 15180944-10 2004 Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release. Lovastatin 83-93 BCL2-associated X protein Mus musculus 181-184 15180944-10 2004 Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release. Lovastatin 109-119 BCL2-associated X protein Mus musculus 56-59 15180944-10 2004 Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release. Lovastatin 109-119 BCL2-associated X protein Mus musculus 181-184 15180944-11 2004 These results suggest that lovastatin may be useful as an adjuvant therapy in breast cancers containing p53 mutations due to its ability to both suppress DNA synthesis and induce p53-independent mitochondria-mediated apoptosis. Lovastatin 27-37 transformation related protein 53, pseudogene Mus musculus 104-107 15180944-11 2004 These results suggest that lovastatin may be useful as an adjuvant therapy in breast cancers containing p53 mutations due to its ability to both suppress DNA synthesis and induce p53-independent mitochondria-mediated apoptosis. Lovastatin 27-37 transformation related protein 53, pseudogene Mus musculus 179-182 15309370-4 2004 As a result of modification of the AB-DHP composite, the electrochemical response of lovastatin at GCE was apparently enhanced; this was apparent as amplification of the oxidation current and the negative shift of the oxidation potential. Lovastatin 85-95 dihydropyrimidinase Homo sapiens 38-41 16295046-5 2004 LDL receptor activity, measured by the capacity of lovastatin to revert the inhibition of lymphocyte proliferation with increasing amounts of LDL in the medium, was greater in the rats fed with palmitic acid, and was similar to the other groups when small amounts of PUFA were added. Lovastatin 51-61 low density lipoprotein receptor Rattus norvegicus 0-12 15532546-7 2004 In contrast, only lovastatin significantly increased levels of IL-1beta and of TNFalpha in a dose-dependent manner. Lovastatin 18-28 interleukin 1 beta Homo sapiens 63-71 15532546-7 2004 In contrast, only lovastatin significantly increased levels of IL-1beta and of TNFalpha in a dose-dependent manner. Lovastatin 18-28 tumor necrosis factor Homo sapiens 79-87 15374955-0 2004 Blocking the Raf/MEK/ERK pathway sensitizes acute myelogenous leukemia cells to lovastatin-induced apoptosis. Lovastatin 80-90 zinc fingers and homeoboxes 2 Homo sapiens 13-16 15374955-0 2004 Blocking the Raf/MEK/ERK pathway sensitizes acute myelogenous leukemia cells to lovastatin-induced apoptosis. Lovastatin 80-90 mitogen-activated protein kinase kinase 7 Homo sapiens 17-20 15374955-0 2004 Blocking the Raf/MEK/ERK pathway sensitizes acute myelogenous leukemia cells to lovastatin-induced apoptosis. Lovastatin 80-90 mitogen-activated protein kinase 1 Homo sapiens 21-24 15374955-9 2004 By establishing and evaluating the inducible Raf-1:ER system in AML cells, we show that constitutive activation of the Raf/MAPK kinase (MEK)/ERK pathway significantly represses but does not completely block lovastatin-induced apoptosis. Lovastatin 207-217 mitogen-activated protein kinase kinase 7 Homo sapiens 136-139 15374955-11 2004 Indeed, down-regulation of the Raf/MEK/ERK pathway potentiates statin-induced apoptosis because exposure to the MEK1 inhibitor PD98059 sensitizes AML cells to low, physiologically achievable concentrations of lovastatin. Lovastatin 209-219 zinc fingers and homeoboxes 2 Homo sapiens 31-34 15374955-11 2004 Indeed, down-regulation of the Raf/MEK/ERK pathway potentiates statin-induced apoptosis because exposure to the MEK1 inhibitor PD98059 sensitizes AML cells to low, physiologically achievable concentrations of lovastatin. Lovastatin 209-219 mitogen-activated protein kinase kinase 7 Homo sapiens 35-38 15374955-11 2004 Indeed, down-regulation of the Raf/MEK/ERK pathway potentiates statin-induced apoptosis because exposure to the MEK1 inhibitor PD98059 sensitizes AML cells to low, physiologically achievable concentrations of lovastatin. Lovastatin 209-219 mitogen-activated protein kinase 1 Homo sapiens 39-42 15374955-11 2004 Indeed, down-regulation of the Raf/MEK/ERK pathway potentiates statin-induced apoptosis because exposure to the MEK1 inhibitor PD98059 sensitizes AML cells to low, physiologically achievable concentrations of lovastatin. Lovastatin 209-219 mitogen-activated protein kinase kinase 1 Homo sapiens 112-116 15374955-12 2004 Our study suggests that lovastatin, alone or in combination with a MEK1 inhibitor, may represent a new and immediately available therapeutic approach to combat tumors with activated ERK1/2, such as AML. Lovastatin 24-34 mitogen-activated protein kinase kinase 1 Homo sapiens 67-71 15374955-12 2004 Our study suggests that lovastatin, alone or in combination with a MEK1 inhibitor, may represent a new and immediately available therapeutic approach to combat tumors with activated ERK1/2, such as AML. Lovastatin 24-34 mitogen-activated protein kinase 3 Homo sapiens 182-188 15309370-4 2004 As a result of modification of the AB-DHP composite, the electrochemical response of lovastatin at GCE was apparently enhanced; this was apparent as amplification of the oxidation current and the negative shift of the oxidation potential. Lovastatin 85-95 aminomethyltransferase Homo sapiens 99-102 15309370-6 2004 The enhanced oxidation of lovastatin at AB-DHP/GCE was due to enlargement of the effective electrode area, catalysis of lovastatin oxidation by AB, and accumulation of lovastatin at the hydrophobic surface of the DHP layer, which would be enhanced by the coherence with Triton X-100. Lovastatin 26-36 dihydropyrimidinase Homo sapiens 43-46 15309370-6 2004 The enhanced oxidation of lovastatin at AB-DHP/GCE was due to enlargement of the effective electrode area, catalysis of lovastatin oxidation by AB, and accumulation of lovastatin at the hydrophobic surface of the DHP layer, which would be enhanced by the coherence with Triton X-100. Lovastatin 120-130 aminomethyltransferase Homo sapiens 26-50 15309370-6 2004 The enhanced oxidation of lovastatin at AB-DHP/GCE was due to enlargement of the effective electrode area, catalysis of lovastatin oxidation by AB, and accumulation of lovastatin at the hydrophobic surface of the DHP layer, which would be enhanced by the coherence with Triton X-100. Lovastatin 120-130 dihydropyrimidinase Homo sapiens 43-46 15540478-7 2004 AFCAPS/TexCAPS researchers found that lovastatin provded a 14.8% reduction in the median levels of CRP (p < 0.001). Lovastatin 38-48 C-reactive protein Homo sapiens 99-102 15309370-2 2004 It is based on the enhanced oxidation of lovastatin at a novel acetylene black-dihexadecyl hydrogen phosphate composite-modified glassy-carbon electrode (AB-DHP/GCE) in the presence of Triton X-100. Lovastatin 41-51 dihydropyrimidinase Homo sapiens 157-160 15309370-2 2004 It is based on the enhanced oxidation of lovastatin at a novel acetylene black-dihexadecyl hydrogen phosphate composite-modified glassy-carbon electrode (AB-DHP/GCE) in the presence of Triton X-100. Lovastatin 41-51 aminomethyltransferase Homo sapiens 161-164 15301716-0 2004 [Effects of lovastatin on cell cycle distribution in MCF-7 cells transfected with BRCA1]. Lovastatin 12-22 BRCA1 DNA repair associated Homo sapiens 82-87 15242975-9 2004 Mevinolin-inhibited chemotaxis was restored by farnesylpyrophosphate but not by geranylgeranylpyrophosphate; in the absence of mevinolin, inhibition of farnesyltransferase reduced ERK phosphorylation and blocked chemotaxis, indicating a role for the Ras family of GTPases (MAPK pathway) under these conditions. Lovastatin 0-9 mitogen-activated protein kinase 3 Homo sapiens 180-183 15301716-14 2004 CONCLUSIONS: Overexpression of BRCA1 protein may amplify sensibility of breast cancer to lovastatin,and enhance the anti-tumor effect of lovastatin. Lovastatin 89-99 BRCA1 DNA repair associated Homo sapiens 31-36 15301716-14 2004 CONCLUSIONS: Overexpression of BRCA1 protein may amplify sensibility of breast cancer to lovastatin,and enhance the anti-tumor effect of lovastatin. Lovastatin 137-147 BRCA1 DNA repair associated Homo sapiens 31-36 14988223-8 2004 Combined treatment with lovastatin and at-RA exerted additive inhibitory effects on radiation-induced E-selectin expression and tumor cell adhesion. Lovastatin 24-34 selectin E Homo sapiens 102-112 15073034-0 2004 Endothelial cell expression of tissue factor in sickle mice is augmented by hypoxia/reoxygenation and inhibited by lovastatin. Lovastatin 115-125 coagulation factor III Mus musculus 31-44 15073034-7 2004 Pretreatment with lovastatin eliminated excessive expression of TF in the posthypoxic mild sickle mouse (approximately 16% positive) and in the more severe mouse at ambient air (approximately 21% positive). Lovastatin 18-28 coagulation factor III Mus musculus 64-66 14988223-0 2004 Ionizing radiation-induced E-selectin gene expression and tumor cell adhesion is inhibited by lovastatin and all-trans retinoic acid. Lovastatin 94-104 selectin E Homo sapiens 27-37 14988223-4 2004 The HMG-CoA reductase inhibitor lovastatin impairs IR-stimulated E-selectin expression as analyzed at the level of the protein, mRNA and promoter. Lovastatin 32-42 selectin E Homo sapiens 65-75 14988223-7 2004 Abrogation of IR-stimulated E-selectin expression by lovastatin and at-RA reduced tumor cell adhesion in a dose-dependent manner. Lovastatin 53-63 selectin E Homo sapiens 28-38 15287896-5 2004 In contrast, cytochalasin D, lovastatin (a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor) and Y-27632 (a rho-kinase inhibitor) prevented both cyclin D3 expression and BrdU incorporation. Lovastatin 29-39 cyclin D3 Rattus norvegicus 147-156 15287896-6 2004 FAK phosphorylation by ET-1 was inhibited by cytochalasin D, lovastatin and Y-27632, but not by PD98059 or PP-2. Lovastatin 61-71 protein tyrosine kinase 2 Rattus norvegicus 0-3 15287896-6 2004 FAK phosphorylation by ET-1 was inhibited by cytochalasin D, lovastatin and Y-27632, but not by PD98059 or PP-2. Lovastatin 61-71 endothelin 1 Rattus norvegicus 23-27 15284534-1 2004 Individuals expressing the polymorphic CYP3A5 enzyme might show a more than average efficiency in the metabolism of lovastatin, simvastatin and atorvastatin. Lovastatin 116-126 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 39-45 15284534-3 2004 Lovastatin, simvastatin and atorvastatin were significantly less effective in CYP3A5 expressors than in non-expressors. Lovastatin 0-10 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 78-84 15274359-2 2004 Both the HMG-CoA reductase inhibitor (HRI) lovastatin (LOV) and the selective apoptotic antineoplastic drug (SAAND) exisulind (EXS) have shown remarkable chemopreventive effects in previous studies, in cell lines and limited studies in rodents. Lovastatin 43-53 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 9-26 15274359-2 2004 Both the HMG-CoA reductase inhibitor (HRI) lovastatin (LOV) and the selective apoptotic antineoplastic drug (SAAND) exisulind (EXS) have shown remarkable chemopreventive effects in previous studies, in cell lines and limited studies in rodents. Lovastatin 55-58 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 9-26 15118409-7 2004 Furthermore, the i-HUVEC lines maintain normal p53-independent checkpoint control, inducing expression of p27(Kip1) in response to lovastatin treatment, with a subsequent decrease in pRb phosphorylation. Lovastatin 131-141 interferon alpha inducible protein 27 Homo sapiens 106-109 15118409-7 2004 Furthermore, the i-HUVEC lines maintain normal p53-independent checkpoint control, inducing expression of p27(Kip1) in response to lovastatin treatment, with a subsequent decrease in pRb phosphorylation. Lovastatin 131-141 cyclin dependent kinase inhibitor 1B Homo sapiens 110-114 15030401-0 2004 Lovastatin-induced up-regulation of the BH3-only protein, Bim, and cell death in glioblastoma cells. Lovastatin 0-10 BCL2 like 11 Homo sapiens 58-61 15033469-3 2004 We tested the effects of four different statins (fluvastatin, atorvastatin, simvastatin, and lovastatin) on ABCA1 expression in macrophages in vitro. Lovastatin 93-103 ATP binding cassette subfamily A member 1 Homo sapiens 108-113 15034047-5 2004 Additionally, the cholesterol-interfering drugs lovastatin, cholesterol oxidase, and filipin increased CD30 shedding. Lovastatin 48-58 TNF receptor superfamily member 8 Homo sapiens 103-107 15030401-4 2004 Lovastatin-induced death occurs in correlation with significantly increased levels of the BH3-only protein, Bim. Lovastatin 0-10 BCL2 like 11 Homo sapiens 108-111 15030401-6 2004 Lovastatin treatment in U87 cells results in activation of targets of three major mitogen-activating protein kinase cascades including Erk1/2, JNK and p38. Lovastatin 0-10 mitogen-activated protein kinase 3 Homo sapiens 135-141 15030401-6 2004 Lovastatin treatment in U87 cells results in activation of targets of three major mitogen-activating protein kinase cascades including Erk1/2, JNK and p38. Lovastatin 0-10 mitogen-activated protein kinase 8 Homo sapiens 143-146 15030401-6 2004 Lovastatin treatment in U87 cells results in activation of targets of three major mitogen-activating protein kinase cascades including Erk1/2, JNK and p38. Lovastatin 0-10 mitogen-activated protein kinase 1 Homo sapiens 151-154 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Lovastatin 126-136 BCL2 like 11 Homo sapiens 21-24 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Lovastatin 126-136 mitogen-activated protein kinase 3 Homo sapiens 65-71 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Lovastatin 126-136 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Lovastatin 126-136 mitogen-activated protein kinase 1 Homo sapiens 84-87 15030401-9 2004 Further elucidation of the mechanisms of lovastatin-induced up-regulation of Bim and apoptosis in glioblastoma cells are important in determining a potential role for lovastatin as a chemotherapy agent. Lovastatin 41-51 BCL2 like 11 Homo sapiens 77-80 15164758-5 2004 However, only toxin A triggers an increased sPLA2-IIA activity consistent with the elevated levels of protein expression, whereas Y27632 and lovastatin rather reduced IL-1beta-induced sPLA2-IIA activity. Lovastatin 141-151 interleukin 1 beta Rattus norvegicus 167-175 15164758-8 2004 Western blot analyses of toxin A-, Y27632- and lovastatin-stimulated cells reveal that the cytosolic group IV PLA2 (cPLA2) and the cytosolic PGE2 synthase (cPGES), but not the sPLA2-IIA, cyclooxygenase-2 or the microsomal PGE2 synthase (mPGES), are upregulated compared to unstimulated cells. Lovastatin 47-57 phospholipase A2 group IVA Rattus norvegicus 116-121 15164758-8 2004 Western blot analyses of toxin A-, Y27632- and lovastatin-stimulated cells reveal that the cytosolic group IV PLA2 (cPLA2) and the cytosolic PGE2 synthase (cPGES), but not the sPLA2-IIA, cyclooxygenase-2 or the microsomal PGE2 synthase (mPGES), are upregulated compared to unstimulated cells. Lovastatin 47-57 prostaglandin E synthase 3 Rattus norvegicus 131-154 15164758-8 2004 Western blot analyses of toxin A-, Y27632- and lovastatin-stimulated cells reveal that the cytosolic group IV PLA2 (cPLA2) and the cytosolic PGE2 synthase (cPGES), but not the sPLA2-IIA, cyclooxygenase-2 or the microsomal PGE2 synthase (mPGES), are upregulated compared to unstimulated cells. Lovastatin 47-57 prostaglandin E synthase 3 Rattus norvegicus 156-161 15164758-8 2004 Western blot analyses of toxin A-, Y27632- and lovastatin-stimulated cells reveal that the cytosolic group IV PLA2 (cPLA2) and the cytosolic PGE2 synthase (cPGES), but not the sPLA2-IIA, cyclooxygenase-2 or the microsomal PGE2 synthase (mPGES), are upregulated compared to unstimulated cells. Lovastatin 47-57 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 187-203 15164758-8 2004 Western blot analyses of toxin A-, Y27632- and lovastatin-stimulated cells reveal that the cytosolic group IV PLA2 (cPLA2) and the cytosolic PGE2 synthase (cPGES), but not the sPLA2-IIA, cyclooxygenase-2 or the microsomal PGE2 synthase (mPGES), are upregulated compared to unstimulated cells. Lovastatin 47-57 prostaglandin E synthase Mus musculus 237-242 14691063-9 2004 To validate the use of USPIOs as a non-invasive tool to evaluate therapeutic strategies, EAE animals were treated with the immunomodulator 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitor, lovastatin, which ameliorated clinical scores. Lovastatin 198-208 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 139-186 15025528-10 2004 Treatment of the cells with Lovastatin, which inhibits HMG-Co reductase and increases expression of LDL receptor, stimulates luciferase expression, suggesting that the gene delivery is specifically mediated by LDL receptor. Lovastatin 28-38 low density lipoprotein receptor Homo sapiens 100-112 15025528-10 2004 Treatment of the cells with Lovastatin, which inhibits HMG-Co reductase and increases expression of LDL receptor, stimulates luciferase expression, suggesting that the gene delivery is specifically mediated by LDL receptor. Lovastatin 28-38 low density lipoprotein receptor Homo sapiens 210-222 14871314-3 2004 The hmg1 and hmg2 mutants were both more sensitive than the wild type (WT) to lovastatin, an inhibitor of HMGR. Lovastatin 78-88 hydroxy methylglutaryl CoA reductase 1 Arabidopsis thaliana 4-8 14871314-3 2004 The hmg1 and hmg2 mutants were both more sensitive than the wild type (WT) to lovastatin, an inhibitor of HMGR. Lovastatin 78-88 3-hydroxy-3-methylglutaryl-CoA reductase 2 Arabidopsis thaliana 13-17 14698450-4 2004 Lovastatin also tends to reduce, although not in a significant manner, basal and interleukin-1beta-stimulated PGE2 release from astrocytes. Lovastatin 0-10 interleukin 1 beta Rattus norvegicus 81-98 14969398-10 2004 Gamma,delta-T-cell proliferation and activation (interferon gamma [IFNgamma] and TNFalpha release) was prevented by mevastatin or lovastatin, which inhibit HMG-CoA reductase upstream of FPP synthase and prevent the synthesis of isopentenyl diphosphate/dimethylallyl diphosphate. Lovastatin 130-140 farnesyl diphosphate synthase Homo sapiens 186-198 14707106-3 2004 Lovastatin induced the expression of GATA3 and the phosphorylation of STAT6, whereas it inhibited tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT4. Lovastatin 0-10 GATA binding protein 3 Mus musculus 37-42 14707106-3 2004 Lovastatin induced the expression of GATA3 and the phosphorylation of STAT6, whereas it inhibited tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT4. Lovastatin 0-10 signal transducer and activator of transcription 6 Mus musculus 70-75 14707106-3 2004 Lovastatin induced the expression of GATA3 and the phosphorylation of STAT6, whereas it inhibited tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT4. Lovastatin 0-10 Janus kinase 2 Mus musculus 126-140 14707106-3 2004 Lovastatin induced the expression of GATA3 and the phosphorylation of STAT6, whereas it inhibited tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT4. Lovastatin 0-10 tyrosine kinase 2 Mus musculus 142-159 14707106-3 2004 Lovastatin induced the expression of GATA3 and the phosphorylation of STAT6, whereas it inhibited tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT4. Lovastatin 0-10 signal transducer and activator of transcription 4 Mus musculus 165-170 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 signal transducer and activator of transcription 4 Mus musculus 31-36 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 negative elongation factor complex member C/D, Th1l Mus musculus 75-78 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 interferon gamma Mus musculus 117-126 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 tumor necrosis factor Mus musculus 131-140 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 interleukin 4 Mus musculus 183-187 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 interleukin 5 Mus musculus 189-193 14707106-4 2004 Inhibition of the Janus kinase-STAT4 pathway by lovastatin modulated T0 to Th1 differentiation and reduced cytokine (IFN-gamma and TNF-alpha) production, thus inducing Th2 cytokines (IL-4, IL-5, and IL-10). Lovastatin 48-58 interleukin 10 Mus musculus 199-204 14707106-7 2004 Moreover, lovastatin-exposed macrophage and BV2 (microglia) in allogeneic MLRs induced the production of the anti-inflammatory cytokine IL-10. Lovastatin 10-20 interleukin 10 Mus musculus 136-141 14675561-9 2004 Lovastatin and simvastatin significantly inhibited butyrylcholinesterase, while mevastatin, pravastatin and the "non-statins" did not. Lovastatin 0-10 butyrylcholinesterase Homo sapiens 51-72 15563400-0 2004 Cytoskeletal actin degradation induced by lovastatin in cardiomyocytes is mediated through caspase-2. Lovastatin 42-52 actin, beta Gallus gallus 13-18 15563400-0 2004 Cytoskeletal actin degradation induced by lovastatin in cardiomyocytes is mediated through caspase-2. Lovastatin 42-52 caspase 2 Gallus gallus 91-100 15563400-4 2004 Lovastatin induced a dramatic and concentration-dependent loss of intact F-actin. Lovastatin 0-10 actin, beta Gallus gallus 75-80 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 32-42 actin, beta Gallus gallus 0-5 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 32-42 caspase 2 Gallus gallus 67-76 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 32-42 caspase 2 Gallus gallus 93-102 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 32-42 actin, beta Gallus gallus 181-186 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 32-42 caspase 3 Gallus gallus 196-205 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 149-159 actin, beta Gallus gallus 0-5 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 149-159 caspase 2 Gallus gallus 67-76 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 149-159 caspase 2 Gallus gallus 93-102 15563400-7 2004 Actin fragmentation produced by lovastatin was operative through a caspase-2 pathway, as the caspase-2 inhibitor, z-VDVAD-fmk, significantly blocked lovastatin-induced changes in F-actin, but the caspase-3 inhibitor, Ac-DEVD-CHO, did not. Lovastatin 149-159 actin, beta Gallus gallus 181-186 15563400-8 2004 Interruption of the mevalonate pathway was in part responsible for lovastatin"s action, as the downstream metabolite mevalonate partially reversed the effect of lovastatin on actin fragmentation. Lovastatin 67-77 actin, beta Gallus gallus 175-180 15563400-8 2004 Interruption of the mevalonate pathway was in part responsible for lovastatin"s action, as the downstream metabolite mevalonate partially reversed the effect of lovastatin on actin fragmentation. Lovastatin 161-171 actin, beta Gallus gallus 175-180 14531947-1 2003 AIM: To examine protective effects of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on endothelial dysfunction induced by a single intravenous injection of natural low density lipoprotein (n-LDL) and analyze the possible action mechanism of lovastatin. Lovastatin 38-48 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 66-123 14644448-2 2003 In this study, we showed that lovastatin and fluvastatin are able to upregulate the mRNA expression of the suppressor of cytokine signaling-3 (SOCS-3) gene. Lovastatin 30-40 suppressor of cytokine signaling 3 Homo sapiens 107-141 14644448-2 2003 In this study, we showed that lovastatin and fluvastatin are able to upregulate the mRNA expression of the suppressor of cytokine signaling-3 (SOCS-3) gene. Lovastatin 30-40 suppressor of cytokine signaling 3 Homo sapiens 143-149 14630701-0 2004 Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion. Lovastatin 0-10 selectin E Homo sapiens 48-58 14630701-0 2004 Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion. Lovastatin 0-10 tumor necrosis factor Homo sapiens 62-70 14630701-3 2004 As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Lovastatin 73-83 tumor necrosis factor Homo sapiens 96-105 14630701-3 2004 As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Lovastatin 73-83 selectin E Homo sapiens 129-139 14630701-4 2004 Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. Lovastatin 114-124 selectin E Homo sapiens 34-44 14630701-6 2004 Lovastatin-mediated block of TNF-alpha induced E-selectin expression is due to inhibition of protein geranylgeranylation rather than farnesylation. Lovastatin 0-10 tumor necrosis factor Homo sapiens 29-38 14630701-6 2004 Lovastatin-mediated block of TNF-alpha induced E-selectin expression is due to inhibition of protein geranylgeranylation rather than farnesylation. Lovastatin 0-10 selectin E Homo sapiens 47-57 14630701-8 2004 Inhibition of E-selectin expression by lovastatin gives rise to a significant reduction in TNF-alpha stimulated adhesion of colon carcinoma cells to HUVEC. Lovastatin 39-49 selectin E Homo sapiens 14-24 14630701-8 2004 Inhibition of E-selectin expression by lovastatin gives rise to a significant reduction in TNF-alpha stimulated adhesion of colon carcinoma cells to HUVEC. Lovastatin 39-49 tumor necrosis factor Homo sapiens 91-100 14630701-9 2004 Furthermore, low concentration of lovastatin (i.e., < or =1 microM) attenuated TNF-alpha induced tumor cell invasion in vitro. Lovastatin 34-44 tumor necrosis factor Homo sapiens 82-91 15584598-7 2004 Body weight loss and diminished insulin resistance in patients with AH concurrent MS require long use of lovastatin along with low-calorie diet and exercises. Lovastatin 105-115 insulin Homo sapiens 32-39 14678744-0 2003 Lovastatin-induced cardiac toxicity involves both oncotic and apoptotic cell death with the apoptotic component blunted by both caspase-2 and caspase-3 inhibitors. Lovastatin 0-10 caspase 2 Gallus gallus 128-137 14678744-0 2003 Lovastatin-induced cardiac toxicity involves both oncotic and apoptotic cell death with the apoptotic component blunted by both caspase-2 and caspase-3 inhibitors. Lovastatin 0-10 caspase 3 Gallus gallus 142-151 14678744-1 2003 The objective of this study was to evaluate the cardiac toxicity of the HMG-CoA reductase inhibitors by testing the hypothesis that lovastatin induces apoptotic and/or oncotic cell death in the myocyte element of the heart and further that cell death is mediated through interruption of the mevalonate pathway and that apoptosis is induced through activation of caspase-2 and caspase-3. Lovastatin 132-142 caspase 2 Gallus gallus 362-371 14678744-1 2003 The objective of this study was to evaluate the cardiac toxicity of the HMG-CoA reductase inhibitors by testing the hypothesis that lovastatin induces apoptotic and/or oncotic cell death in the myocyte element of the heart and further that cell death is mediated through interruption of the mevalonate pathway and that apoptosis is induced through activation of caspase-2 and caspase-3. Lovastatin 132-142 caspase 3 Gallus gallus 376-385 14678744-7 2003 The caspase-2 inhibitor z-VDVAD-fmk and the caspase-3 inhibitor Ac-DEVD-CHO reduced the extent of lovastatin-induced cardiac apoptosis. Lovastatin 98-108 caspase 2 Gallus gallus 4-13 14678744-7 2003 The caspase-2 inhibitor z-VDVAD-fmk and the caspase-3 inhibitor Ac-DEVD-CHO reduced the extent of lovastatin-induced cardiac apoptosis. Lovastatin 98-108 caspase 3 Gallus gallus 44-53 14678744-9 2003 In summary, lovastatin-induced cardiotoxicity is complex and represents the sum of two distinct modes of cell death operating in part through the mevalonate pathway with the apoptotic component subject to modification by inhibitors of the initiator caspase, caspase-2, as well as the effector caspase, caspase-3. Lovastatin 12-22 caspase 2 Gallus gallus 249-256 14678744-9 2003 In summary, lovastatin-induced cardiotoxicity is complex and represents the sum of two distinct modes of cell death operating in part through the mevalonate pathway with the apoptotic component subject to modification by inhibitors of the initiator caspase, caspase-2, as well as the effector caspase, caspase-3. Lovastatin 12-22 caspase 2 Gallus gallus 258-267 14678744-9 2003 In summary, lovastatin-induced cardiotoxicity is complex and represents the sum of two distinct modes of cell death operating in part through the mevalonate pathway with the apoptotic component subject to modification by inhibitors of the initiator caspase, caspase-2, as well as the effector caspase, caspase-3. Lovastatin 12-22 caspase 2 Gallus gallus 258-265 14678744-9 2003 In summary, lovastatin-induced cardiotoxicity is complex and represents the sum of two distinct modes of cell death operating in part through the mevalonate pathway with the apoptotic component subject to modification by inhibitors of the initiator caspase, caspase-2, as well as the effector caspase, caspase-3. Lovastatin 12-22 caspase 3 Gallus gallus 302-311 14563711-3 2003 Here we demonstrated that the statins tested, ie, cerivastatin, simvastatin, lovastatin, and atorvastatin, promoted Th2 polarization through both inhibition of Th1 development and augmentation of Th2 development of CD4+ T cells primed in vitro with anti-CD3 antibody and splenic antigen-presenting cells. Lovastatin 77-87 heart and neural crest derivatives expressed 2 Mus musculus 116-119 14563711-3 2003 Here we demonstrated that the statins tested, ie, cerivastatin, simvastatin, lovastatin, and atorvastatin, promoted Th2 polarization through both inhibition of Th1 development and augmentation of Th2 development of CD4+ T cells primed in vitro with anti-CD3 antibody and splenic antigen-presenting cells. Lovastatin 77-87 negative elongation factor complex member C/D, Th1l Mus musculus 160-163 14563711-3 2003 Here we demonstrated that the statins tested, ie, cerivastatin, simvastatin, lovastatin, and atorvastatin, promoted Th2 polarization through both inhibition of Th1 development and augmentation of Th2 development of CD4+ T cells primed in vitro with anti-CD3 antibody and splenic antigen-presenting cells. Lovastatin 77-87 heart and neural crest derivatives expressed 2 Mus musculus 196-199 14672267-8 2003 3) Following lovastatin treatment, p16 expression exhibits no change, but pronounced increases of p27KIP1 protein are observed in all examined cell lines. Lovastatin 13-23 cyclin dependent kinase inhibitor 2A Homo sapiens 35-38 14672267-8 2003 3) Following lovastatin treatment, p16 expression exhibits no change, but pronounced increases of p27KIP1 protein are observed in all examined cell lines. Lovastatin 13-23 cyclin dependent kinase inhibitor 1B Homo sapiens 98-105 14672267-10 2003 4) Following lovastatin treatment, increased p53 protein is detected only in D341 Med, and bax protein is unchanged in all cell lines. Lovastatin 13-23 tumor protein p53 Homo sapiens 45-48 14672267-11 2003 CONCLUSIONS: Lovastatin-induced growth inhibition and apoptosis in medulloblastoma are not dependent on the regulation of Ras and c-myc gene expression, but may be mediated by p27KIP1 gene expression. Lovastatin 13-23 cyclin dependent kinase inhibitor 1B Homo sapiens 176-183 14672267-12 2003 Lovastatin-induced apoptosis in medulloblastoma is probably p53 independent, but p53 and p21WAF1 gene expression may also mediate anti-proliferative effects of lovastatin on specific medulloblastoma cell lines. Lovastatin 0-10 tumor protein p53 Homo sapiens 60-63 14672267-12 2003 Lovastatin-induced apoptosis in medulloblastoma is probably p53 independent, but p53 and p21WAF1 gene expression may also mediate anti-proliferative effects of lovastatin on specific medulloblastoma cell lines. Lovastatin 160-170 tumor protein p53 Homo sapiens 81-84 14572607-2 2003 Treatment with lovastatin resulted in the induction of LPS/IFN-gamma-mediated iNOS mRNA and increased nitric oxide (NO) production. Lovastatin 15-25 interferon regulatory factor 6 Homo sapiens 55-58 14572607-2 2003 Treatment with lovastatin resulted in the induction of LPS/IFN-gamma-mediated iNOS mRNA and increased nitric oxide (NO) production. Lovastatin 15-25 interferon gamma Homo sapiens 59-68 14572607-2 2003 Treatment with lovastatin resulted in the induction of LPS/IFN-gamma-mediated iNOS mRNA and increased nitric oxide (NO) production. Lovastatin 15-25 nitric oxide synthase 2 Homo sapiens 78-82 14572607-4 2003 An inhibitor of geranylgeranyltransferase inhibitor (GGTI 298) further induced the cytokine and lovastatin-mediated iNOS expression, suggesting the involvement of geranylgeranylated proteins in the regulation of iNOS. Lovastatin 96-106 nitric oxide synthase 2 Homo sapiens 116-120 14572607-4 2003 An inhibitor of geranylgeranyltransferase inhibitor (GGTI 298) further induced the cytokine and lovastatin-mediated iNOS expression, suggesting the involvement of geranylgeranylated proteins in the regulation of iNOS. Lovastatin 96-106 nitric oxide synthase 2 Homo sapiens 212-216 14572607-6 2003 Lovastatin treatment induced NO by increasing NF-kappaB translocation and its association with the CREB-binding protein (CBP/p300) via the downregulation of RhoA. Lovastatin 0-10 nuclear factor kappa B subunit 1 Homo sapiens 46-55 14572607-6 2003 Lovastatin treatment induced NO by increasing NF-kappaB translocation and its association with the CREB-binding protein (CBP/p300) via the downregulation of RhoA. Lovastatin 0-10 CREB binding protein Homo sapiens 99-119 14572607-6 2003 Lovastatin treatment induced NO by increasing NF-kappaB translocation and its association with the CREB-binding protein (CBP/p300) via the downregulation of RhoA. Lovastatin 0-10 CREB binding protein Homo sapiens 121-129 14572607-6 2003 Lovastatin treatment induced NO by increasing NF-kappaB translocation and its association with the CREB-binding protein (CBP/p300) via the downregulation of RhoA. Lovastatin 0-10 ras homolog family member A Homo sapiens 157-161 14572607-9 2003 Taken together, these studies show that downregulation of RhoA by lovastatin resulted in increased iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells. Lovastatin 66-76 ras homolog family member A Homo sapiens 58-62 14572607-9 2003 Taken together, these studies show that downregulation of RhoA by lovastatin resulted in increased iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells. Lovastatin 66-76 nitric oxide synthase 2 Homo sapiens 99-103 14572607-9 2003 Taken together, these studies show that downregulation of RhoA by lovastatin resulted in increased iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells. Lovastatin 66-76 nuclear factor kappa B subunit 1 Homo sapiens 137-146 14572607-9 2003 Taken together, these studies show that downregulation of RhoA by lovastatin resulted in increased iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells. Lovastatin 66-76 CREB binding protein Homo sapiens 147-150 14572607-9 2003 Taken together, these studies show that downregulation of RhoA by lovastatin resulted in increased iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells. Lovastatin 66-76 E1A binding protein p300 Homo sapiens 151-155 12942316-0 2003 Epidermal growth factor receptor-targeted therapy potentiates lovastatin-induced apoptosis in head and neck squamous cell carcinoma cells. Lovastatin 62-72 epidermal growth factor receptor Homo sapiens 0-32 12942316-3 2003 In this study, we evaluated the potential of a number of chemotherapeutics that demonstrate activity in HNSCC, including an inhibitor of epidermal growth factor receptor (EGFR) to potentiate the cytotoxic effects of lovastatin. Lovastatin 216-226 epidermal growth factor receptor Homo sapiens 137-169 12942316-3 2003 In this study, we evaluated the potential of a number of chemotherapeutics that demonstrate activity in HNSCC, including an inhibitor of epidermal growth factor receptor (EGFR) to potentiate the cytotoxic effects of lovastatin. Lovastatin 216-226 epidermal growth factor receptor Homo sapiens 171-175 12942316-6 2003 Expression levels of EGFR and ligand activated EGFR following lovastatin treatment were analyzed by Western blotting. Lovastatin 62-72 epidermal growth factor receptor Homo sapiens 21-25 12942316-6 2003 Expression levels of EGFR and ligand activated EGFR following lovastatin treatment were analyzed by Western blotting. Lovastatin 62-72 epidermal growth factor receptor Homo sapiens 47-51 12942316-10 2003 In contrast to the chemotherapeutics analyzed, the AG1478 tyrosine kinase inhibitor of the EGFR demonstrated additive cytotoxic effects in combination with lovastatin in HNSCC cells. Lovastatin 156-166 epidermal growth factor receptor Homo sapiens 91-95 12942316-11 2003 Mevalonate metabolites may regulate EGFR function, suggesting that lovastatin may inhibit the activity of this receptor. Lovastatin 67-77 epidermal growth factor receptor Homo sapiens 36-40 12942316-12 2003 Indeed, lovastatin treatment inhibited EGF-induced autophosphorylation of the EGFR in the SCC9 and SCC25 cell lines. Lovastatin 8-18 epidermal growth factor receptor Homo sapiens 78-82 12942316-13 2003 Pretreatment of SCC9 and SCC25 cell lines for 24 h with 10 microM lovastatin, conditions that demonstrated significant inhibition of EGF-induced EGFR autophosphorylation, induced significant additive effects in combination with AG1478. Lovastatin 66-76 epidermal growth factor receptor Homo sapiens 145-149 12942316-14 2003 CONCLUSION: These results demonstrated the ability of EGFR pathway inhibitors to potentiate lovastatin-induced apoptosis and suggested that lovastatin may target the EGFR pathway in HNSCC cells. Lovastatin 92-102 epidermal growth factor receptor Homo sapiens 54-58 12942316-14 2003 CONCLUSION: These results demonstrated the ability of EGFR pathway inhibitors to potentiate lovastatin-induced apoptosis and suggested that lovastatin may target the EGFR pathway in HNSCC cells. Lovastatin 140-150 epidermal growth factor receptor Homo sapiens 54-58 12942316-14 2003 CONCLUSION: These results demonstrated the ability of EGFR pathway inhibitors to potentiate lovastatin-induced apoptosis and suggested that lovastatin may target the EGFR pathway in HNSCC cells. Lovastatin 140-150 epidermal growth factor receptor Homo sapiens 166-170 14581565-5 2003 Treatment of infected cells with lovastatin, a drug that disrupts protein prenylation, changed the relative electrophoretic mobility of Us2 in sodium dodecyl sulfate-polyacrylamide gels. Lovastatin 33-43 usherin Homo sapiens 136-139 14581565-6 2003 In addition, lovastatin treatment caused a dramatic relocalization of Us2 to cytoplasmic punctate structures associated with microtubules, which appeared to concentrate over the microtubule organizing center. Lovastatin 13-23 usherin Homo sapiens 70-73 14581565-7 2003 When the CAAX motif was changed to GAAX and the mutant protein was synthesized from an expression plasmid, it concentrated in punctate cytoplasmic structures reminiscent of Us2 localization in infected cells treated with lovastatin. Lovastatin 221-231 usherin Homo sapiens 173-176 14612202-5 2003 Different statins (atorvastatin, simvastatin and lovastatin, 1-10 micromol/l) significantly reduced basal and cytokine-, nitric oxide- or lysophosphatidylcholine (LPC)-induced VEGF synthesis in HMEC-1 and HVSMC. Lovastatin 49-59 vascular endothelial growth factor A Homo sapiens 176-180 14612203-4 2003 Lovastatin, simvastatin, atorvastatin, fluvastatin and cerivastatin, which are hydrophobic statins, markedly reduced cell viability associated with DNA fragmentation, DNA laddering and activation of caspase-3, suggesting apoptotic cell death. Lovastatin 0-10 caspase 3 Rattus norvegicus 199-208 14517078-5 2003 Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. Lovastatin 27-37 HRas proto-oncogene, GTPase Homo sapiens 52-58 14555271-0 2003 Lovastatin inhibits adipogenic and stimulates osteogenic differentiation by suppressing PPARgamma2 and increasing Cbfa1/Runx2 expression in bone marrow mesenchymal cell cultures. Lovastatin 0-10 RUNX family transcription factor 2 Homo sapiens 114-119 14555271-0 2003 Lovastatin inhibits adipogenic and stimulates osteogenic differentiation by suppressing PPARgamma2 and increasing Cbfa1/Runx2 expression in bone marrow mesenchymal cell cultures. Lovastatin 0-10 RUNX family transcription factor 2 Homo sapiens 120-125 14555271-6 2003 Lovastatin enhanced osteoblast differentiation as assessed by a 1.8x increase in expression of Cbfa1/Runx2 and by a 5x increase in osteocalcin promoter activity. Lovastatin 0-10 RUNX family transcription factor 2 Homo sapiens 95-100 14555271-6 2003 Lovastatin enhanced osteoblast differentiation as assessed by a 1.8x increase in expression of Cbfa1/Runx2 and by a 5x increase in osteocalcin promoter activity. Lovastatin 0-10 RUNX family transcription factor 2 Homo sapiens 101-106 14555271-6 2003 Lovastatin enhanced osteoblast differentiation as assessed by a 1.8x increase in expression of Cbfa1/Runx2 and by a 5x increase in osteocalcin promoter activity. Lovastatin 0-10 bone gamma-carboxyglutamate protein Homo sapiens 131-142 14522569-4 2003 Since certain lipophilic statins (i.e. simvastatin, atorvastatin, lovastatin) are a substrate of CYP3A4, we were interested in potential drug interactions between clopidogrel and statins. Lovastatin 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 14605511-3 2003 Previously, the ADvicor Vs. Other Cholesterol-modulating Agents Trial Evaluation demonstrated that niacin extended release/lovastatin provided greater global improvement in lipid parameters such as low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, lipoprotein (a), apolipoprotein B, and apolipoprotein A-I blood levels compared with atorvastatin and simvastatin monotherapies. Lovastatin 123-133 apolipoprotein B Homo sapiens 305-321 14605511-3 2003 Previously, the ADvicor Vs. Other Cholesterol-modulating Agents Trial Evaluation demonstrated that niacin extended release/lovastatin provided greater global improvement in lipid parameters such as low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, lipoprotein (a), apolipoprotein B, and apolipoprotein A-I blood levels compared with atorvastatin and simvastatin monotherapies. Lovastatin 123-133 apolipoprotein A1 Homo sapiens 327-345 14517078-5 2003 Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. Lovastatin 27-37 insulin Homo sapiens 80-87 14517078-5 2003 Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. Lovastatin 103-113 HRas proto-oncogene, GTPase Homo sapiens 52-58 14517078-5 2003 Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. Lovastatin 103-113 insulin Homo sapiens 80-87 14517078-5 2003 Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. Lovastatin 103-113 HRas proto-oncogene, GTPase Homo sapiens 211-217 12933658-6 2003 Treatment of the cells with 50 microM lovastatin induced cytochrome c translocation from mitochondria to cytosol; increases in caspase-2, -3, and -9 activity; and poly (ADP-ribose) polymerase degradation in a time-dependent manner. Lovastatin 38-48 cytochrome c, somatic Homo sapiens 57-69 14527367-4 2003 RESULTS: Lovastatin was found to have inhibitory effects on human mesangial cell (HMC) proliferation and lipopolysaccharide (LPS)-mediated human mesangine cell HMC mRNA expression of proinflammatory cytokines via activation of NF-kappa B. Lovastatin 9-19 nuclear factor kappa B subunit 1 Homo sapiens 227-237 14527367-6 2003 CONCLUSION: Lovastatin may decrease HMC proliferation and production of proinflammatory cytokines through the inhibition of NF-kappa B activation. Lovastatin 12-22 nuclear factor kappa B subunit 1 Homo sapiens 124-134 12933658-6 2003 Treatment of the cells with 50 microM lovastatin induced cytochrome c translocation from mitochondria to cytosol; increases in caspase-2, -3, and -9 activity; and poly (ADP-ribose) polymerase degradation in a time-dependent manner. Lovastatin 38-48 caspase 2 Homo sapiens 127-148 12933658-7 2003 However, administration of mevalonate or geranylgeraniol, but not farnesol, dose-dependently prevented lovastatin-induced poly (ADP-ribose) polymerase degradation and the occurrence of apoptosis, but treatment with geranylgeranyl transferase inhibitor, GGTI-298, which blocks the geranylgeranylation, induced an increase in the percentage of the apoptotic cells. Lovastatin 103-113 protein geranylgeranyltransferase type I subunit beta Homo sapiens 253-257 12933658-9 2003 To support this notion, we demonstrate that lovastatin dose-dependently decreased the translocation of RhoA and Rac1, but not Ras, from cytosol to membrane fraction. Lovastatin 44-54 ras homolog family member A Homo sapiens 103-107 12933658-9 2003 To support this notion, we demonstrate that lovastatin dose-dependently decreased the translocation of RhoA and Rac1, but not Ras, from cytosol to membrane fraction. Lovastatin 44-54 Rac family small GTPase 1 Homo sapiens 112-116 12933658-10 2003 Moreover, the lovastatin-induced translocation inhibitions in RhoA and Rac1 were prevented by mevalonate and geranylgeraniol but not farnesol. Lovastatin 14-24 ras homolog family member A Homo sapiens 62-66 12933658-10 2003 Moreover, the lovastatin-induced translocation inhibitions in RhoA and Rac1 were prevented by mevalonate and geranylgeraniol but not farnesol. Lovastatin 14-24 Rac family small GTPase 1 Homo sapiens 71-75 12760743-12 2003 Whereas mevinolin increased the mRNA for EBP and DHCR7 (delta7-sterol reductase) in HepG2 cells, it had no effect on mRNAs for EBPL and sigma1 receptor, indicating that EBP and EBPL expression are not co-ordinated. Lovastatin 8-17 EBP cholestenol delta-isomerase Homo sapiens 41-44 12885571-0 2003 Lovastatin enhances Abeta production and senile plaque deposition in female Tg2576 mice. Lovastatin 0-10 amyloid beta (A4) precursor protein Mus musculus 20-25 12760743-12 2003 Whereas mevinolin increased the mRNA for EBP and DHCR7 (delta7-sterol reductase) in HepG2 cells, it had no effect on mRNAs for EBPL and sigma1 receptor, indicating that EBP and EBPL expression are not co-ordinated. Lovastatin 8-17 7-dehydrocholesterol reductase Homo sapiens 49-54 14555343-8 2003 Radiation-stimulated activation of ERKs was attenuated by lovastatin. Lovastatin 58-68 mitogen-activated protein kinase 1 Homo sapiens 35-39 12907238-0 2003 Treatment with lovastatin, cholestyramine or niacin alters K-ras membrane association in mouse lung in a strain-dependent manner: results in females. Lovastatin 15-25 Kirsten rat sarcoma viral oncogene homolog Mus musculus 59-64 12859971-2 2003 Inhibition of UV-C-triggered JNK/SAPK activation by lovastatin is due to inhibition of Rac-SEK1/MKK4-mediated phosphorylation of JNKs/SAPKs at Thr183/Tyr185. Lovastatin 52-62 mitogen-activated protein kinase 8 Homo sapiens 29-32 12859971-2 2003 Inhibition of UV-C-triggered JNK/SAPK activation by lovastatin is due to inhibition of Rac-SEK1/MKK4-mediated phosphorylation of JNKs/SAPKs at Thr183/Tyr185. Lovastatin 52-62 mitogen-activated protein kinase kinase 4 Homo sapiens 96-100 12859971-8 2003 Based on the data, we suggest that lovastatin-provoked resistance to UV-C light is due to the inhibition of UV-C-inducible Rac-SEK1/MKK4-JNK/SAPK-dependent signal mechanisms regulating cell cycle progression and activation of caspases and apoptotic death. Lovastatin 35-45 mitogen-activated protein kinase kinase 4 Homo sapiens 132-136 12859971-8 2003 Based on the data, we suggest that lovastatin-provoked resistance to UV-C light is due to the inhibition of UV-C-inducible Rac-SEK1/MKK4-JNK/SAPK-dependent signal mechanisms regulating cell cycle progression and activation of caspases and apoptotic death. Lovastatin 35-45 mitogen-activated protein kinase 8 Homo sapiens 137-140 12736259-3 2003 Treatment of Tobacco Bright Yellow-2 (TBY-2) cells by the HMGR-specific inhibitor mevinolin led to growth reduction and induction of apparent HMGR activity, in parallel to an increase in protein representing two HMGR isozymes. Lovastatin 82-91 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 58-62 12736259-3 2003 Treatment of Tobacco Bright Yellow-2 (TBY-2) cells by the HMGR-specific inhibitor mevinolin led to growth reduction and induction of apparent HMGR activity, in parallel to an increase in protein representing two HMGR isozymes. Lovastatin 82-91 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 142-146 12736259-3 2003 Treatment of Tobacco Bright Yellow-2 (TBY-2) cells by the HMGR-specific inhibitor mevinolin led to growth reduction and induction of apparent HMGR activity, in parallel to an increase in protein representing two HMGR isozymes. Lovastatin 82-91 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 142-146 12736259-5 2003 Furthermore, DX partially re-established feedback repression of mevinolin-induced HMGR activity. Lovastatin 64-73 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 82-86 12801507-12 2003 Lovastatin, another statin, also induced the HSP27 accumulation and SB203580 suppressed the HSP27 accumulation. Lovastatin 0-10 heat shock protein 1 Mus musculus 45-50 12792788-8 2003 IFN-alpha 2b alone showed little effect on protein phosphorylation but strongly enhanced lovastatin driven loss of phosphorylation. Lovastatin 89-99 interferon alpha 1 Homo sapiens 0-9 12843138-0 2003 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, induces apoptosis and differentiation in human anaplastic thyroid carcinoma cells. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-61 12824699-7 2003 We found that LPS-induced I kappa B kinase and nuclear factor-kappa B (NF-kappa B) activation, as well as IFN-gamma-induced signal transducer and activator of transcription 1 (STAT1) phosphorylation, were reduced by lovastatin. Lovastatin 216-226 interferon gamma Mus musculus 106-115 12824699-7 2003 We found that LPS-induced I kappa B kinase and nuclear factor-kappa B (NF-kappa B) activation, as well as IFN-gamma-induced signal transducer and activator of transcription 1 (STAT1) phosphorylation, were reduced by lovastatin. Lovastatin 216-226 signal transducer and activator of transcription 1 Mus musculus 124-174 12824699-7 2003 We found that LPS-induced I kappa B kinase and nuclear factor-kappa B (NF-kappa B) activation, as well as IFN-gamma-induced signal transducer and activator of transcription 1 (STAT1) phosphorylation, were reduced by lovastatin. Lovastatin 216-226 signal transducer and activator of transcription 1 Mus musculus 176-181 12633795-7 2003 Niacin ER/lovastatin also provided significant improvements in triglycerides, lipoprotein(a), apolipoprotein A-1, apolipoprotein B, and HDL subfractions. Lovastatin 10-20 apolipoprotein A1 Homo sapiens 94-112 12820652-0 2003 Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Lovastatin 62-72 heat shock protein family B (small) member 1 Homo sapiens 0-5 12820652-0 2003 Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Lovastatin 62-72 heat shock protein family A (Hsp70) member 4 Homo sapiens 10-15 12820652-7 2003 Moreover, sarcomas showed the highest expression levels of Hsp25 in the viable tumor cells growing under untreated conditions, and these levels increased after DOX and LOV administration. Lovastatin 168-171 heat shock protein family B (small) member 1 Homo sapiens 59-64 12921559-0 2003 [Effect of lovastatin on the expression of IkappaBalpha and cell-cycle regulating protein in MCF-7 cells]. Lovastatin 11-21 NFKB inhibitor alpha Homo sapiens 43-55 12921559-1 2003 OBJECTIVE: To study the effect of lovastatin on the expression of IkappaBalpha and cell-cycle regulating proteins in MCF-7 cells. Lovastatin 34-44 NFKB inhibitor alpha Homo sapiens 66-78 12921559-4 2003 RESULTS: Lovastatin could arrest cellcycle in the G(0)/G(1) phase in a dose- and time-dependent manner, obviously lowering the expression of IkappaBalpha, CDK4 and pRb protein level in the cytoplasm and increasing IkappaBalpha in the nucleus, but not on p16 protein level. Lovastatin 9-19 NFKB inhibitor alpha Homo sapiens 141-153 12921559-4 2003 RESULTS: Lovastatin could arrest cellcycle in the G(0)/G(1) phase in a dose- and time-dependent manner, obviously lowering the expression of IkappaBalpha, CDK4 and pRb protein level in the cytoplasm and increasing IkappaBalpha in the nucleus, but not on p16 protein level. Lovastatin 9-19 cyclin dependent kinase 4 Homo sapiens 155-159 12921559-4 2003 RESULTS: Lovastatin could arrest cellcycle in the G(0)/G(1) phase in a dose- and time-dependent manner, obviously lowering the expression of IkappaBalpha, CDK4 and pRb protein level in the cytoplasm and increasing IkappaBalpha in the nucleus, but not on p16 protein level. Lovastatin 9-19 RB transcriptional corepressor 1 Homo sapiens 164-167 12921559-4 2003 RESULTS: Lovastatin could arrest cellcycle in the G(0)/G(1) phase in a dose- and time-dependent manner, obviously lowering the expression of IkappaBalpha, CDK4 and pRb protein level in the cytoplasm and increasing IkappaBalpha in the nucleus, but not on p16 protein level. Lovastatin 9-19 NFKB inhibitor alpha Homo sapiens 214-226 12921559-4 2003 RESULTS: Lovastatin could arrest cellcycle in the G(0)/G(1) phase in a dose- and time-dependent manner, obviously lowering the expression of IkappaBalpha, CDK4 and pRb protein level in the cytoplasm and increasing IkappaBalpha in the nucleus, but not on p16 protein level. Lovastatin 9-19 cyclin dependent kinase inhibitor 2A Homo sapiens 254-257 12921559-5 2003 CONCLUSION: Lovastatin can induce the arrest of cell cycle in G(0)/G(1) phase by affecting the expression of IkappaBalpha and cell-cycle regulating protein in MCF-7 cells. Lovastatin 12-22 NFKB inhibitor alpha Homo sapiens 109-121 12914758-4 2003 Lovastatin inhibited MHC class II and CD40 expression on DC in a dose-dependent manner, but had lesser effects on CD16, CD80, CD86, and CD11b expression. Lovastatin 0-10 CD40 molecule Homo sapiens 38-42 12914758-5 2003 Nuclear extracts of lovastatin treated DC had decreased NF-kappaB DNA binding activity. Lovastatin 20-30 nuclear factor kappa B subunit 1 Homo sapiens 56-65 12694870-10 2003 Furthermore, lovastatin inhibited induction of alpha-smooth muscle actin expression in the course of primary culture. Lovastatin 13-23 actin gamma 2, smooth muscle Rattus norvegicus 47-72 12694870-11 2003 Immunoblot experiments indicated that lovastatin suppressed both Ras-mediated ERK 1/2 activation and platelet-derived growth factor-induced membrane translocation of RhoA. Lovastatin 38-48 mitogen activated protein kinase 3 Rattus norvegicus 78-85 12694870-11 2003 Immunoblot experiments indicated that lovastatin suppressed both Ras-mediated ERK 1/2 activation and platelet-derived growth factor-induced membrane translocation of RhoA. Lovastatin 38-48 ras homolog family member A Rattus norvegicus 166-170 12633795-7 2003 Niacin ER/lovastatin also provided significant improvements in triglycerides, lipoprotein(a), apolipoprotein A-1, apolipoprotein B, and HDL subfractions. Lovastatin 10-20 apolipoprotein B Homo sapiens 114-130 12615656-4 2003 In contrast, PON3 lactonase activity toward lovastatin was markedly reduced (by 29% to 57%) compared with control cells. Lovastatin 44-54 paraoxonase 3 Mus musculus 13-17 12663504-2 2003 Lovastatin inhibited cell growth in vitro in a dose-dependent manner for both mammary and prostate cancer cell lines, which was associated with p53-independent apoptosis. Lovastatin 0-10 transformation related protein 53, pseudogene Mus musculus 144-147 12663504-4 2003 p21(Waf1) and p27(Kip1) were induced by lovastatin in both types of cancer cells. Lovastatin 40-50 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 0-3 12663504-4 2003 p21(Waf1) and p27(Kip1) were induced by lovastatin in both types of cancer cells. Lovastatin 40-50 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 4-8 12663504-4 2003 p21(Waf1) and p27(Kip1) were induced by lovastatin in both types of cancer cells. Lovastatin 40-50 cyclin-dependent kinase inhibitor 1B Mus musculus 14-17 12663504-4 2003 p21(Waf1) and p27(Kip1) were induced by lovastatin in both types of cancer cells. Lovastatin 40-50 cyclin-dependent kinase inhibitor 1B Mus musculus 18-22 12613664-1 2003 The "statin story" began in 1987 when the first-generation, fungal HMG-CoA reductase inhibitor lovastatin received FDA approval in the USA. Lovastatin 95-105 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 67-84 12612910-11 2003 Finally, the mGSH depletion induced by acetaldehyde sensitized HepG2 cells to tumor necrosis factor (TNF)-alpha-induced apoptosis that was prevented by cyclosporin A, GSH ethyl ester, and lovastatin. Lovastatin 188-198 tumor necrosis factor Homo sapiens 78-111 12593849-0 2003 Lovastatin stimulates human vascular smooth muscle cell expression of bone morphogenetic protein-2, a potent inhibitor of low-density lipoprotein-stimulated cell growth. Lovastatin 0-10 bone morphogenetic protein 2 Homo sapiens 70-98 12593849-3 2003 Treatment with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitor lovastatin (34 microM) increased BMP-2 gene transcription >14-fold as measured by real-time PCR analysis (P<0.05 vs. solvent control). Lovastatin 67-77 bone morphogenetic protein 2 Homo sapiens 100-105 12524225-3 2003 METHODS AND RESULTS: Simvastatin, atorvastatin, and lovastatin (0.1 to 10 micro mol/L) inhibited the binding of nuclear proteins to both the nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA consensus oligonucleotides in human endothelial and vascular smooth muscle cells as assessed by electrophoretic mobility shift assay (EMSA). Lovastatin 52-62 nuclear factor kappa B subunit 1 Homo sapiens 141-163 12524225-3 2003 METHODS AND RESULTS: Simvastatin, atorvastatin, and lovastatin (0.1 to 10 micro mol/L) inhibited the binding of nuclear proteins to both the nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA consensus oligonucleotides in human endothelial and vascular smooth muscle cells as assessed by electrophoretic mobility shift assay (EMSA). Lovastatin 52-62 nuclear factor kappa B subunit 1 Homo sapiens 165-174 12524225-3 2003 METHODS AND RESULTS: Simvastatin, atorvastatin, and lovastatin (0.1 to 10 micro mol/L) inhibited the binding of nuclear proteins to both the nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA consensus oligonucleotides in human endothelial and vascular smooth muscle cells as assessed by electrophoretic mobility shift assay (EMSA). Lovastatin 52-62 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 180-199 12524225-3 2003 METHODS AND RESULTS: Simvastatin, atorvastatin, and lovastatin (0.1 to 10 micro mol/L) inhibited the binding of nuclear proteins to both the nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA consensus oligonucleotides in human endothelial and vascular smooth muscle cells as assessed by electrophoretic mobility shift assay (EMSA). Lovastatin 52-62 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 201-205 12524230-3 2003 METHODS AND RESULTS: Our studies uncovered several new features that distinguish SCAP ligand from lovastatin, a classic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, and from OM, which utilize an SREBP-independent regulatory pathway. Lovastatin 98-108 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 219-224 12699076-2 2003 Random screening of chemical libraries identified the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin as an inhibitor of the LFA-1/intercellular adhesion molecule (ICAM)-1 interaction. Lovastatin 122-132 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 54-111 12699076-2 2003 Random screening of chemical libraries identified the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin as an inhibitor of the LFA-1/intercellular adhesion molecule (ICAM)-1 interaction. Lovastatin 122-132 integrin subunit alpha L Homo sapiens 156-161 12699076-3 2003 The effect of lovastatin on LFA-1 was found to be unrelated to the inhibition of HMG-CoA reductase and to be mediated by lovastatin binding to a novel allosteric site within LFA-1. Lovastatin 14-24 integrin subunit alpha L Homo sapiens 28-33 12699076-3 2003 The effect of lovastatin on LFA-1 was found to be unrelated to the inhibition of HMG-CoA reductase and to be mediated by lovastatin binding to a novel allosteric site within LFA-1. Lovastatin 14-24 integrin subunit alpha L Homo sapiens 174-179 12699076-3 2003 The effect of lovastatin on LFA-1 was found to be unrelated to the inhibition of HMG-CoA reductase and to be mediated by lovastatin binding to a novel allosteric site within LFA-1. Lovastatin 121-131 integrin subunit alpha L Homo sapiens 28-33 12699076-3 2003 The effect of lovastatin on LFA-1 was found to be unrelated to the inhibition of HMG-CoA reductase and to be mediated by lovastatin binding to a novel allosteric site within LFA-1. Lovastatin 121-131 integrin subunit alpha L Homo sapiens 174-179 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 cyclin dependent kinase 20 Homo sapiens 145-148 12485399-7 2003 Finally when using primary cultures of mouse hippocampus the synaptophysin/synaptobrevin complex was down-regulated after depleting the endogenous cholesterol content by the HMG-CoA-reductase inhibitor lovastatin. Lovastatin 202-212 synaptophysin Mus musculus 61-74 12514264-5 2003 We tested the hypothesis that plant-derived isoprenoids also regulate mammalian HMG-CoA reductase synthesis at a post-transcriptional level by incubating lovastatin-treated C100 cells with mevalonate or a plant-derived isoprenoid (the monoterpenes, limonene, perillyl alcohol or geraniol) either alone or combined with the oxysterol, 25-hydroxycholesterol (25-OH C). Lovastatin 154-164 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 80-97 12526087-4 2002 In this study we investigated the expression of intercellular cell adhesion molecule-1 (ICAM-1) in transformed endothelial cell line ECV304 cells as influenced by lovastatin, tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma. Lovastatin 163-173 intercellular adhesion molecule 1 Homo sapiens 48-86 12526087-4 2002 In this study we investigated the expression of intercellular cell adhesion molecule-1 (ICAM-1) in transformed endothelial cell line ECV304 cells as influenced by lovastatin, tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma. Lovastatin 163-173 intercellular adhesion molecule 1 Homo sapiens 88-94 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 intercellular adhesion molecule 1 Homo sapiens 54-60 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 interferon gamma Homo sapiens 79-88 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 mitogen-activated protein kinase 1 Homo sapiens 97-134 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 mitogen-activated protein kinase 1 Homo sapiens 136-139 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 interferon induced protein 44 Homo sapiens 141-144 12505310-2 2002 With the exception of pravastatin, the remaining 15 compounds transactivated the CYP3A4 reporter gene with differing inductive abilities (I(max):EC(50)) over two orders of magnitude, ranging from 1.1 (phenytoin) to 222.9 (lovastatin) in a receptor-supplemented system and it is proposed that the lack of response to pravastatin is due to loss of the known hepatic uptake transporter in HepG2 cells. Lovastatin 222-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 12433810-2 2002 Treatment of 2- to 3-day-old human hepatocyte cultures with 3 x 10(-5) M lovastatin, simvastatin, fluvastatin, or atorvastatin for 24 h increased the amounts of CYP2B6 and CYP3A mRNA by an average of 3.8- to 9.2-fold and 24- to 36-fold, respectively. Lovastatin 73-83 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 161-167 12433810-2 2002 Treatment of 2- to 3-day-old human hepatocyte cultures with 3 x 10(-5) M lovastatin, simvastatin, fluvastatin, or atorvastatin for 24 h increased the amounts of CYP2B6 and CYP3A mRNA by an average of 3.8- to 9.2-fold and 24- to 36-fold, respectively. Lovastatin 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-177 12501010-3 2002 CRV similar to another statin, lovastatin (LOV), significantly inhibited PAI-1 expression and its release from endothelial cells, nonstimulated and stimulated with TNF-alpha. Lovastatin 31-41 serpin family E member 1 Homo sapiens 73-78 12501010-3 2002 CRV similar to another statin, lovastatin (LOV), significantly inhibited PAI-1 expression and its release from endothelial cells, nonstimulated and stimulated with TNF-alpha. Lovastatin 31-41 tumor necrosis factor Homo sapiens 164-173 12501010-3 2002 CRV similar to another statin, lovastatin (LOV), significantly inhibited PAI-1 expression and its release from endothelial cells, nonstimulated and stimulated with TNF-alpha. Lovastatin 43-46 serpin family E member 1 Homo sapiens 73-78 12501010-3 2002 CRV similar to another statin, lovastatin (LOV), significantly inhibited PAI-1 expression and its release from endothelial cells, nonstimulated and stimulated with TNF-alpha. Lovastatin 43-46 tumor necrosis factor Homo sapiens 164-173 12514251-5 2002 In addition, lovastatin lowered the transcription level of the ADP-glucose pyrophosphorylase small subunit (AgpS) gene. Lovastatin 13-23 glucose-1-phosphate adenylyltransferase small subunit, chloroplastic/amyloplastic-like Nicotiana tabacum 63-106 12514251-5 2002 In addition, lovastatin lowered the transcription level of the ADP-glucose pyrophosphorylase small subunit (AgpS) gene. Lovastatin 13-23 glucose-1-phosphate adenylyltransferase small subunit, chloroplastic/amyloplastic-like Nicotiana tabacum 108-112 12208479-10 2002 These results demonstrate that inhibition of cholesterol biosynthesis by lovastatin and simvastatin modifies the normal diurnal rhythm of cholesterol biosynthesis in female FH patients. Lovastatin 73-83 low density lipoprotein receptor Homo sapiens 173-175 12593493-12 2003 Lovastatin reduced (p < 0.01) TC (18.0%), LDL-C (22.6%), and (p < 0.05) triglycerides (9.8%). Lovastatin 0-10 component of oligomeric golgi complex 2 Homo sapiens 45-50 12429374-5 2002 Splenocytes from Lovastatin-treated EAE rats showed decreased levels of interferon-gamma, a Th1 type cytokine, while interleukin (IL)-10, a Th2 type cytokine, was markedly increased as compared to untreated EAE animals. Lovastatin 17-27 interferon gamma Rattus norvegicus 72-88 12429374-6 2002 In addition, we also observed reduced levels of IL-6 and nitric oxide production in lipopolysaccharide-stimulated splenocytes isolated from Lovastatin-treated animals. Lovastatin 140-150 interleukin 6 Rattus norvegicus 48-52 12427032-5 2002 Either FPP or GGPP completely prevents lovastatin-induced upregulation of RhoB mRNA. Lovastatin 39-49 ras homolog family member B Homo sapiens 74-78 12412808-3 2002 Additionally, oral simvastatin and lovastatin increased the cancellous bone volume in rats, presumably an effect of the increase of BMP-2. Lovastatin 35-45 bone morphogenetic protein 2 Rattus norvegicus 132-137 12534147-1 2002 We assessed the short and long-term efficacy and safety of the lipid lowering drugs, nicotinic acid, and the HMG-CoA reductase inhibitor, lovastatin, in combination with cholestyramine in four renal transplant patients. Lovastatin 138-148 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 109-126 12526087-5 2002 Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. Lovastatin 18-28 signal transducer and activator of transcription 1 Homo sapiens 149-154 12526087-6 2002 In cells treated with lovastatin and IFN-gamma, ICAM-1 was expressed at a lower level than in cells treated with IFN-gamma alone. Lovastatin 22-32 intercellular adhesion molecule 1 Homo sapiens 48-54 12526087-6 2002 In cells treated with lovastatin and IFN-gamma, ICAM-1 was expressed at a lower level than in cells treated with IFN-gamma alone. Lovastatin 22-32 interferon gamma Homo sapiens 113-122 12526087-11 2002 But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1. Lovastatin 4-14 interferon gamma Homo sapiens 32-41 12526087-11 2002 But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1. Lovastatin 4-14 mitogen-activated protein kinase 3 Homo sapiens 70-74 12526087-11 2002 But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1. Lovastatin 4-14 mitogen-activated protein kinase 1 Homo sapiens 75-79 12526087-11 2002 But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1. Lovastatin 4-14 signal transducer and activator of transcription 1 Homo sapiens 120-125 12235235-0 2002 Potent suppression of proliferation of a10 vascular smooth muscle cells by combined treatment with lovastatin and 3-allylfarnesol, an inhibitor of protein farnesyltransferase. Lovastatin 99-109 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 39-42 12434292-8 2002 In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells. Lovastatin 39-49 H3 histone pseudogene 16 Homo sapiens 82-85 12434292-8 2002 In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells. Lovastatin 39-49 KRAS proto-oncogene, GTPase Homo sapiens 156-161 12384940-6 2002 RESULTS: Lovastatin induced a 15-fold rise in IL-1beta secretion by normal anti-CD2 + CD28-stimulated cells (P < 0.001). Lovastatin 9-19 interleukin 1 beta Homo sapiens 46-54 12384940-6 2002 RESULTS: Lovastatin induced a 15-fold rise in IL-1beta secretion by normal anti-CD2 + CD28-stimulated cells (P < 0.001). Lovastatin 9-19 CD2 molecule Homo sapiens 80-83 12384940-6 2002 RESULTS: Lovastatin induced a 15-fold rise in IL-1beta secretion by normal anti-CD2 + CD28-stimulated cells (P < 0.001). Lovastatin 9-19 CD28 molecule Homo sapiens 86-90 12384940-10 2002 The effect of lovastatin on IL-1beta secretion was reduced by mevalonate, FOH, and GGOH. Lovastatin 14-24 interleukin 1 beta Homo sapiens 28-36 12235235-4 2002 We have therefore assayed the effect of lovastatin on both the growth of A10 vascular smooth muscle cells and the status of their Ras and RhoB proteins. Lovastatin 40-50 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 73-76 12235235-5 2002 We find that < or =1 microM lovastatin potently inhibits the proliferation of A10 cultures, and higher concentrations (> or =3 microM) induce apoptosis. Lovastatin 31-41 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 81-84 12235235-8 2002 We also find that lovastatin and 3-alFOH exhibit synergism to cause the up-regulation and relocalization of RhoB from the membrane to cytosolic compartments. Lovastatin 18-28 ras homolog family member B Homo sapiens 108-112 12235235-9 2002 This relocalization of RhoB, which is presumed to reflect an inhibition of its prenylation, correlates with the proapoptotic activities of combined 3-alFOH and lovastatin treatment. Lovastatin 160-170 ras homolog family member B Homo sapiens 23-27 12392621-6 2002 RESULTS: Addition of 0.1 to 50 micromol/L lovastatin into culture medium had no toxicity to hepatic stellate cells, but could significantly inhibit hepatic stellate cell proliferation and provoke G0/G1 phase arrest in dose-dependent manner, and could also markedly inhibit the c-jun and c-fos expression and type IV collagen and laminin secretion, which could partly be antagonized by geranyl geranypyrophosphate. Lovastatin 42-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 287-292 12239596-0 2002 The HMG-CoA reductase inhibitor lovastatin protects cells from the antineoplastic drugs doxorubicin and etoposide. Lovastatin 32-42 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-21 12119193-0 2002 Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-alpha activated human vascular endothelial cells. Lovastatin 0-10 selectin E Homo sapiens 40-50 12119193-0 2002 Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-alpha activated human vascular endothelial cells. Lovastatin 0-10 intercellular adhesion molecule 1 Homo sapiens 52-58 12119193-0 2002 Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-alpha activated human vascular endothelial cells. Lovastatin 0-10 vascular cell adhesion molecule 1 Homo sapiens 63-69 12119193-0 2002 Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-alpha activated human vascular endothelial cells. Lovastatin 0-10 tumor necrosis factor Homo sapiens 73-82 12119193-7 2002 The lovastatin-potentiated increase of E-selectin and CAMs is correlated with a corresponding increase of selectin- and CAM-specific mRNA. Lovastatin 4-14 selectin E Homo sapiens 39-49 12106604-0 2002 Alterations in membrane-bound and cytoplasmic K-ras protein levels in mouse lung induced by treatment with lovastatin, cholestyramine, or niacin: effects are highly mouse strain dependent. Lovastatin 107-117 Kirsten rat sarcoma viral oncogene homolog Mus musculus 46-51 12196129-6 2002 In humans, lovastatin, an HMG-CoA reductase inhibitor, has been shown to reduce A beta levels in blood of patients by up to 40%. Lovastatin 11-21 amyloid beta precursor protein Homo sapiens 80-86 12048122-9 2002 Comparative studies of simvastatin and lovastatin indicated a differential ability to induce apoAI synthesis and secretion, with simvastatin having a more significant effect. Lovastatin 39-49 apolipoprotein A1 Homo sapiens 93-98 12174823-0 2002 Lovastatin increases longitudinal bone growth and bone morphogenetic protein-2 levels in the growth plate of Sprague-Dawley rats. Lovastatin 0-10 bone morphogenetic protein 2 Rattus norvegicus 50-78 12082550-10 2002 Because rhoA requires GGPP for its function, this links the microarray and biochemical data and identifies rhoA as a potential mediator of the anticancer properties of lovastatin. Lovastatin 168-178 ras homolog family member A Homo sapiens 8-12 12115596-2 2002 Lovastatin has also been proved to potentiate antitumor effects of both cisplatin and TNF-alpha in murine melanoma models. Lovastatin 0-10 tumor necrosis factor Mus musculus 86-95 12115596-6 2002 In the present report, we supplement our preliminary observations and demonstrate in 2 murine and 2 human melanoma cell lines that lovastatin effectively potentiates the cytostatic/cytotoxic activity of doxorubicin in vitro via an augmentation of apoptosis (estimated with PARP-cleavage assay, annexin V assay and TUNEL). Lovastatin 131-141 collagen type XI alpha 2 chain Homo sapiens 273-277 12115596-6 2002 In the present report, we supplement our preliminary observations and demonstrate in 2 murine and 2 human melanoma cell lines that lovastatin effectively potentiates the cytostatic/cytotoxic activity of doxorubicin in vitro via an augmentation of apoptosis (estimated with PARP-cleavage assay, annexin V assay and TUNEL). Lovastatin 131-141 annexin A5 Homo sapiens 294-303 12094262-5 2002 This effect was not the consequence of a change in the protein expression levels of Bcl-2 or Bax induced by lovastatin. Lovastatin 108-118 BCL2 associated X, apoptosis regulator Homo sapiens 93-96 12094262-8 2002 The cytotoxic activity of lovastatin was higher in Pgp expressing cell lines, but did not correlate with the multidrug resistance (MDR)-related proteins LRP, Bcl-2 and Bax. Lovastatin 26-36 phosphoglycolate phosphatase Homo sapiens 51-54 12066225-3 2002 The aim of the present study was to examine the bFGF-induced growth inhibition in the presence of lovastatin, a farnesyl transferase inhibitor, which impaired ras signaling by preventing its association with the plasma membrane. Lovastatin 98-108 fibroblast growth factor 2 Homo sapiens 48-52 12066226-7 2002 Combination of a specific COX-2 inhibitor, MF-tricyclic, may increase antiproliferative effects of lovastatin in colon cancer cells and this effect was due to an augmented apoptosis. Lovastatin 99-109 cytochrome c oxidase II, mitochondrial Mus musculus 26-31 12082550-10 2002 Because rhoA requires GGPP for its function, this links the microarray and biochemical data and identifies rhoA as a potential mediator of the anticancer properties of lovastatin. Lovastatin 168-178 ras homolog family member A Homo sapiens 107-111 11888511-2 2002 We report that mevinolin and mevastatin, two inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase are able to completely abolish the vasoactive properties of A beta in rat aortae. Lovastatin 15-24 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 102-120 12008177-0 2002 Comparison of effect of intensive lipid lowering with atorvastatin to less intensive lowering with lovastatin on C-reactive protein in patients with stable angina pectoris and inducible myocardial ischemia. Lovastatin 99-109 C-reactive protein Homo sapiens 113-131 11875067-4 2002 We report that inhibition of Rho, by either lovastatin or C3 exoenzyme, can increase the translational efficiency of p27 mRNA. Lovastatin 44-54 interferon alpha inducible protein 27 Homo sapiens 117-120 11978159-2 2002 CASE REPORT: Rhabdomyolysis occurring in transplant patients receiving both cyclosporine and the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin has been well documented. Lovastatin 160-170 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 97-149 12125979-4 2002 The temporal expression of Nedd5 in U373 astrocytoma cells at various timepoints throughout the cell cycle was determined by an analysis of lovastatin- and nocodazole-treated, synchronized cell populations. Lovastatin 140-150 septin 2 Homo sapiens 27-32 11888511-2 2002 We report that mevinolin and mevastatin, two inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase are able to completely abolish the vasoactive properties of A beta in rat aortae. Lovastatin 15-24 amyloid beta precursor protein Rattus norvegicus 181-187 11888511-3 2002 Mevinolin also appears to oppose the increased vascular reactivity to ET-1 induced by interleukin 1-beta and phospholipase A(2) suggesting that statins display some anti-inflammatory properties. Lovastatin 0-9 endothelin 1 Rattus norvegicus 70-74 11888511-3 2002 Mevinolin also appears to oppose the increased vascular reactivity to ET-1 induced by interleukin 1-beta and phospholipase A(2) suggesting that statins display some anti-inflammatory properties. Lovastatin 0-9 interleukin 1 beta Rattus norvegicus 86-104 11888511-3 2002 Mevinolin also appears to oppose the increased vascular reactivity to ET-1 induced by interleukin 1-beta and phospholipase A(2) suggesting that statins display some anti-inflammatory properties. Lovastatin 0-9 phospholipase A2 group IB Rattus norvegicus 109-127 11888511-4 2002 We show that freshly solubilized A beta stimulates prostaglandin E(2) and F(2 alpha) production (by 6 and 3.6 times, respectively) in isolated rat aortae and that mevinolin completely antagonizes this effect confirming the anti-inflammatory action of mevinolin ex vivo in rat aortae. Lovastatin 163-172 amyloid beta precursor protein Rattus norvegicus 33-39 11888511-4 2002 We show that freshly solubilized A beta stimulates prostaglandin E(2) and F(2 alpha) production (by 6 and 3.6 times, respectively) in isolated rat aortae and that mevinolin completely antagonizes this effect confirming the anti-inflammatory action of mevinolin ex vivo in rat aortae. Lovastatin 251-260 amyloid beta precursor protein Rattus norvegicus 33-39 11900994-10 2002 Our results suggest a mechanism by which hypercholesterolemia may increase risk for AD and indicate that lovastatin reduces Abeta formation and may thereby be effective in delaying the onset and/or slowing the progression of AD. Lovastatin 105-115 amyloid beta precursor protein Homo sapiens 124-129 11894121-12 2002 These findings further support the hypothesis that HMGCo-R and COX-2 activities play important roles in apoptosis and regulation of apoptosis by selective agents such as lovastatin and celecoxib would provide effective strategies for the prevention of colon cancer. Lovastatin 170-180 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 11696371-1 2001 Lovastatin treatment caused down-regulation of the insulin-responsive glucose transporter 4 (Glut4) and up-regulation of Glut1 in 3T3-L1 adipocytes. Lovastatin 0-10 insulin Homo sapiens 51-58 11884371-0 2002 Lovastatin enhances ecto-5"-nucleotidase activity and cell surface expression in endothelial cells: implication of rho-family GTPases. Lovastatin 0-10 5'-nucleotidase ecto Homo sapiens 20-40 11884371-4 2002 Lovastatin enhanced Ecto-5"-Nu activity in a dose-dependent manner. Lovastatin 0-10 5'-nucleotidase ecto Homo sapiens 20-30 11884371-6 2002 By contrast, lovastatin enhanced cell surface expression of Ecto-5"-Nu and decreased endocytosis of Ecto-5"-Nu, as evidenced by immunostaining. Lovastatin 13-23 5'-nucleotidase ecto Homo sapiens 60-70 11884371-6 2002 By contrast, lovastatin enhanced cell surface expression of Ecto-5"-Nu and decreased endocytosis of Ecto-5"-Nu, as evidenced by immunostaining. Lovastatin 13-23 5'-nucleotidase ecto Homo sapiens 100-110 11884371-9 2002 Stimulation of Ecto-5"-Nu by lovastatin enhanced the inhibition of platelet aggregation induced by endothelial cells. Lovastatin 29-39 tripartite motif containing 33 Homo sapiens 15-19 11884371-10 2002 In conclusion, lovastatin enhances Ecto-5"-Nu activity and membrane expression in endothelial cells. Lovastatin 15-25 5'-nucleotidase ecto Homo sapiens 35-45 11902809-5 2002 In conclusion, simvastatin and lovastatin are susceptible to interaction with or via MDR1, but pravastatin is not. Lovastatin 31-41 ATP-binding cassette, sub-family B (MDR/TAP), member 1 Sus scrofa 85-89 11884211-12 2002 Addition of lovastatin as a complementary therapy to HRT revealed a significant 27% increment in HDLC and 48% decrement in CRP concentrations. Lovastatin 12-22 C-reactive protein Rattus norvegicus 123-126 11908910-2 2002 Treatment of cells with lovastatin, a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, depletes cells of mevalonic acid and thus blocks the isoprenylation of proteins in the RAS superfamily. Lovastatin 24-34 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 38-90 12429913-6 2002 Both simvastatin and lovastatin significantly augmented TRAIL-induced apoptosis in tumor cells, but not in normal keratinocytes. Lovastatin 21-31 TNF superfamily member 10 Homo sapiens 56-61 11879577-8 2002 The increased steroid hormone production in mutant K-ras-transfected cells was reversed by lovastatin, a pharmacologic inhibitor of p21ras function. Lovastatin 91-101 KRAS proto-oncogene, GTPase Homo sapiens 51-56 11879577-8 2002 The increased steroid hormone production in mutant K-ras-transfected cells was reversed by lovastatin, a pharmacologic inhibitor of p21ras function. Lovastatin 91-101 HRas proto-oncogene, GTPase Homo sapiens 132-138 11716532-8 2001 Wortmannin and LY294002, PI3-kinase inhibitors, as well as lovastatin and PD152440, Ras farnesylation inhibitors, and MEK inhibitor PD98059 abolished the insulin repression of ALAS transcription. Lovastatin 59-69 insulin Homo sapiens 154-161 11716532-8 2001 Wortmannin and LY294002, PI3-kinase inhibitors, as well as lovastatin and PD152440, Ras farnesylation inhibitors, and MEK inhibitor PD98059 abolished the insulin repression of ALAS transcription. Lovastatin 59-69 5'-aminolevulinate synthase 1 Homo sapiens 176-180 11728391-3 2001 Atorvastatin and lovastatin increased low-density lipoprotein receptor mRNA (2.5-fold at 3 x 10(-7) M) and the transcription rate at the promoter of the low-density lipoprotein receptor gene (>5-fold at 10(-6) M). Lovastatin 17-27 low density lipoprotein receptor Homo sapiens 38-70 11728391-3 2001 Atorvastatin and lovastatin increased low-density lipoprotein receptor mRNA (2.5-fold at 3 x 10(-7) M) and the transcription rate at the promoter of the low-density lipoprotein receptor gene (>5-fold at 10(-6) M). Lovastatin 17-27 low density lipoprotein receptor Homo sapiens 153-185 11728391-5 2001 Atorvastatin and lovastatin increased the nuclear form of sterol regulatory element binding protein (SREBP)-2, but not of SREBP-1. Lovastatin 17-27 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 58-99 11728391-5 2001 Atorvastatin and lovastatin increased the nuclear form of sterol regulatory element binding protein (SREBP)-2, but not of SREBP-1. Lovastatin 17-27 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 101-106 11697864-1 2001 RNA from various mouse organs was analyzed by Northern hybridization to determine the response of squalene synthase (SQS) mRNA to dietary cholesterol, or lovastatin and cholestyramine, administration. Lovastatin 154-164 farnesyl diphosphate farnesyl transferase 1 Mus musculus 98-115 11697864-1 2001 RNA from various mouse organs was analyzed by Northern hybridization to determine the response of squalene synthase (SQS) mRNA to dietary cholesterol, or lovastatin and cholestyramine, administration. Lovastatin 154-164 farnesyl diphosphate farnesyl transferase 1 Mus musculus 117-120 11900994-0 2002 Pharmacological concentrations of the HMG-CoA reductase inhibitor lovastatin decrease the formation of the Alzheimer beta-amyloid peptide in vitro and in patients. Lovastatin 66-76 amyloid beta precursor protein Homo sapiens 117-137 11902809-0 2002 Simvastatin and lovastatin, but not pravastatin, interact with MDR1. Lovastatin 16-26 ATP-binding cassette, sub-family B (MDR/TAP), member 1 Sus scrofa 63-67 11890736-6 2002 Pretreatment of the neural cells with lovastatin, an inhibitor of p21(ras) signaling, greatly inhibited the accumulation of p53 induced by SIN-1. Lovastatin 38-48 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 66-69 11890736-6 2002 Pretreatment of the neural cells with lovastatin, an inhibitor of p21(ras) signaling, greatly inhibited the accumulation of p53 induced by SIN-1. Lovastatin 38-48 transformation related protein 53, pseudogene Mus musculus 124-127 11890736-6 2002 Pretreatment of the neural cells with lovastatin, an inhibitor of p21(ras) signaling, greatly inhibited the accumulation of p53 induced by SIN-1. Lovastatin 38-48 mitogen-activated protein kinase associated protein 1 Mus musculus 139-144 11857349-5 2002 These effects were at least in part due to apoptosis induction that occurred after 12 hr of incubation with lovastatin and butyrate and was preceded by changes in cell cycle distribution of treated cells and expression of p21, p53 and cyclin D1. Lovastatin 108-118 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 222-225 11857349-5 2002 These effects were at least in part due to apoptosis induction that occurred after 12 hr of incubation with lovastatin and butyrate and was preceded by changes in cell cycle distribution of treated cells and expression of p21, p53 and cyclin D1. Lovastatin 108-118 transformation related protein 53, pseudogene Mus musculus 227-230 11857349-5 2002 These effects were at least in part due to apoptosis induction that occurred after 12 hr of incubation with lovastatin and butyrate and was preceded by changes in cell cycle distribution of treated cells and expression of p21, p53 and cyclin D1. Lovastatin 108-118 cyclin D1 Mus musculus 235-244 11839370-5 2002 We therefore hypothesize that the addition of lovastatin caused an increase in plasma quetiapine levels through competitive inhibition of the cytochrome P(450) (CYP) isoenzyme 3A4. Lovastatin 46-56 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 142-159 11839370-5 2002 We therefore hypothesize that the addition of lovastatin caused an increase in plasma quetiapine levels through competitive inhibition of the cytochrome P(450) (CYP) isoenzyme 3A4. Lovastatin 46-56 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 161-164 11840288-8 2002 Not surprisingly, lovastatin also induces G0/G1 arrest and apoptosis in Bcr/Abl-transformed cells, however, TPA protects cells from both apoptosis and G0/G1 arrest caused by lovastatin. Lovastatin 18-28 BCR activator of RhoGEF and GTPase Homo sapiens 72-75 11840288-9 2002 Thus, in Bcr/Abl-transformed cells, POH and lovastatin cause growth arrest by different mechanisms. Lovastatin 44-54 BCR activator of RhoGEF and GTPase Homo sapiens 9-12 14727985-10 2002 Simvastatin and lovastatin are significantly metabolized by cytochrome P450 enzymes (CYP3A4) and are therefore not recommended for coadministration with protease inhibitors. Lovastatin 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 11786505-9 2002 Only simvastatin and lovastatin increased t-PA production in endothelial cells. Lovastatin 21-31 plasminogen activator, tissue type Homo sapiens 42-46 11779217-4 2002 Using cells stably transfected with a cyclin B1 promoter-luciferase reporter, luciferase activity was measured throughout the cell cycle in lovastatin synchronized cells and in G1 and S/G2 phases of asynchronized cells by flow cytometry. Lovastatin 140-150 cyclin B1 Homo sapiens 38-47 12405293-10 2002 In addition, lovastatin induced a dose-dependent inhibition in the secretion of urokinase, a key proteolytic enzyme during tumor invasion and metastasis, and a significant increase of tissue-type plasminogen activator, a marker of good prognosis in mammary cancer. Lovastatin 13-23 plasminogen activator, tissue Mus musculus 184-217 11995814-4 2002 In this study, we evaluated lovastatin effects on meningioma cell proliferation and activation of the MEK-1-MAPK/ERK pathway. Lovastatin 28-38 mitogen-activated protein kinase kinase 1 Homo sapiens 102-107 11995814-4 2002 In this study, we evaluated lovastatin effects on meningioma cell proliferation and activation of the MEK-1-MAPK/ERK pathway. Lovastatin 28-38 mitogen-activated protein kinase 1 Homo sapiens 108-112 11995814-4 2002 In this study, we evaluated lovastatin effects on meningioma cell proliferation and activation of the MEK-1-MAPK/ERK pathway. Lovastatin 28-38 mitogen-activated protein kinase 1 Homo sapiens 113-116 11995814-6 2002 Concomitant lovastatin effects on phosphorylation/activation of mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) kinase (MEK-1) and MAPK/ERK were assessed by Western blot. Lovastatin 12-22 mitogen-activated protein kinase 1 Homo sapiens 141-144 11995814-6 2002 Concomitant lovastatin effects on phosphorylation/activation of mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) kinase (MEK-1) and MAPK/ERK were assessed by Western blot. Lovastatin 12-22 mitogen-activated protein kinase kinase 1 Homo sapiens 154-159 11995814-6 2002 Concomitant lovastatin effects on phosphorylation/activation of mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) kinase (MEK-1) and MAPK/ERK were assessed by Western blot. Lovastatin 12-22 mitogen-activated protein kinase 1 Homo sapiens 136-140 11995814-6 2002 Concomitant lovastatin effects on phosphorylation/activation of mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) kinase (MEK-1) and MAPK/ERK were assessed by Western blot. Lovastatin 12-22 mitogen-activated protein kinase 1 Homo sapiens 170-173 11995814-10 2002 Concomitant with its growth inhibitory effects, lovastatin reduced phosphorylation/activation of MEK-1/2 in five meningiomas and MAPK/ERK in seven. Lovastatin 48-58 mitogen-activated protein kinase kinase 1 Homo sapiens 97-104 11995814-12 2002 Lovastatin is a potent inhibitor of meningioma cell proliferation which may act in part by reducing activation of MEK-1-MAPK/ERK pathway. Lovastatin 0-10 mitogen-activated protein kinase kinase 1 Homo sapiens 114-119 11995814-12 2002 Lovastatin is a potent inhibitor of meningioma cell proliferation which may act in part by reducing activation of MEK-1-MAPK/ERK pathway. Lovastatin 0-10 mitogen-activated protein kinase 1 Homo sapiens 120-124 11995814-12 2002 Lovastatin is a potent inhibitor of meningioma cell proliferation which may act in part by reducing activation of MEK-1-MAPK/ERK pathway. Lovastatin 0-10 mitogen-activated protein kinase 1 Homo sapiens 125-128 11591701-6 2001 Treatment of cells with 25 microm mevastatin or lovastatin resulted in the induction of COX-2 and increase in prostacyclin production. Lovastatin 48-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 12467231-1 2001 The hydroxymethylglutaryl-CoA reductase inhibitor lovastatin is used widely to treat hypercholesterolemia and has been shown to have cell cycle-specific effects. Lovastatin 50-60 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-39 12467231-5 2001 In addition, Annexin V apoptotic studies revealed that lovastatin enhances paclitaxel-induced apoptosis in HL-60 cells. Lovastatin 55-65 annexin A5 Homo sapiens 13-22 12467231-7 2001 Whereas lovastatin induced an accumulation of unmodified Ras and caused an up-regulation of both RhoB and Rap1A, paclitaxel was found to have no effect on the isoprenylated proteins. Lovastatin 8-18 ras homolog family member B Homo sapiens 97-101 12467231-7 2001 Whereas lovastatin induced an accumulation of unmodified Ras and caused an up-regulation of both RhoB and Rap1A, paclitaxel was found to have no effect on the isoprenylated proteins. Lovastatin 8-18 RAP1A, member of RAS oncogene family Homo sapiens 106-111 12467231-8 2001 Studies of the centromere-associated protein mitosin revealed that treatment with lovastatin and paclitaxel resulted in increased mitosin levels and that lovastatin altered the association of mitosin with condensed chromosomes. Lovastatin 82-92 centromere protein F Homo sapiens 45-52 12467231-8 2001 Studies of the centromere-associated protein mitosin revealed that treatment with lovastatin and paclitaxel resulted in increased mitosin levels and that lovastatin altered the association of mitosin with condensed chromosomes. Lovastatin 82-92 centromere protein F Homo sapiens 130-137 12467231-8 2001 Studies of the centromere-associated protein mitosin revealed that treatment with lovastatin and paclitaxel resulted in increased mitosin levels and that lovastatin altered the association of mitosin with condensed chromosomes. Lovastatin 82-92 centromere protein F Homo sapiens 130-137 12467231-8 2001 Studies of the centromere-associated protein mitosin revealed that treatment with lovastatin and paclitaxel resulted in increased mitosin levels and that lovastatin altered the association of mitosin with condensed chromosomes. Lovastatin 154-164 centromere protein F Homo sapiens 45-52 12901109-6 2001 RESULTS: Both lovastatin and CsA inhibited PBMC proliferation, expression of IL-2 and IFN-gamma, and NK cell cytotoxicity in a dose-dependent manner. Lovastatin 14-24 interleukin 2 Homo sapiens 77-81 12901109-6 2001 RESULTS: Both lovastatin and CsA inhibited PBMC proliferation, expression of IL-2 and IFN-gamma, and NK cell cytotoxicity in a dose-dependent manner. Lovastatin 14-24 interferon gamma Homo sapiens 86-95 11696371-1 2001 Lovastatin treatment caused down-regulation of the insulin-responsive glucose transporter 4 (Glut4) and up-regulation of Glut1 in 3T3-L1 adipocytes. Lovastatin 0-10 solute carrier family 2 member 4 Homo sapiens 93-98 11696371-1 2001 Lovastatin treatment caused down-regulation of the insulin-responsive glucose transporter 4 (Glut4) and up-regulation of Glut1 in 3T3-L1 adipocytes. Lovastatin 0-10 solute carrier family 2 member 1 Homo sapiens 121-126 11696371-3 2001 Lovastatin had no effect on cell cholesterol levels, but its effects were reversed by mevalonate, demonstrating that inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes. Lovastatin 0-10 insulin Homo sapiens 162-169 11720089-12 2001 In contrast, lovastatin exhibited an inhibitory effect on the plasma and hepatic lipid peroxidation and increased the hepatic catalase activity in high-cholesterol fed rabbits. Lovastatin 13-23 catalase Oryctolagus cuniculus 126-134 11720089-5 2001 The naringin supplementation significantly increased the activities of both hepatic SOD and catalase by 33% and 20%, respectively, whereas the lovastatin supplementation only increased the catalase activity by 23% compared to control group. Lovastatin 143-153 catalase Oryctolagus cuniculus 189-197 11729502-0 2001 Lovastatin increases nitric oxide synthesis in IL-1 beta-stimulated smooth muscle cells. Lovastatin 0-10 interleukin 1 beta Rattus norvegicus 47-56 11729502-6 2001 RESULTS: Lovastatin (10(-5) mol/L) significantly increased interleukin-1 beta (IL-1 beta, 10 ng/mL)-induced nitrite accumulation in a time (0-24 hours)-dependent manner. Lovastatin 9-19 interleukin 1 beta Rattus norvegicus 59-77 11729502-6 2001 RESULTS: Lovastatin (10(-5) mol/L) significantly increased interleukin-1 beta (IL-1 beta, 10 ng/mL)-induced nitrite accumulation in a time (0-24 hours)-dependent manner. Lovastatin 9-19 interleukin 1 beta Rattus norvegicus 79-88 11729502-8 2001 Furthermore, inhibition of Rho by C3 exoenzyme mimicked the increase in IL-1 beta-induced nitrite accumulation induced by lovastatin in the vascular smooth muscle cells. Lovastatin 122-132 interleukin 1 beta Rattus norvegicus 72-81 11729502-9 2001 CONCLUSION: These results demonstrate that lovastatin up-regulates NO formation in rat vascular smooth muscle cells stimulated by IL-1 beta, and the effect may be associated with the inhibition of Rho activity. Lovastatin 43-53 interleukin 1 beta Rattus norvegicus 130-139 11720884-0 2001 Lovastatin-induced apoptosis in thyroid cells: involvement of cytochrome c and lamin B. Lovastatin 0-10 cytochrome c, somatic Homo sapiens 62-74 11720884-1 2001 OBJECTIVE: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin, induces apoptosis in the thyroid cell line TAD-2 and in proliferating normal human thyroid cells in culture, through a p53-independent mechanism involving caspase-3-like proteases. Lovastatin 74-84 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 15-62 11720884-1 2001 OBJECTIVE: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin, induces apoptosis in the thyroid cell line TAD-2 and in proliferating normal human thyroid cells in culture, through a p53-independent mechanism involving caspase-3-like proteases. Lovastatin 74-84 adenosine deaminase tRNA specific 2 Homo sapiens 129-134 11720884-1 2001 OBJECTIVE: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin, induces apoptosis in the thyroid cell line TAD-2 and in proliferating normal human thyroid cells in culture, through a p53-independent mechanism involving caspase-3-like proteases. Lovastatin 74-84 tumor protein p53 Homo sapiens 205-208 11720884-1 2001 OBJECTIVE: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin, induces apoptosis in the thyroid cell line TAD-2 and in proliferating normal human thyroid cells in culture, through a p53-independent mechanism involving caspase-3-like proteases. Lovastatin 74-84 caspase 3 Homo sapiens 241-250 11720884-4 2001 Based on this premise, we analyzed in more detail the role of some molecular effectors and the role of the caspase family proteases in the lovastatin-induced apoptotic pathway in TAD-2 cells. Lovastatin 139-149 adenosine deaminase tRNA specific 2 Homo sapiens 179-184 11720884-5 2001 METHODS: TAD-2 cells were treated with lovastatin to induce apoptosis, and expression of p53, Bc1-2, Bcl-XL and Bax was analyzed by Western blot. Lovastatin 39-49 adenosine deaminase tRNA specific 2 Homo sapiens 9-14 11592110-2 2001 We report that Lovastatin treatment blocks the clinical disease and induction of inflammatory cytokines and iNOS in spinal cords of MBP induced EAE rats. Lovastatin 15-25 nitric oxide synthase 2 Rattus norvegicus 108-112 11720884-12 2001 CONCLUSIONS: These data demonstrate that, in TAD-2 thyroid cells, lovastatin induces lamin B proteolysis and inhibits its nuclear localization and induces cytochrome c release from mitochondria into the cytosol. Lovastatin 66-76 adenosine deaminase tRNA specific 2 Homo sapiens 45-50 11720884-12 2001 CONCLUSIONS: These data demonstrate that, in TAD-2 thyroid cells, lovastatin induces lamin B proteolysis and inhibits its nuclear localization and induces cytochrome c release from mitochondria into the cytosol. Lovastatin 66-76 cytochrome c, somatic Homo sapiens 155-167 11711492-7 2001 Similarly, simvastatin and lovastatin (34 micromol/L) caused robust upregulation of the iNOS protein level. Lovastatin 27-37 nitric oxide synthase 2 Homo sapiens 88-92 11592110-2 2001 We report that Lovastatin treatment blocks the clinical disease and induction of inflammatory cytokines and iNOS in spinal cords of MBP induced EAE rats. Lovastatin 15-25 myelin basic protein Rattus norvegicus 132-135 11592110-5 2001 The data presented here documents that Lovastatin treatment attenuates the transmigration of mononuclear cells possibly by down regulating the expression of LFA-1, a ligand for ICAM, in endothelial-leukocyte interaction. Lovastatin 39-49 integrin subunit alpha L Rattus norvegicus 157-162 11592110-5 2001 The data presented here documents that Lovastatin treatment attenuates the transmigration of mononuclear cells possibly by down regulating the expression of LFA-1, a ligand for ICAM, in endothelial-leukocyte interaction. Lovastatin 39-49 intercellular adhesion molecule 1 Rattus norvegicus 177-181 11590226-15 2001 In contrast, if the cells were depleted of cholesterol by incubating them with lovastatin and cyclodextrin, the mature forms of SREBP-1 and SREBP-2 were increased, as were mRNA levels for the sterol-responsive genes. Lovastatin 79-89 sterol regulatory element binding transcription factor 1 Homo sapiens 128-135 11577016-0 2001 Lovastatin-induced E2F-1 modulation and its effect on prostate cancer cell death. Lovastatin 0-10 E2F transcription factor 1 Homo sapiens 19-24 11577016-1 2001 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, induces growth arrest in a variety of cancer cell lines. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-71 11577016-4 2001 We have shown in this study that transcriptional regulation and proteasomal degradation of E2F-1 are critical regulatory events in lovastatin-induced cell death. Lovastatin 131-141 E2F transcription factor 1 Homo sapiens 91-96 11577016-7 2001 Although expression of E2F-1 was reduced in three prostate cancer cell lines-PC-3, LNCaP and DU-145-the p21 and p27 protein levels were not increased in all the cell lines treated, suggesting that increase in p21 and p27 protein expression per se is not responsible for lovastatin-mediated down-regulation of E2F-1. Lovastatin 270-280 E2F transcription factor 1 Homo sapiens 23-28 11577016-8 2001 The subsequent apoptotic death of these cells in the presence of lovastatin can be prevented by forced ectopic expression of E2F-1. Lovastatin 65-75 E2F transcription factor 1 Homo sapiens 125-130 11590226-15 2001 In contrast, if the cells were depleted of cholesterol by incubating them with lovastatin and cyclodextrin, the mature forms of SREBP-1 and SREBP-2 were increased, as were mRNA levels for the sterol-responsive genes. Lovastatin 79-89 sterol regulatory element binding transcription factor 2 Homo sapiens 140-147 11516100-7 2001 In support of this hypothesis, the geranylgeranyl transferase inhibitor (GGTI-298) mimicked the effect of lovastatin, whereas the farnesyl transferase inhibitor (FTI-277) was much less effective at triggering apoptosis in AML cells. Lovastatin 106-116 protein geranylgeranyltransferase type I subunit beta Homo sapiens 73-77 11487529-3 2001 Incubation of the cells with simvastatin or lovastatin time-dependently and reversibly changed cell morphology and the actin cytoskeleton with maximal effects observed after about 18 h. Within the same time period, statins reduced the basal expression of CTGF and interfered with CTGF induction by lysophosphatidic acid (LPA) or transforming growth factor beta. Lovastatin 44-54 cellular communication network factor 2 Homo sapiens 255-259 11487529-3 2001 Incubation of the cells with simvastatin or lovastatin time-dependently and reversibly changed cell morphology and the actin cytoskeleton with maximal effects observed after about 18 h. Within the same time period, statins reduced the basal expression of CTGF and interfered with CTGF induction by lysophosphatidic acid (LPA) or transforming growth factor beta. Lovastatin 44-54 cellular communication network factor 2 Homo sapiens 280-284 11483865-1 2001 The effect of lovastatin, an inhibitor of 3-hydroxymethyl-3-glutaryl coenzyme A (HMG CoA) reductase, was examined on human vascular smooth muscle cells (HVSMC). Lovastatin 14-24 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 42-99 11160853-6 2001 Binucleation was also induced by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin and by the squalene synthase inhibitor zaragozic acid A and was prevented by adding low-density lipoprotein. Lovastatin 95-105 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 37-84 11438939-7 2001 Cholera toxin, stimulating Gs, and lovastatin, which blocks isoprenylation of Rho, reduced thrombin-induced calcium mobilization. Lovastatin 35-45 coagulation factor II, thrombin Homo sapiens 91-99 11438656-7 2001 Analysis on the expression pattern of NoBP mRNA throughout the cell cycle in HeLa cells synchronized by lovastatin demonstrated a substantial upregulation during the late G(1)/early S phase. Lovastatin 104-114 EBNA1 binding protein 2 Homo sapiens 38-42 11453651-8 2001 Lovastatin, an inhibitor of geranylgeranylation, also induced an accumulation of the acidic form of rab3D. Lovastatin 0-10 RAB3D, member RAS oncogene family Rattus norvegicus 100-105 11444504-5 2001 The lipophilic statins fluvastatin and lovastatin significantly increased interleukin-1beta-induced nitrite production by cardiac myocytes, whereas hydrophilic pravastatin did not. Lovastatin 39-49 interleukin 1 beta Rattus norvegicus 74-91 11430324-4 2001 METHODS: The level of C-reactive protein was measured at base line and after one year in 5742 participants in a five-year randomized trial of lovastatin for the primary prevention of acute coronary events. Lovastatin 142-152 C-reactive protein Homo sapiens 22-40 11430324-6 2001 Lovastatin therapy reduced the C-reactive protein level by 14.8 percent (P<0.001), an effect not explained by lovastatin-induced changes in the lipid profile. Lovastatin 0-10 C-reactive protein Homo sapiens 31-49 11430324-8 2001 However, lovastatin was also effective among those with a ratio of total to HDL cholesterol that was lower than the median and a C-reactive protein level higher than the median (number needed to treat, 43; P=0.02). Lovastatin 9-19 C-reactive protein Homo sapiens 129-147 11466161-0 2001 Treatment with controlled-release lovastatin decreases serum concentrations of human beta-amyloid (A beta) peptide. Lovastatin 34-44 amyloid beta precursor protein Homo sapiens 85-105 11466161-2 2001 Studies in vitro have shown that inhibiting cholesterol metabolism with lovastatin, or its active metabolite lovastatin acid, lowers A beta production. Lovastatin 72-82 amyloid beta precursor protein Homo sapiens 133-139 11309494-6 2001 Several mechanisms were elucidated as being the basis of enhanced alpha-secretase activity: increased membrane fluidity and impaired internalization of APP were responsible for the effect observed with methyl-beta-cyclodextrin; treatment with lovastatin resulted in higher expression of the alpha-secretase ADAM 10. Lovastatin 243-253 ADAM metallopeptidase domain 10 Homo sapiens 307-314 11368995-5 2001 Cholesterol 7alpha-hydroxylase activity was increased by lovastatin (11%) and by lovastatin plus TRF(25) (19%). Lovastatin 57-67 cytochrome P450 family 7 subfamily A member 1 Gallus gallus 0-30 11368995-5 2001 Cholesterol 7alpha-hydroxylase activity was increased by lovastatin (11%) and by lovastatin plus TRF(25) (19%). Lovastatin 81-91 cytochrome P450 family 7 subfamily A member 1 Gallus gallus 0-30 11368995-6 2001 TRF(25)+lovastatin decreased levels of serum total cholesterol (22%), LDL cholesterol (42%), apolipoprotein B (13-38%), triglycerides (19%), thromboxane B(2) (34%) and platelet factor 4 (26%), although high-density lipoprotein (HDL) cholesterol, and apolipoprotein A1 levels were unaffected. Lovastatin 8-18 apolipoprotein B Gallus gallus 93-109 11368995-6 2001 TRF(25)+lovastatin decreased levels of serum total cholesterol (22%), LDL cholesterol (42%), apolipoprotein B (13-38%), triglycerides (19%), thromboxane B(2) (34%) and platelet factor 4 (26%), although high-density lipoprotein (HDL) cholesterol, and apolipoprotein A1 levels were unaffected. Lovastatin 8-18 apolipoprotein AI Gallus gallus 250-267 11262181-3 2001 Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Lovastatin 87-97 tumor necrosis factor Homo sapiens 132-140 11262181-3 2001 Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Lovastatin 87-97 NFKB inhibitor alpha Homo sapiens 164-176 11262181-3 2001 Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Lovastatin 87-97 nuclear factor kappa B subunit 1 Homo sapiens 228-237 11322384-0 2001 Lovastatin blocks basic fibroblast growth factor-induced mitogen-activated protein kinase signaling in coronary smooth muscle cells via phosphatase inhibition. Lovastatin 0-10 fibroblast growth factor 2 Homo sapiens 18-48 11322384-2 2001 In this study, we investigated the effects of the 3hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin on bFGF-induced signal transduction in cSMC. Lovastatin 118-128 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 77-107 11322384-2 2001 In this study, we investigated the effects of the 3hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin on bFGF-induced signal transduction in cSMC. Lovastatin 118-128 fibroblast growth factor 2 Homo sapiens 132-136 11322384-3 2001 The present study shows that lovastatin inhibits bFGF-stimulated DNA synthesis in cSMC, and that this inhibition is reversed by mevalonate (50 micromol/l) and by geranylgeranyl-pyrophosphate (1-5 micromol/l). Lovastatin 29-39 fibroblast growth factor 2 Homo sapiens 49-53 11322384-4 2001 Although lovastatin prevented Ras farnesylation the amount of bFGF-stimulated MAPK phosphorylation decreased only partially after lovastatin treatment. Lovastatin 9-19 fibroblast growth factor 2 Homo sapiens 62-66 11322384-4 2001 Although lovastatin prevented Ras farnesylation the amount of bFGF-stimulated MAPK phosphorylation decreased only partially after lovastatin treatment. Lovastatin 130-140 fibroblast growth factor 2 Homo sapiens 62-66 11322384-8 2001 Lovastatin inhibited the expression of the PP-1 protein, which is involved in bFGF-induced DNA synthesis in cSMC. Lovastatin 0-10 inorganic pyrophosphatase 1 Homo sapiens 43-47 11322384-8 2001 Lovastatin inhibited the expression of the PP-1 protein, which is involved in bFGF-induced DNA synthesis in cSMC. Lovastatin 0-10 fibroblast growth factor 2 Homo sapiens 78-82 11322384-9 2001 Thus, our data suggest that, lovastatin possibly affects the dephosphorylation processes of PKC and MAPK by inhibition of PP-1/PP-2A protein phosphatases which are involved in the bFGF-induced mitogenesis in cSMC. Lovastatin 29-39 inorganic pyrophosphatase 1 Homo sapiens 122-126 11322384-9 2001 Thus, our data suggest that, lovastatin possibly affects the dephosphorylation processes of PKC and MAPK by inhibition of PP-1/PP-2A protein phosphatases which are involved in the bFGF-induced mitogenesis in cSMC. Lovastatin 29-39 protein phosphatase 2 phosphatase activator Homo sapiens 127-132 11322384-9 2001 Thus, our data suggest that, lovastatin possibly affects the dephosphorylation processes of PKC and MAPK by inhibition of PP-1/PP-2A protein phosphatases which are involved in the bFGF-induced mitogenesis in cSMC. Lovastatin 29-39 fibroblast growth factor 2 Homo sapiens 180-184 11226249-5 2001 Lovastatin, which binds under the conformationally mobile C-terminal alpha-helix of the I domain, inhibited binding to ICAM-1 by alphaLbeta2 with wild-type, but not locked-open I domains. Lovastatin 0-10 intercellular adhesion molecule 1 Homo sapiens 119-125 11215845-6 2001 The effects of four HMG-CoA reductase inhibitors (atorvastatin, lovastatin, simvastatin, pravastatin) on fibrinogen have been evaluated. Lovastatin 64-74 fibrinogen beta chain Homo sapiens 105-115 11215845-8 2001 This method also demonstrated that lovastatin use was associated with a 24.4% increase (p < 0.0001) in plasma fibrinogen concentration. Lovastatin 35-45 fibrinogen beta chain Homo sapiens 113-123 11178870-3 2001 Apoptosis was accompanied by a decrease in both Bcl-2 and Bcl-xL protein levels, suggesting that changes in the expression of these genes may contribute to apoptosis following lovastatin treatment. Lovastatin 176-186 BCL2, apoptosis regulator Rattus norvegicus 48-53 11178870-3 2001 Apoptosis was accompanied by a decrease in both Bcl-2 and Bcl-xL protein levels, suggesting that changes in the expression of these genes may contribute to apoptosis following lovastatin treatment. Lovastatin 176-186 Bcl2-like 1 Rattus norvegicus 58-64 11584328-7 2001 Several drugs have been shown to significantly inhibit the CYP3A4 pathway; in combination with statins such as lovastatin, simvastatin, atorvastatin, and cerivastatin, they have been shown to elevate serum concentrations of these statins, or may increase the risk of myopathy. Lovastatin 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 11406567-8 2001 The induction of cancer cell invasion by EGF was inhibited by the addition of fluvastatin or lovastatin in a dose-dependent manner. Lovastatin 93-103 epidermal growth factor Homo sapiens 41-44 11474784-6 2001 RESULTS: Lovastatin and simvastatin are very potent and effective inhibitors of P-gp transport with IC50"s of 26 and 9 microM, respectively, for the human enzyme. Lovastatin 9-19 phosphoglycolate phosphatase Homo sapiens 80-84 11380065-1 2001 OBJECTIVE: In order to suppress de novo cholesterol and VLDL biosynthesis, a long-term therapy trial with lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, was initiated in two patients with cholesteryl ester storage disease (CESD), and concentrations of plasma lipids were monitored over a period of 9 years. Lovastatin 106-116 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 145-202 11303752-0 2001 Differential effects of lovastatin treatment on brain cholesterol levels in normal and apoE-deficient mice. Lovastatin 24-34 apolipoprotein E Mus musculus 87-91 11309234-0 2001 The effects of the statins lovastatin and cerivastatin on signalling by the prostanoid IP-receptor. Lovastatin 27-37 prostaglandin I2 receptor Homo sapiens 76-98 11262181-4 2001 Furthermore, NF-kappaB-regulated gene expression stimulated by either UV irradiation or treatment with TNFalpha was abrogated by lovastatin pretreatment. Lovastatin 129-139 nuclear factor kappa B subunit 1 Homo sapiens 13-22 11262181-4 2001 Furthermore, NF-kappaB-regulated gene expression stimulated by either UV irradiation or treatment with TNFalpha was abrogated by lovastatin pretreatment. Lovastatin 129-139 tumor necrosis factor Homo sapiens 103-111 12214063-4 2001 To test the effects of altering cholesterol on Abeta formation, we incubated cells in the presence of lipid depleted serum, with or without the active metabolite of the HMG-CoA reductase inhibitor lovastatin. Lovastatin 197-207 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 169-186 11307620-3 2001 Lovastatin and phenylacetate promote p21 accumulation but fail to induce cell cycle arrest. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 37-40 11307620-4 2001 BCL-2 gene transfer inhibits apoptosis induced by lovastatin but not apoptosis induced by phenylacetate. Lovastatin 50-60 BCL2 apoptosis regulator Homo sapiens 0-5 11307620-5 2001 Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells. Lovastatin 37-47 tumor protein p53 Homo sapiens 10-13 11307620-5 2001 Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells. Lovastatin 37-47 tumor protein p53 Homo sapiens 69-72 11307620-5 2001 Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells. Lovastatin 37-47 tumor protein p53 Homo sapiens 69-72 11378962-1 2001 The fungal metabolite lovastatin and its derivatives are widely prescribed cholesterol-lowering drugs that act as potent inhibitors of (3S)-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMG-CoA reductase). Lovastatin 22-32 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 187-204 11475198-4 2001 RESULT: More than 50% of the overall CYP metabolism is mediated through the isoenzyme CYP3A4, which is the main elimination route of simvastatin, lovastatin and atorvastatin. Lovastatin 146-156 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 37-40 11475198-4 2001 RESULT: More than 50% of the overall CYP metabolism is mediated through the isoenzyme CYP3A4, which is the main elimination route of simvastatin, lovastatin and atorvastatin. Lovastatin 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 14728043-6 2001 Combination therapy with colesevelam plus hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (lovastatin, simvastatin or atorvastatin) was associated with additive reductions in serum levels of LDL-cholesterol and total cholesterol, relative to either agent alone. Lovastatin 107-117 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 42-94 12213976-0 2001 Lovastatin inhibits phenylephrine-induced ERK activation and growth of cardiac. Lovastatin 0-10 Eph receptor B1 Rattus norvegicus 42-45 11197581-12 2001 CONCLUSIONS: Macrolide antibiotics inhibit the metabolism of HMG-CoA reductase inhibitors that are metabolized by CYP3A4 (i.e., atorvastatin, cerivastatin, lovastatin, simvastatin). Lovastatin 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 11123852-6 2001 Thirdly, preliminary data with a single tablet formulation extended-release niacin and an HMG CoA reductase inhibitor (lovastatin) shows it to be safe and very effective, especially for raising HDL. Lovastatin 119-129 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 90-107 11144997-5 2001 Statistically significant decreases were also seen for total cholesterol and apolipoprotein B (apo B) with doses of 25 mg to 400 mg of SCH 48461 and lovastatin. Lovastatin 149-159 apolipoprotein B Homo sapiens 77-93 11074211-1 2000 The purpose of this study was to determine if long-term use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (atorvastatin, fluvastatin, lovastatin, pravastatin, or simvastatin) resulted in tachyphylaxis (a decreasing response to a physiologically active agent). Lovastatin 150-160 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-110 11162452-4 2000 Activation of phosphatidylinositol-4-phosphate 5-kinase and contraction of mesangial cell-embedded collagen gels in response to fibronectin and laminin were inhibited by pretreatment of mesangial cells with lovastatin and restored by isoprenoid augmentation with geranylgeraniol, supporting a role for the ras-related protein Rho in this process. Lovastatin 207-217 fibronectin 1 Homo sapiens 128-139 11426618-2 2000 Lovastatin, a competitive inhibitor of HMG-CoA reductase, induced a retinoic acid-like differentiation response followed by extensive apoptosis in neuroblastoma cell lines at relatively low concentrations (<20 microM) of this agent. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-56 11426618-6 2000 Lovastatin exposure induced increased expression of CD11b and CD18 markers similar to retinoic acid treatment. Lovastatin 0-10 integrin subunit alpha M Homo sapiens 52-57 11426618-6 2000 Lovastatin exposure induced increased expression of CD11b and CD18 markers similar to retinoic acid treatment. Lovastatin 0-10 integrin subunit beta 2 Homo sapiens 62-66 11426618-7 2000 Following 24 hrs exposure to 20 microM lovastatin, all 7 acute myeloid leukemia cell lines tested showed a decrease in bcl-2 mRNA expression while only 1/5 acute lymphocytic leukemia cell lines showed a similar response. Lovastatin 39-49 BCL2 apoptosis regulator Homo sapiens 119-124 11426618-8 2000 A role for bcl-2 in the apoptotic response of acute myeloid leukemia cells to lovastatin was demonstrated as exogenous constitutive expression of bcl-2 in the AML-5 cell line inhibited apoptosis in a time and dose dependent manner. Lovastatin 78-88 BCL2 apoptosis regulator Homo sapiens 11-16 11426618-8 2000 A role for bcl-2 in the apoptotic response of acute myeloid leukemia cells to lovastatin was demonstrated as exogenous constitutive expression of bcl-2 in the AML-5 cell line inhibited apoptosis in a time and dose dependent manner. Lovastatin 78-88 BCL2 apoptosis regulator Homo sapiens 146-151 11128243-6 2000 This assay was able to measure steady-state lovastatin concentration (Css) at the initial dose level in a phase I trial of lovastatin as a modulator of apoptosis. Lovastatin 44-54 cytidine monophosphate N-acetylneuraminic acid synthetase Homo sapiens 70-73 11128243-6 2000 This assay was able to measure steady-state lovastatin concentration (Css) at the initial dose level in a phase I trial of lovastatin as a modulator of apoptosis. Lovastatin 123-133 cytidine monophosphate N-acetylneuraminic acid synthetase Homo sapiens 70-73 10780669-5 2000 Second, blocking the Ras signal pathway in glioma cells by lovastatin or the Ha-rasAsn17 dominant-negative mutant gene resulted in reduced Fas-L expression. Lovastatin 59-69 Fas ligand Homo sapiens 139-144 11060356-9 2000 Maximum stimulation (4-fold) was seen in the presence LPL (1 microgram/ml) or HTGL (3 microgram/ml) in lovastatin-treated cells. Lovastatin 103-113 lipoprotein lipase Homo sapiens 54-57 11060356-9 2000 Maximum stimulation (4-fold) was seen in the presence LPL (1 microgram/ml) or HTGL (3 microgram/ml) in lovastatin-treated cells. Lovastatin 103-113 lipase C, hepatic type Homo sapiens 78-82 11060356-10 2000 On the other hand, degradation of apoE-depleted VLDL was not significantly increased by the presence of lipases even in lovastatin-treated cells. Lovastatin 120-130 apolipoprotein E Homo sapiens 34-38 11030795-8 2000 CONCLUSIONS: There is a lower prevalence of diagnosed probable AD in patients taking 2 different 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors-lovastatin and pravastatin. Lovastatin 156-166 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 97-144 11032335-3 2000 ALDP-deficient mice were fed chow with 0.01-0.1% lovastatin for 4-8 weeks. Lovastatin 49-59 ATP-binding cassette, sub-family D (ALD), member 1 Mus musculus 0-4 11032335-5 2000 Treatment with 0.1% lovastatin significantly reduced body weight and total cholesterol in the plasma of ALDP-deficient mice. Lovastatin 20-30 ATP-binding cassette, sub-family D (ALD), member 1 Mus musculus 104-108 10997696-1 2000 We have shown that lovastatin, an inhibitor of 3 hydroxy-3-methylglutary coenzyme A (HMG CoA) reductase, delays development and progression of diabetic nephropathy in streptozotocine-induced diabetic rats through suppression of glomerular transforming growth factor (TGF)-beta1 mRNA expression. Lovastatin 19-29 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 49-103 10997696-1 2000 We have shown that lovastatin, an inhibitor of 3 hydroxy-3-methylglutary coenzyme A (HMG CoA) reductase, delays development and progression of diabetic nephropathy in streptozotocine-induced diabetic rats through suppression of glomerular transforming growth factor (TGF)-beta1 mRNA expression. Lovastatin 19-29 transforming growth factor, beta 1 Rattus norvegicus 239-277 10997696-2 2000 We have also shown that lovastatin suppresses both control and high glucose (HG)-induced TGF-beta1 and fibronectin mRNA expression and protein synthesis by rat mesangial cell (RMC) and that this down-regulation by lovastatin is reversed by mevalonate. Lovastatin 24-34 transforming growth factor, beta 1 Rattus norvegicus 89-98 10997696-2 2000 We have also shown that lovastatin suppresses both control and high glucose (HG)-induced TGF-beta1 and fibronectin mRNA expression and protein synthesis by rat mesangial cell (RMC) and that this down-regulation by lovastatin is reversed by mevalonate. Lovastatin 24-34 fibronectin 1 Rattus norvegicus 103-114 10997696-6 2000 Suppression of TGF-beta1 and fibronectin expression by lovastatin was reversed effectively when GGPP was added alone. Lovastatin 55-65 transforming growth factor, beta 1 Rattus norvegicus 15-24 10997696-6 2000 Suppression of TGF-beta1 and fibronectin expression by lovastatin was reversed effectively when GGPP was added alone. Lovastatin 55-65 fibronectin 1 Rattus norvegicus 29-40 10997696-7 2000 Partial reversal of lovastatin effect on fibronectin and TGF-beta1 expression was found when FPP was added alone. Lovastatin 20-30 fibronectin 1 Rattus norvegicus 41-52 10997696-7 2000 Partial reversal of lovastatin effect on fibronectin and TGF-beta1 expression was found when FPP was added alone. Lovastatin 20-30 transforming growth factor, beta 1 Rattus norvegicus 57-66 10997696-8 2000 Adding both GGPP and FPP resulted in complete reversal of lovastatin effect on fibronectin but not TGF-beta1 suggesting that fibronectin and TGF-beta1 are regulated differently. Lovastatin 58-68 fibronectin 1 Rattus norvegicus 79-90 11053993-0 2000 Suppression of invasion and MMP-9 expression in NIH 3T3 and v-H-Ras 3T3 fibroblasts by lovastatin through inhibition of ras isoprenylation. Lovastatin 87-97 matrix metallopeptidase 9 Mus musculus 28-33 11053993-7 2000 To confirm the lovastatin-induced down-regulation of MMP-9 expression, we transfected an MMP-9/luciferase reporter vector, under MMP-9 promoter control, into both NIH 3T3 and v-H-Ras 3T3. Lovastatin 15-25 matrix metallopeptidase 9 Mus musculus 53-58 11053993-7 2000 To confirm the lovastatin-induced down-regulation of MMP-9 expression, we transfected an MMP-9/luciferase reporter vector, under MMP-9 promoter control, into both NIH 3T3 and v-H-Ras 3T3. Lovastatin 15-25 matrix metallopeptidase 9 Mus musculus 89-94 11053993-7 2000 To confirm the lovastatin-induced down-regulation of MMP-9 expression, we transfected an MMP-9/luciferase reporter vector, under MMP-9 promoter control, into both NIH 3T3 and v-H-Ras 3T3. Lovastatin 15-25 matrix metallopeptidase 9 Mus musculus 89-94 11053993-9 2000 In addition, lovastatin also reduced AP-1 and NFkappaB binding activities. Lovastatin 13-23 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 46-54 11053993-11 2000 These results suggest that down-regulation of MMP-9 contributes to the anti-invasive activity of lovastatin. Lovastatin 97-107 matrix metallopeptidase 9 Mus musculus 46-51 10946069-3 2000 METHODS: We treated rabbits and rats for 2 weeks with the HMG CoA reductase inhibitor lovastatin and measured Na(+)-K(+) pump current (I(p)) in isolated rabbit cardiac myocytes using the whole cell patch-clamp technique, K-dependent p-nitrophenyl phosphatase (p-NPPase) activity in crude myocardial and skeletal muscle homogenates, and vanadate-facilitated 3H-ouabain binding in intact skeletal muscle samples from rats. Lovastatin 86-96 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 58-75 10942241-1 2000 Lovastatin, a competitive inhibitor of HMG-CoA reductase, reportedly inhibits proliferation and induces apoptosis of tumor cells with MDR-1 coded P-glycoprotein (Pgp) expression. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-56 10942241-1 2000 Lovastatin, a competitive inhibitor of HMG-CoA reductase, reportedly inhibits proliferation and induces apoptosis of tumor cells with MDR-1 coded P-glycoprotein (Pgp) expression. Lovastatin 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 134-139 10942241-1 2000 Lovastatin, a competitive inhibitor of HMG-CoA reductase, reportedly inhibits proliferation and induces apoptosis of tumor cells with MDR-1 coded P-glycoprotein (Pgp) expression. Lovastatin 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 146-160 10942241-1 2000 Lovastatin, a competitive inhibitor of HMG-CoA reductase, reportedly inhibits proliferation and induces apoptosis of tumor cells with MDR-1 coded P-glycoprotein (Pgp) expression. Lovastatin 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 162-165 10942241-3 2000 MTT and apoptosis assays revealed that K562/ADR, NOMO-1/ADR and NB4/RA/MDR were more sensitive to lovastatin than their parental cell lines, while NB4/MDR showed the same level of sensitivity as parental NB4 cells, which already were very sensitive to lovastatin. Lovastatin 98-108 aldo-keto reductase family 1 member B Homo sapiens 39-47 10942241-3 2000 MTT and apoptosis assays revealed that K562/ADR, NOMO-1/ADR and NB4/RA/MDR were more sensitive to lovastatin than their parental cell lines, while NB4/MDR showed the same level of sensitivity as parental NB4 cells, which already were very sensitive to lovastatin. Lovastatin 98-108 NODAL modulator 1 Homo sapiens 49-55 10942241-3 2000 MTT and apoptosis assays revealed that K562/ADR, NOMO-1/ADR and NB4/RA/MDR were more sensitive to lovastatin than their parental cell lines, while NB4/MDR showed the same level of sensitivity as parental NB4 cells, which already were very sensitive to lovastatin. Lovastatin 98-108 aldo-keto reductase family 1 member B Homo sapiens 44-47 10942241-4 2000 Significant elevation of transcript levels of HMG-CoA reductase was observed by semiquantitative RT-PCR analysis in more than three lovastatin-sensitive MDR sublines, but not in NB4/MDR compared with the parental cell lines. Lovastatin 132-142 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 46-63 10942241-5 2000 HMG-CoA reductase mRNA levels were up-regulated more than two-fold by the exposure to lovastatin in all of the parental non-Pgp-expressing cell lines. Lovastatin 86-96 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-17 10942241-5 2000 HMG-CoA reductase mRNA levels were up-regulated more than two-fold by the exposure to lovastatin in all of the parental non-Pgp-expressing cell lines. Lovastatin 86-96 ATP binding cassette subfamily B member 1 Homo sapiens 124-127 10938345-1 2000 Growth inhibition of tobacco (Nicotiana tabacum L. cv Bright Yellow-2) cells by mevinolin, a specific inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) could be partially overcome by the addition of farnesol. Lovastatin 80-89 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 115-162 10938345-1 2000 Growth inhibition of tobacco (Nicotiana tabacum L. cv Bright Yellow-2) cells by mevinolin, a specific inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) could be partially overcome by the addition of farnesol. Lovastatin 80-89 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 164-168 10938345-6 2000 Both mevinolin and farnesol treatments stimulated apparent HMGR activity. Lovastatin 5-14 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 59-63 10953355-15 2000 Lovastatin acts through isoprenoid depletion, because supplementation of the media with 50-100 microM mevalonate restored all tau eta epsilon effects. Lovastatin 0-10 endothelin receptor type A Homo sapiens 130-133 10856525-2 2000 We found that lovastatin and simvastatin inhibited cell proliferation by provoking G0/G1 phase arrest with concomitant depression of the proliferation antigen Ki-67/MIB-1. Lovastatin 14-24 MIB E3 ubiquitin protein ligase 1 Mus musculus 165-170 10892724-1 2000 Lovastatin is a lipid lowering agent that acts by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a key regulatory enzyme in cholesterol biosynthesis. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 61-118 10815931-1 2000 Lovastatin, a drug commonly used in the clinic to treat hypercholesterolemia, has previously been reported to exert antitumor effects in rodent tumor models and to strengthen the antitumor effects of immune response modifiers (tumor necrosis factor alpha and IFN-gamma) or chemotherapeutic drugs (cisplatin). Lovastatin 0-10 tumor necrosis factor Mus musculus 227-254 10815931-1 2000 Lovastatin, a drug commonly used in the clinic to treat hypercholesterolemia, has previously been reported to exert antitumor effects in rodent tumor models and to strengthen the antitumor effects of immune response modifiers (tumor necrosis factor alpha and IFN-gamma) or chemotherapeutic drugs (cisplatin). Lovastatin 0-10 interferon gamma Mus musculus 259-268 10931838-6 2000 In contrast to PON1, PON3 has very limited arylesterase and no paraoxonase activities but rapidly hydrolyzes lactones such as statin prodrugs (e.g. lovastatin). Lovastatin 148-158 paraoxonase 3 Homo sapiens 21-25 11005703-12 2000 Atorvastatin, cerivastatin, lovastatin and simvastatin are predominantly metabolised by the CYP3A4 isozyme. Lovastatin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 11029845-8 2000 Lovastatin, simvastatin, and atorvastatin are substrates of CYP3A4, whereas fluvastatin is metabolized by CYP2C9. Lovastatin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 11126989-3 2000 Most statins are metabolised by the CYP3A4 izoenzyme (lovastatin, simvastatin, atorvastatin, cerivastatin). Lovastatin 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 10913178-7 2000 In lovastatin-treated MDA468 cells, the mobility of the associated hnRNP C1 and C2 proteins changed, and this correlated with increased p27 expression. Lovastatin 3-13 interferon alpha inducible protein 27 Homo sapiens 136-139 10908155-4 2000 Lovastatin and simvastatin caused a dose-dependent inhibition of MCP-1 production in peripheral blood mononuclear cells exposed to lipopolysaccharide or inactivated Streptococcus hemoliticus and in human endothelial cells exposed to interleukin-1beta. Lovastatin 0-10 C-C motif chemokine ligand 2 Homo sapiens 65-70 10908155-4 2000 Lovastatin and simvastatin caused a dose-dependent inhibition of MCP-1 production in peripheral blood mononuclear cells exposed to lipopolysaccharide or inactivated Streptococcus hemoliticus and in human endothelial cells exposed to interleukin-1beta. Lovastatin 0-10 interleukin 1 beta Homo sapiens 233-250 10908155-8 2000 At the dose of 10 mg/kg, lovastatin and pravastatin reduced by approximately 50% the lipopolysaccharide-induced leukocytes recruitment and the exudate MCP-1 production. Lovastatin 25-35 chemokine (C-C motif) ligand 2 Mus musculus 151-156 10888037-4 2000 In this study we show that inhibition of N-linked glycosylation using tunicamycin or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin resulted in down-regulation of IGF-1R at the cell surface in Ewing"s sarcoma cell lines (RD-ES and ES-1 cells). Lovastatin 157-167 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 89-146 10822111-2 2000 Lovastatin at 1 microM decreases CCK 8 secretion by over 50% in WE cells and in CCK 8 expressing AtT20 cells. Lovastatin 0-10 cholecystokinin Homo sapiens 33-36 10822111-2 2000 Lovastatin at 1 microM decreases CCK 8 secretion by over 50% in WE cells and in CCK 8 expressing AtT20 cells. Lovastatin 0-10 cholecystokinin Homo sapiens 80-83 10822111-6 2000 Our results clearly demonstrate that lovastatin at 1 microM strongly inhibits CCK 8 secretion at multiple levels while having little or no effect on its synthesis. Lovastatin 37-47 cholecystokinin Homo sapiens 78-81 10749150-5 2000 The Ras inhibitors B-1086 and Lovastatin decreased PTHRP mRNA expression. Lovastatin 30-40 parathyroid hormone-like hormone Rattus norvegicus 51-56 10888037-4 2000 In this study we show that inhibition of N-linked glycosylation using tunicamycin or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin resulted in down-regulation of IGF-1R at the cell surface in Ewing"s sarcoma cell lines (RD-ES and ES-1 cells). Lovastatin 157-167 insulin like growth factor 1 receptor Homo sapiens 199-205 10888037-7 2000 Our data suggest that relatively untoxic HMG-CoA reductase inhibitors (e.g. lovastatin) could have therapeutic significance in IGF-1R-dependent neoplasms like Ewing"s sarcoma. Lovastatin 76-86 insulin like growth factor 1 receptor Homo sapiens 127-133 10728920-0 2000 Induction of apoptosis by lovastatin through activation of caspase-3 and DNase II in leukaemia HL-60 cells. Lovastatin 26-36 caspase 3 Homo sapiens 59-68 10728920-5 2000 Treatment of lovastatin caused a rapid release of mitochondrial cytochrome c into cytosol and subsequent induction of caspase-3, but not caspase-1 activity. Lovastatin 13-23 cytochrome c, somatic Homo sapiens 64-76 10728920-5 2000 Treatment of lovastatin caused a rapid release of mitochondrial cytochrome c into cytosol and subsequent induction of caspase-3, but not caspase-1 activity. Lovastatin 13-23 caspase 3 Homo sapiens 118-127 10728920-5 2000 Treatment of lovastatin caused a rapid release of mitochondrial cytochrome c into cytosol and subsequent induction of caspase-3, but not caspase-1 activity. Lovastatin 13-23 caspase 1 Homo sapiens 137-146 10728920-6 2000 Lovastatin also stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP), and followed by the appearance of caspase activity and DNA fragmentation. Lovastatin 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 51-79 10728920-6 2000 Lovastatin also stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP), and followed by the appearance of caspase activity and DNA fragmentation. Lovastatin 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 81-85 10728920-7 2000 Pretreatment with caspase-3 inhibitors, Ac-DEVD-CHO and Z-VAD-FMK, inhibited lovastatin induced caspase-3 activity and DNA fragmentation. Lovastatin 77-87 caspase 3 Homo sapiens 18-27 10728920-7 2000 Pretreatment with caspase-3 inhibitors, Ac-DEVD-CHO and Z-VAD-FMK, inhibited lovastatin induced caspase-3 activity and DNA fragmentation. Lovastatin 77-87 caspase 3 Homo sapiens 96-105 10728920-9 2000 These results suggested that the mechanism of lovastatin induced HL-60 cells apoptosis through activation of caspase-3 and DNase II activities. Lovastatin 46-56 caspase 3 Homo sapiens 109-118 11122720-3 2000 Despite an excellent safety record, CYP 3A4 statins (lovastatin, simvastatin, atorvastatin) taken concomitantly with a potent CYP 3A4 inhibitor may increase the risk for adverse events (myopathy, rhabdomyolysis). Lovastatin 53-63 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 36-39 11154978-1 2000 Lovastatin reduces the isoprenylation of p21ras via suppression of mevalonic acid generation. Lovastatin 0-10 HRas proto-oncogene, GTPase Homo sapiens 41-47 10631097-0 2000 Low-density lipoprotein-induced expression of interleukin-6, a marker of human mesangial cell inflammation: effects of oxidation and modulation by lovastatin. Lovastatin 147-157 interleukin 6 Homo sapiens 46-59 10631097-7 2000 Lovastatin markedly inhibited mesangial cell expression of IL-6 mRNA and reduced IL-6 secretion. Lovastatin 0-10 interleukin 6 Homo sapiens 59-63 10631097-7 2000 Lovastatin markedly inhibited mesangial cell expression of IL-6 mRNA and reduced IL-6 secretion. Lovastatin 0-10 interleukin 6 Homo sapiens 81-85 10673069-2 2000 Lovastatin is a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor that inhibits cholesterol biosynthesis and affects the activity of some signal transduction pathways and liver transcription factors. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 16-56 10616843-6 2000 Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression despite high blood glucose levels. Lovastatin 15-25 transforming growth factor, beta 1 Rattus norvegicus 147-156 10616843-10 2000 These results suggest that lovastatin has a direct cellular effect independent of a cholesterol-lowering effect and delays the onset and progression of diabetic nephropathy, at least in part, through suppression of glomerular expression of TGF-beta1. Lovastatin 27-37 transforming growth factor, beta 1 Rattus norvegicus 240-249 10794499-4 2000 The action of L-arginine was compared to vitamin E and the HMG CoA reductase inhibitor lovastatin which are known to attenuate progression of atherosclerosis. Lovastatin 87-97 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 59-76 10574973-8 1999 Consistent with their inhibition of the mevalonate pathway, apoptosis and cleavage of Mst1 kinase induced by alendronate, risedronate, and lovastatin, but not clodronate, are blocked by geranylgeraniol, a precursor of geranylgeranyl diphosphate. Lovastatin 139-149 macrophage stimulating 1 Homo sapiens 86-90 10601278-7 1999 Cis-inhibition studies indicate that both OATP2 and roatp1 also transport other statins including lovastatin, simvastatin, and atorvastatin. Lovastatin 98-108 solute carrier organic anion transporter family member 1B1 Homo sapiens 42-47 10591153-1 1999 It has been shown previously that inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, such as compactin, lovastatin, and pravastatin, block cholesterol synthesis, suppress lymphocyte functions, and beneficially affect atherogenesis. Lovastatin 126-136 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 48-105 11387965-0 1999 [Effects of lovastatin on plasma lipid, plasma glucose and insulin metabolism of patients with type II B hyperlipemia]. Lovastatin 12-22 insulin Homo sapiens 59-66 11387965-1 1999 This study was directed at the effects of lovastatin on plasma glucose and insulin metabolism of patients with Type II B hyperlipemia. Lovastatin 42-52 insulin Homo sapiens 75-82 10665838-7 1999 Simvastatin, lovastatin, cerivastatin, and atorvastatin are biotransformed in the liver primarily by cytochrome P450-3A4, and are susceptible to drug interactions when co-administered with potential inhibitors of this enzyme. Lovastatin 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-120 10559211-2 1999 Pretreatment of Jurkat T-cells with the 3-hydroxymethylglutaryl-coenzyme A reductase inhibitor, lovastatin, markedly reduced (IC(50) approximately 1-2 microM) alpha(4)beta(1)-dependent adhesion to fibronectin (FN) stimulated by phorbol 12-myristate 13-acetate (PMA) which modulates post-receptor events. Lovastatin 96-106 fibronectin 1 Homo sapiens 197-208 10559211-2 1999 Pretreatment of Jurkat T-cells with the 3-hydroxymethylglutaryl-coenzyme A reductase inhibitor, lovastatin, markedly reduced (IC(50) approximately 1-2 microM) alpha(4)beta(1)-dependent adhesion to fibronectin (FN) stimulated by phorbol 12-myristate 13-acetate (PMA) which modulates post-receptor events. Lovastatin 96-106 fibronectin 1 Homo sapiens 210-212 10559211-6 1999 The inhibitory effect of lovastatin on PMA-stimulated leukocyte adhesion was reversed by co-incubation with geranylgeraniol, but not with farnesol, with concurrent reversal of the inhibition of protein prenylation as shown by protein RhoA geranylgeranylation. Lovastatin 25-35 ras homolog family member A Homo sapiens 234-238 10557091-6 1999 These effects were dose-dependent, augmented with repeated insults, and were prevented by culturing cells in the presence of lovastatin, a competitive inhibitor of HMGR. Lovastatin 125-135 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 164-168 10534570-4 1999 A negative growth regulator, the HMG-CoA reductase inhibitor lovastatin was found to induce loss of p107 protein which was reversible by a specific protease inhibitor lactacystin as well as calpain inhibitor. Lovastatin 61-71 RB transcriptional corepressor like 1 Homo sapiens 100-104 10534570-5 1999 Following treatment with lovastatin higher molecular weight ubiquitinated forms of p107 were detected by anti-p107 immunoprecipitation and anti-ubiquitin Western blotting. Lovastatin 25-35 RB transcriptional corepressor like 1 Homo sapiens 83-87 10534570-5 1999 Following treatment with lovastatin higher molecular weight ubiquitinated forms of p107 were detected by anti-p107 immunoprecipitation and anti-ubiquitin Western blotting. Lovastatin 25-35 RB transcriptional corepressor like 1 Homo sapiens 110-114 10502407-6 1999 We demonstrated that pRB phosphorylation, cdk2 activity needed for this phosphorylation, and the levels of cyclin A, D, and E were inhibited after 24 h of lovastatin treatment, while the levels of p27(Kip1) were elevated. Lovastatin 155-165 RB transcriptional corepressor 1 Homo sapiens 21-24 10502407-6 1999 We demonstrated that pRB phosphorylation, cdk2 activity needed for this phosphorylation, and the levels of cyclin A, D, and E were inhibited after 24 h of lovastatin treatment, while the levels of p27(Kip1) were elevated. Lovastatin 155-165 cyclin dependent kinase 2 Homo sapiens 42-46 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 116-126 choline kinase alpha Homo sapiens 21-24 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 116-126 H3 histone pseudogene 16 Homo sapiens 345-348 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 116-126 interferon alpha inducible protein 27 Homo sapiens 353-356 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 116-126 cyclin dependent kinase 2 Homo sapiens 399-403 10502413-4 1999 The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity. Lovastatin 253-263 choline kinase alpha Homo sapiens 21-24 10502413-9 1999 Last, treatment of MDA-MB-157 cells with lovastatin, another known cAMP modulator which also causes growth arrest, resulted in the induction of p21 and p27 without any increase in PKA activity. Lovastatin 41-51 H3 histone pseudogene 16 Homo sapiens 144-147 10502407-6 1999 We demonstrated that pRB phosphorylation, cdk2 activity needed for this phosphorylation, and the levels of cyclin A, D, and E were inhibited after 24 h of lovastatin treatment, while the levels of p27(Kip1) were elevated. Lovastatin 155-165 cyclin A2 Homo sapiens 107-115 10502413-9 1999 Last, treatment of MDA-MB-157 cells with lovastatin, another known cAMP modulator which also causes growth arrest, resulted in the induction of p21 and p27 without any increase in PKA activity. Lovastatin 41-51 interferon alpha inducible protein 27 Homo sapiens 152-155 10502407-6 1999 We demonstrated that pRB phosphorylation, cdk2 activity needed for this phosphorylation, and the levels of cyclin A, D, and E were inhibited after 24 h of lovastatin treatment, while the levels of p27(Kip1) were elevated. Lovastatin 155-165 dynactin subunit 6 Homo sapiens 197-200 10502407-6 1999 We demonstrated that pRB phosphorylation, cdk2 activity needed for this phosphorylation, and the levels of cyclin A, D, and E were inhibited after 24 h of lovastatin treatment, while the levels of p27(Kip1) were elevated. Lovastatin 155-165 cyclin dependent kinase inhibitor 1B Homo sapiens 201-205 10506194-0 1999 Impaired regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase degradation in lovastatin-resistant cells. Lovastatin 86-96 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 23-70 10506194-1 1999 L-90 cells were selected to grow in the presence of serum lipoproteins and 90 microM lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR). Lovastatin 85-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 113-160 10506194-1 1999 L-90 cells were selected to grow in the presence of serum lipoproteins and 90 microM lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR). Lovastatin 85-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 162-166 10543307-8 1999 Expression of thrombospondin-1 was significantly decreased after 24 h incubations with lovastatin in concentrations as low as 1 micromol/L. Lovastatin 87-97 thrombospondin 1 Homo sapiens 14-30 10543307-11 1999 In contrast, lovastatin did not affect expression of fibronectin, whereas collagen type I and biglycan expression decreased only after long incubations with high, toxic lovastatin concentrations. Lovastatin 169-179 biglycan Homo sapiens 94-102 10575059-5 1999 The lipophilic drugs lovastatin, simvastatin, atorvastatin, cerivastatin and fluvastatin are metabolized via the cytochrome P450 (CYP450) system in the liver and the gut, making them subject to potential interactions with concomitantly administered drugs that are competing for metabolism via this system. Lovastatin 21-31 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 113-128 10543307-13 1999 In summary, lovastatin and simvastatin predominantly decrease the expression of the glycoprotein thrombospondin-1, which is functionally associated with smooth muscle cell migration and proliferation. Lovastatin 12-22 thrombospondin 1 Homo sapiens 97-113 10490896-0 1999 Small intestinal metabolism of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin and comparison with pravastatin. Lovastatin 93-103 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 35-82 10490896-1 1999 We compared the intestinal metabolism of the structurally related 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors lovastatin and pravastatin in vitro. Lovastatin 125-135 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 66-113 10490896-8 1999 It was concluded that lovastatin is metabolized by cytochrome P-450 3A enzymes in the small intestine. Lovastatin 22-32 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 51-67 10521709-1 1999 Inhibition of esterified and non-esterified cholesterol synthesis by lovastatin in primary rat hepatocytes suppressed the net synthesis and very-low-density lipoprotein (VLDL) secretion of apolipoprotein B (apoB)-48 and apoB-100. Lovastatin 69-79 apolipoprotein B Rattus norvegicus 189-215 10521709-1 1999 Inhibition of esterified and non-esterified cholesterol synthesis by lovastatin in primary rat hepatocytes suppressed the net synthesis and very-low-density lipoprotein (VLDL) secretion of apolipoprotein B (apoB)-48 and apoB-100. Lovastatin 69-79 apolipoprotein B Rattus norvegicus 220-228 10521709-7 1999 The inhibitory effect of lovastatin alone on the net synthesis of apoB-48 and apoB-100 was reversed by the simultaneous presence of 25-hydroxycholesterol, suggesting a role for newly synthesised cholesteryl ester. Lovastatin 25-35 apolipoprotein B Rattus norvegicus 66-73 10521709-7 1999 The inhibitory effect of lovastatin alone on the net synthesis of apoB-48 and apoB-100 was reversed by the simultaneous presence of 25-hydroxycholesterol, suggesting a role for newly synthesised cholesteryl ester. Lovastatin 25-35 apolipoprotein B Rattus norvegicus 78-86 10521709-9 1999 In the presence of lovastatin, restoration of the net synthesis of apoB by 25-hydroxycholesterol was not accompanied by an increased VLDL output of apoB-48 and apoB-100. Lovastatin 19-29 apolipoprotein B Rattus norvegicus 67-71 10440923-3 1999 Lovastatin treatment (10 microM) of control 3T3 cells resulted in growth arrest at G1 accompanied by actin stress fiber disassembly, cell rounding, and decreased active RhoA from the membranous protein fraction. Lovastatin 0-10 ras homolog family member A Mus musculus 169-173 10493852-0 1999 Structural basis for LFA-1 inhibition upon lovastatin binding to the CD11a I-domain. Lovastatin 43-53 integrin subunit alpha L Homo sapiens 21-26 10493852-2 1999 We report here that lovastatin, a drug clinically used for lowering cholesterol levels, inhibits the interaction of human LFA-1 with its counter-receptor intercellular adhesion molecule-1. Lovastatin 20-30 integrin subunit alpha L Homo sapiens 122-127 10575059-6 1999 Clinically important interactions with simvastatin or lovastatin and drugs that inhibit the 3A4 isoenzyme (part of the CYP450 system) may result in myopathy and rhabdomyolysis, which can be fatal. Lovastatin 54-64 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 119-125 10508262-2 1999 Activation of cell adhesion by AIF4- was abrogated by lovastatin, thereby establishing a link between heterotrimeric G-proteins and small GTP-binding proteins in the regulation of alpha4beta7-mediated cell adhesion. Lovastatin 54-64 itchy E3 ubiquitin protein ligase Homo sapiens 31-35 10473109-6 1999 Lovastatin treatment resulted in decreased expression of the antiapoptotic protein bcl-2 and increased the expression of the proapoptotic protein bax. Lovastatin 0-10 BCL2 apoptosis regulator Homo sapiens 83-88 10473109-6 1999 Lovastatin treatment resulted in decreased expression of the antiapoptotic protein bcl-2 and increased the expression of the proapoptotic protein bax. Lovastatin 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 10430507-8 1999 Administration of lovastatin inhibited the expression of iNOS, TNF-alpha and IFN-gamma in the CNS of EAE rats and improved the clinical signs of EAE suggesting that this compound may have therapeutic potential in the treatment of neuroinflammatory diseases like MS. Lovastatin 18-28 nitric oxide synthase 2 Rattus norvegicus 57-61 10430507-8 1999 Administration of lovastatin inhibited the expression of iNOS, TNF-alpha and IFN-gamma in the CNS of EAE rats and improved the clinical signs of EAE suggesting that this compound may have therapeutic potential in the treatment of neuroinflammatory diseases like MS. Lovastatin 18-28 tumor necrosis factor Rattus norvegicus 63-72 10430507-8 1999 Administration of lovastatin inhibited the expression of iNOS, TNF-alpha and IFN-gamma in the CNS of EAE rats and improved the clinical signs of EAE suggesting that this compound may have therapeutic potential in the treatment of neuroinflammatory diseases like MS. Lovastatin 18-28 interferon gamma Rattus norvegicus 77-86 10440099-0 1999 Lovastatin prevents angiotensin II-induced cardiac hypertrophy in cultured neonatal rat heart cells. Lovastatin 0-10 angiotensinogen Rattus norvegicus 20-34 10440099-5 1999 Lipid-soluble HMG-CoA reductase inhibitors, lovastatin (10(-6) M) and simvastatin (10(-6) M) partially and significantly inhibited the angiotensin II-induced increases in these parameters, but a water-soluble HMG-CoA reductase inhibitor, pravastatin (10(-6) M) did not. Lovastatin 44-54 angiotensinogen Rattus norvegicus 135-149 10440099-6 1999 Mevalonate (10(-4) M) overcame the inhibitory effects of lovastatin and simvastatin on angiotensin II-induced increases in these parameters. Lovastatin 57-67 angiotensinogen Rattus norvegicus 87-101 10440099-9 1999 These studies demonstrate that a lipid-soluble HMG-CoA reductase inhibitor, lovastatin, may prevent angiotensin II-induced cardiac hypertrophy, at least in part, through p21ras/MAP kinase pathway, which is linked to mevalonate metabolism. Lovastatin 76-86 angiotensinogen Rattus norvegicus 100-114 10440099-9 1999 These studies demonstrate that a lipid-soluble HMG-CoA reductase inhibitor, lovastatin, may prevent angiotensin II-induced cardiac hypertrophy, at least in part, through p21ras/MAP kinase pathway, which is linked to mevalonate metabolism. Lovastatin 76-86 HRas proto-oncogene, GTPase Rattus norvegicus 170-176 10416996-1 1999 A 54 year old man developed rhabdomyolysis one year after beginning treatment with a combination of lovastatin (an HMGCoA reductase inhibitor) and niacin. Lovastatin 100-110 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 115-131 10412747-5 1999 Lovastatin reduced membrane-bound p21ras and fetal calf serum-induced c-fos and c-jun protein expression. Lovastatin 0-10 HRas proto-oncogene, GTPase Rattus norvegicus 34-40 10412747-5 1999 Lovastatin reduced membrane-bound p21ras and fetal calf serum-induced c-fos and c-jun protein expression. Lovastatin 0-10 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 70-75 10399961-2 1999 We have previously shown that blocking the mevalonate pathway with lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, inhibits medulloblastoma proliferation and induces apoptosis in vitro. Lovastatin 67-77 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 106-163 10399961-4 1999 We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis. Lovastatin 46-56 H3 histone pseudogene 16 Homo sapiens 13-16 10399961-4 1999 We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis. Lovastatin 123-133 H3 histone pseudogene 16 Homo sapiens 13-16 10399961-9 1999 In both lovastatin- and manumycin A-treated cells, cellular cysteine protease precursor (CPP32) was activated, confirming the occurrence of apoptosis. Lovastatin 8-18 caspase 3 Homo sapiens 89-94 10409615-15 1999 The effects of SM depletion contrasted with those previously obtained with the cholesterol inhibitor lovastatin, which reduced PrP(Sc) and removed it from detergent-insoluble complexes. Lovastatin 101-111 prp Drosophila melanogaster 127-130 10393901-1 1999 In this paper we present the finding that lovastatin arrests cells by inhibiting the proteasome, which results in the accumulation of p21 and p27, leading to G1 arrest. Lovastatin 42-52 cyclin dependent kinase inhibitor 1A Homo sapiens 134-137 10393901-1 1999 In this paper we present the finding that lovastatin arrests cells by inhibiting the proteasome, which results in the accumulation of p21 and p27, leading to G1 arrest. Lovastatin 42-52 interferon alpha inducible protein 27 Homo sapiens 142-145 10393901-2 1999 Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 30-72 10393901-3 1999 Previously, we reported that lovastatin can be used to arrest cultured cells in the G1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27. Lovastatin 29-39 cyclin dependent kinase inhibitor 1A Homo sapiens 192-195 10393901-3 1999 Previously, we reported that lovastatin can be used to arrest cultured cells in the G1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27. Lovastatin 29-39 interferon alpha inducible protein 27 Homo sapiens 200-203 10393901-4 1999 In this report we show that this stabilization of p21 and p27 may be the result of a previously unknown function of the pro-drug, beta-lactone ring form of lovastatin to inhibit the proteasome degradation of these CKIs. Lovastatin 156-166 cyclin dependent kinase inhibitor 1A Homo sapiens 50-53 10393901-4 1999 In this report we show that this stabilization of p21 and p27 may be the result of a previously unknown function of the pro-drug, beta-lactone ring form of lovastatin to inhibit the proteasome degradation of these CKIs. Lovastatin 156-166 interferon alpha inducible protein 27 Homo sapiens 58-61 10652602-5 1999 Analysis of G1 regulatory proteins demonstrated that the protein levels of cyclin-dependent kinase (CDK) 2, CDK4, CDK6 and cyclin E were decreased after treatment with lovastatin (10 microM) in a time-dependent manner, but not cyclin D1. Lovastatin 168-178 cyclin dependent kinase 2 Homo sapiens 100-106 10652602-5 1999 Analysis of G1 regulatory proteins demonstrated that the protein levels of cyclin-dependent kinase (CDK) 2, CDK4, CDK6 and cyclin E were decreased after treatment with lovastatin (10 microM) in a time-dependent manner, but not cyclin D1. Lovastatin 168-178 cyclin dependent kinase 4 Homo sapiens 108-112 10652602-5 1999 Analysis of G1 regulatory proteins demonstrated that the protein levels of cyclin-dependent kinase (CDK) 2, CDK4, CDK6 and cyclin E were decreased after treatment with lovastatin (10 microM) in a time-dependent manner, but not cyclin D1. Lovastatin 168-178 cyclin dependent kinase 6 Homo sapiens 114-118 10652602-5 1999 Analysis of G1 regulatory proteins demonstrated that the protein levels of cyclin-dependent kinase (CDK) 2, CDK4, CDK6 and cyclin E were decreased after treatment with lovastatin (10 microM) in a time-dependent manner, but not cyclin D1. Lovastatin 168-178 cyclin D1 Homo sapiens 227-236 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 cyclin dependent kinase inhibitor 3 Homo sapiens 59-92 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 cyclin dependent kinase inhibitor 3 Homo sapiens 94-98 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 dynactin subunit 6 Homo sapiens 101-104 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 dynactin subunit 6 Homo sapiens 143-146 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 cyclin dependent kinase 2 Homo sapiens 152-156 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 cyclin dependent kinase 4 Homo sapiens 161-165 10652602-6 1999 In addition, lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. Lovastatin 13-23 cyclin dependent kinase 6 Homo sapiens 176-180 10652602-7 1999 At higher doses of lovastatin (50 mM, 100 mM, 200 mM), a significant apoptosis was observed as evidenced by FACS analysis with annexin V staining, which was associated with downregulation of Bcl-2 protein. Lovastatin 19-29 BCL2 apoptosis regulator Homo sapiens 191-196 10652602-8 1999 These results suggest that lovastatin inhibits the proliferation of myeloid leukemic cells via G1 arrest in association with p27 induction and is an effective inducer of apoptosis in HL-60 cells. Lovastatin 27-37 dynactin subunit 6 Homo sapiens 125-128 10393211-4 1999 Both VLDL binding and degradation were significantly increased (4-fold) when LDL receptors were up-regulated by treatment with lovastatin. Lovastatin 127-137 CD320 antigen Mus musculus 5-9 10412776-12 1999 Lovastatin suppressed DNA synthesis and reduced the expression of cyclin D1 and cyclin E, whereas p27Kip1 expression was strongly induced by lovastatin pretreatment. Lovastatin 0-10 cyclin D1 Rattus norvegicus 66-75 10412776-12 1999 Lovastatin suppressed DNA synthesis and reduced the expression of cyclin D1 and cyclin E, whereas p27Kip1 expression was strongly induced by lovastatin pretreatment. Lovastatin 0-10 cyclin E1 Rattus norvegicus 80-88 10412776-12 1999 Lovastatin suppressed DNA synthesis and reduced the expression of cyclin D1 and cyclin E, whereas p27Kip1 expression was strongly induced by lovastatin pretreatment. Lovastatin 141-151 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 98-105 10412776-15 1999 Lovastatin may suppress DNA synthesis in VSMCs by inducing p27Kip1 and reducing expression of cyclins D1 and E. Lovastatin 0-10 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 59-66 10412776-15 1999 Lovastatin may suppress DNA synthesis in VSMCs by inducing p27Kip1 and reducing expression of cyclins D1 and E. Lovastatin 0-10 cyclin D1 Rattus norvegicus 94-110 10575059-5 1999 The lipophilic drugs lovastatin, simvastatin, atorvastatin, cerivastatin and fluvastatin are metabolized via the cytochrome P450 (CYP450) system in the liver and the gut, making them subject to potential interactions with concomitantly administered drugs that are competing for metabolism via this system. Lovastatin 21-31 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 130-136 10405975-6 1999 Mevinolin (lovastatin), an inhibitor of 3-hydroxy-3-methylglutaryl-CoA(HMG-CoA) reductase, at 2 microM concentration, inhibited CH synthesis from 14C-acetate by 80%. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 71-89 10385497-3 1999 BACKGROUND: The NHLBI Post Coronary Artery Bypass Graft trial (Post CABG) showed that aggressive compared with moderate lowering of low-density lipoprotein-cholesterol (LDL-C) decreased obstructive changes in saphenous vein grafts (SVGs) by 31%.1 Using lovastatin and cholestyramine when necessary, the annually determined mean LDL-C level ranged from 93 to 97 mg/dL in aggressively treated patients and from 132 to 136 mg/dL in the others (P<0.001). Lovastatin 253-263 component of oligomeric golgi complex 2 Homo sapiens 132-167 10385497-3 1999 BACKGROUND: The NHLBI Post Coronary Artery Bypass Graft trial (Post CABG) showed that aggressive compared with moderate lowering of low-density lipoprotein-cholesterol (LDL-C) decreased obstructive changes in saphenous vein grafts (SVGs) by 31%.1 Using lovastatin and cholestyramine when necessary, the annually determined mean LDL-C level ranged from 93 to 97 mg/dL in aggressively treated patients and from 132 to 136 mg/dL in the others (P<0.001). Lovastatin 253-263 component of oligomeric golgi complex 2 Homo sapiens 169-174 10501560-1 1999 Addition of the beta-hydroxy-beta-methylglutaryl-CoA (HmG-CoA) reductase inhibitor lovastatin to human HEK cells transfected with the amyloid precursor protein (APP) reduces intracellular cholesterol/protein ratios by 50%, and markedly inhibits beta-secretase cleavage of newly-synthesized APP. Lovastatin 83-93 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 16-72 10501560-1 1999 Addition of the beta-hydroxy-beta-methylglutaryl-CoA (HmG-CoA) reductase inhibitor lovastatin to human HEK cells transfected with the amyloid precursor protein (APP) reduces intracellular cholesterol/protein ratios by 50%, and markedly inhibits beta-secretase cleavage of newly-synthesized APP. Lovastatin 83-93 amyloid beta precursor protein Homo sapiens 134-159 10405975-6 1999 Mevinolin (lovastatin), an inhibitor of 3-hydroxy-3-methylglutaryl-CoA(HMG-CoA) reductase, at 2 microM concentration, inhibited CH synthesis from 14C-acetate by 80%. Lovastatin 11-21 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 71-89 10225445-0 1999 Lovastatin and tumor necrosis factor-alpha exhibit potentiated antitumor effects against Ha-ras-transformed murine tumor via inhibition of tumor-induced angiogenesis. Lovastatin 0-10 Harvey rat sarcoma virus oncogene Mus musculus 89-95 10329655-9 1999 Feeding rats 5% cholestyramine plus 0.1% lovastatin in chow resulted in both approximately a 3-fold induction of DHCR mRNA and a 5-fold increase of the enzymic activity in the liver. Lovastatin 41-51 7-dehydrocholesterol reductase Rattus norvegicus 113-117 10225445-3 1999 In in vitro studies, lovastatin inhibited the growth of cells transformed with Ha-ras oncogene (Ras-3T3 and HBL100-ras cells) more effectively than control NIH-3T3 and HBL100-neo cells. Lovastatin 21-31 Harvey rat sarcoma virus oncogene Mus musculus 79-85 10225445-6 1999 Ras-3T3 tumor cells produced increased amounts of vascular endothelial growth factor (VEGF) and lovastatin effectively suppressed VEGF production by these cells. Lovastatin 96-106 vascular endothelial growth factor A Mus musculus 130-134 10225445-7 1999 Our results suggest that lovastatin increases antitumor activity of TNF-alpha against tumor cells transformed with v-Ha-ras oncogene via inhibition of tumor-induced blood-vessel formation. Lovastatin 25-35 tumor necrosis factor Mus musculus 68-77 10225445-7 1999 Our results suggest that lovastatin increases antitumor activity of TNF-alpha against tumor cells transformed with v-Ha-ras oncogene via inhibition of tumor-induced blood-vessel formation. Lovastatin 25-35 Harvey rat sarcoma virus oncogene Mus musculus 117-123 10412747-10 1999 Lovastatin increased tissue-type plasminogen activator (PA) and decreased PA inhibitor activities and antigens; these effects were prevented by mevalonate and GGPP but not FPP, and were reproduced by C3 exoenzyme in a manner insensitive to GGPP. Lovastatin 0-10 plasminogen activator, tissue type Rattus norvegicus 21-54 10225445-1 1999 Lovastatin, a drug commonly used in the treatment of hypercholesterolemia, has previously been reported to exert potentiated antitumor activity when combined with either tumor necrosis factor-alpha (TNF-alpha), cisplatin or doxorubicin in a melanoma model in mice. Lovastatin 0-10 tumor necrosis factor Mus musculus 170-197 10225445-1 1999 Lovastatin, a drug commonly used in the treatment of hypercholesterolemia, has previously been reported to exert potentiated antitumor activity when combined with either tumor necrosis factor-alpha (TNF-alpha), cisplatin or doxorubicin in a melanoma model in mice. Lovastatin 0-10 tumor necrosis factor Mus musculus 199-208 10374838-1 1999 Hydroxymethyl-glutaryl-CoA-reductase (HMG-CoA-reductase), the key enzyme for cholesterol synthesis and essential for the synthesis of the precursor for p21ras farnesylation, was inhibited in neuroblastoma cells by lovastatin or L-ascorbic acid. Lovastatin 214-224 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-55 9927296-2 1999 Lovastatin, a 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase inhibitor, displays proapoptotic activity in tumor cells blocking the synthesis of isoprenoids compounds. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-71 9927296-4 1999 In an immortalized human thyroid cell line (TAD-2) and in neoplastic cells, lovastatin induced cell rounding within 24 h of treatment. Lovastatin 76-86 adenosine deaminase tRNA specific 2 Homo sapiens 44-49 9929499-0 1999 Comparison of cytochrome P-450-dependent metabolism and drug interactions of the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors lovastatin and pravastatin in the liver. Lovastatin 133-143 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 14-30 9929499-1 1999 In an in vitro study, the cytochrome P-450 3A (CYP3A)-dependent metabolism and drug interactions of the 3-hydroxy-3-methylglutaryl-Co A reductase inhibitors lovastatin and pravastatin were compared. Lovastatin 157-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 9929499-1 1999 In an in vitro study, the cytochrome P-450 3A (CYP3A)-dependent metabolism and drug interactions of the 3-hydroxy-3-methylglutaryl-Co A reductase inhibitors lovastatin and pravastatin were compared. Lovastatin 157-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 10192749-8 1999 The CETP activity correlated with the LDL cholesterol concentration (r = 0.52, P = 0.01) and the change in the LDL cholesterol during colestipol (r = 0.51, P = 0.02) and lovastatin (r = 0.65, P = 0.001) treatment, but only in patients without the apo E 4 allele. Lovastatin 170-180 cholesteryl ester transfer protein Homo sapiens 4-8 10192749-9 1999 CONCLUSION: Colestipol and lovastatin reduced CETP activity to the same amount, regardless of the apo E phenotype. Lovastatin 27-37 cholesteryl ester transfer protein Homo sapiens 46-50 11563401-9 1999 Simvastatin has no effect on platelet-thrombus formation or fibrinogen levels, while atorvastatin and lovastatin have been shown to increase fibrinogen in some studies. Lovastatin 102-112 fibrinogen beta chain Homo sapiens 141-151 11563401-10 1999 Plasminogen activator inhibitor-1 levels are decreased by pravastatin, are not affected by atorvastatin, and are significantly increased by lovastatin and simvastatin. Lovastatin 140-150 serpin family E member 1 Homo sapiens 0-33 10205288-6 1999 Lovastatin inhibited, PDGF-, angiotensin II- and PMA-mediated induction. Lovastatin 0-10 angiotensinogen Homo sapiens 29-43 10205288-10 1999 The data demonstrate that lovastatin can suppress PDGF- and angiotensin II-mediated induction of c-Jun and c-Fos protein in human SMC. Lovastatin 26-36 angiotensinogen Homo sapiens 60-74 10205288-10 1999 The data demonstrate that lovastatin can suppress PDGF- and angiotensin II-mediated induction of c-Jun and c-Fos protein in human SMC. Lovastatin 26-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 97-102 10205288-10 1999 The data demonstrate that lovastatin can suppress PDGF- and angiotensin II-mediated induction of c-Jun and c-Fos protein in human SMC. Lovastatin 26-36 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 107-112 10401660-1 1999 The cholesterol lowering drug lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, blocks DNA synthesis and proliferation of thyrotropin (TSH) primed FRTL-5 rat thyroid cells. Lovastatin 30-40 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 69-126 10401660-5 1999 It is suggested that the HMG-CoA reductase inhibitor lovastatin affects cell proliferation mainly through inhibition of protein farnesylation which results in altered function proteins relevant for proliferation control, notably p21ras and/or other small GTPases. Lovastatin 53-63 HRas proto-oncogene, GTPase Rattus norvegicus 229-235 10213372-5 1999 RESULTS: Some (terfenadine, erythromycin and lovastatin) but not all (nifedipine and midazolam) CYP3A substrates were found to be P-gp substrates. Lovastatin 45-55 phosphoglycolate phosphatase Homo sapiens 130-134 9933026-0 1999 The expression of the lectin-like oxidized low-density lipoprotein receptor (LOX-1) on human vascular smooth muscle cells and monocytes and its down-regulation by lovastatin. Lovastatin 163-173 oxidized low density lipoprotein receptor 1 Homo sapiens 77-82 9933026-6 1999 LOX-1 mRNA expression in monocytes could be significantly suppressed by lovastatin. Lovastatin 72-82 oxidized low density lipoprotein receptor 1 Homo sapiens 0-5 10390143-1 1999 The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models. Lovastatin 31-41 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 4-20 10390143-1 1999 The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models. Lovastatin 31-41 KRAS proto-oncogene, GTPase Rattus norvegicus 81-84 10390143-1 1999 The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models. Lovastatin 43-46 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 4-20 10390143-1 1999 The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models. Lovastatin 43-46 KRAS proto-oncogene, GTPase Rattus norvegicus 81-84 9882513-1 1999 The Ewing"s sarcoma cell line RD-ES, which carries the EWS/FLI-1 fusion gene, responded to the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin with growth arrest. Lovastatin 163-173 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 95-152 10374838-1 1999 Hydroxymethyl-glutaryl-CoA-reductase (HMG-CoA-reductase), the key enzyme for cholesterol synthesis and essential for the synthesis of the precursor for p21ras farnesylation, was inhibited in neuroblastoma cells by lovastatin or L-ascorbic acid. Lovastatin 214-224 HRas proto-oncogene, GTPase Homo sapiens 152-158 10374838-3 1999 However, while the addition of mevalonate, the product of HMG-CoA-reductase, circumvented the inhibition by lovastatin it had no reversing effect on the inhibition by L-ascorbic acid. Lovastatin 108-118 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 58-75 9872842-5 1999 Studies in our laboratory have demonstrated that lovastatin potently induces apoptosis in fibroblasts constitutively expressing Myc, and that lung fibroblasts isolated from fibrotic lesions constitutively express growth-promoting genes. Lovastatin 49-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 128-131 10202552-1 1999 It was shown in vitro that high concentrations of lovastatin, a competitive inhibitor of hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibited human malignant cells MOLT-4. Lovastatin 50-60 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 89-142 10423270-7 1999 Lovastatin-treated cells were shown to be synchronized in the G1 phase and to migrate simultaneously after FGF-1 stimulation. Lovastatin 0-10 fibroblast growth factor 1 Rattus norvegicus 107-112 10037258-11 1999 Lovastatin, which blocks 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreased the induction of DNA synthesis, but not of protein synthesis induced by insulin or TSH in PC Cl3 cells. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 25-72 10579901-7 1999 In contrast, we found that the expression of gas3 mRNA was neither upregulated in senescent cells nor in cells arrested in G1 using Lovastatin. Lovastatin 132-142 peripheral myelin protein 22 Homo sapiens 45-49 10037258-12 1999 In FRTL-5 cells, lovastatin reduced protein and DNA synthesis stimulated by insulin but not TSH-induced protein synthesis. Lovastatin 17-27 insulin Canis lupus familiaris 76-83 9864387-0 1999 Lovastatin induces p21WAF1/Cip1 in human vascular smooth muscle cells: influence on protein phosphorylation, cell cycle, induction of apoptosis, and growth inhibition. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 27-31 10037258-13 1999 Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin. Lovastatin 301-311 insulin Canis lupus familiaris 44-51 10037258-13 1999 Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin. Lovastatin 381-391 insulin Canis lupus familiaris 44-51 10372657-0 1999 High lovastatin doses combined with hypercholesterolemic diet induce hepatic damage and are lethal to the CD-1 mouse. Lovastatin 5-15 CD1 antigen complex Mus musculus 106-110 9869647-5 1999 Mevinolin (HMGR inhibitor) produced predicted increases in HMGR activity that were related to the degree of cholesterolgenesis inhibition (e.g., 4-fold, 9-fold, and 17-fold increases relative to 50%, 76%, and 90% inhibition, respectively). Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 11-15 9869647-5 1999 Mevinolin (HMGR inhibitor) produced predicted increases in HMGR activity that were related to the degree of cholesterolgenesis inhibition (e.g., 4-fold, 9-fold, and 17-fold increases relative to 50%, 76%, and 90% inhibition, respectively). Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-63 10372657-1 1999 The addition of 1% lovastatin (LVT) to hypercholesterolemic diets [1% cholesterol or 1% cholesterol plus 0.1% sodium deoxycholate (HD)] induced hepatic damage and was lethal to CD-1 mice in the first days of treatment; the females were more resistant than males. Lovastatin 19-29 CD1 antigen complex Mus musculus 177-181 9811471-4 1998 However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1. Lovastatin 102-112 H3 histone pseudogene 16 Homo sapiens 24-27 9920144-5 1999 Lovastatin caused a greater decline in total apolipoprotein B (apo B) and LDL apo B than gemfibrozil, whereas VLDL apo B decreased only after gemfibrozil therapy. Lovastatin 0-10 apolipoprotein B Homo sapiens 45-61 10548883-11 1999 Many of the PXR activators are widely used drugs such as dexamethasone, lovastatin, and rifampicin, whose induction of CYP3A levels causes them to promote the metabolism of other drugs, often with adverse consequences. Lovastatin 72-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 9862703-2 1998 Previous evidence that the pan-prenylation inhibitor lovastatin blocks Ag-stimulated Ca2+ influx, secretion, and membrane/cytoskeletal responses implicated isoprenylated proteins in the Fc epsilonRI-coupled signaling cascade but could not distinguish between contributions of C15 (farnesylated) and C20 (geranylgeranylated) species. Lovastatin 53-63 nuclear distribution C, dynein complex regulator Rattus norvegicus 276-279 9862703-8 1998 Additionally, only lovastatin inhibits phospholipase Cgamma-mediated inositol (1,4,5) trisphosphate production, sustained Ca2+ influx, and Ca2+-dependent IL-4 production, suggesting novel roles for geranylgeranylated (lovastatin-sensitive, BZA-5B-insensitive) proteins in Fc epsilonRI signal propagation. Lovastatin 19-29 interleukin 4 Rattus norvegicus 154-158 9848777-0 1998 Lovastatin inhibits mesangial cell proliferation via p27Kip1. Lovastatin 0-10 cyclin dependent kinase inhibitor 1B Homo sapiens 53-60 9848777-5 1998 Lovastatin increased the p27Kip1 protein level but produced no changes in the abundance of the p27Kip1 mRNA level both in the presence and absence of mitogens. Lovastatin 0-10 cyclin dependent kinase inhibitor 1B Homo sapiens 25-32 9848777-6 1998 Treatment with lovastatin revealed the increment of both CDK2- and CDK4-bound-p27Kip1. Lovastatin 15-25 cyclin dependent kinase 2 Homo sapiens 57-61 9848777-6 1998 Treatment with lovastatin revealed the increment of both CDK2- and CDK4-bound-p27Kip1. Lovastatin 15-25 cyclin dependent kinase 4 Homo sapiens 67-71 9848777-6 1998 Treatment with lovastatin revealed the increment of both CDK2- and CDK4-bound-p27Kip1. Lovastatin 15-25 cyclin dependent kinase inhibitor 1B Homo sapiens 78-85 9848777-7 1998 The experiment using antisense oligonucleotide against p27Kip1 showed significant amelioration of lovastatin-induced cell cycle arrest. Lovastatin 98-108 cyclin dependent kinase inhibitor 1B Homo sapiens 55-62 9848777-8 1998 Lovastatin reduced both platelet-derived growth factor-stimulated CDK2 and CDK4 kinase activities. Lovastatin 0-10 cyclin dependent kinase 2 Homo sapiens 66-70 9848777-8 1998 Lovastatin reduced both platelet-derived growth factor-stimulated CDK2 and CDK4 kinase activities. Lovastatin 0-10 cyclin dependent kinase 4 Homo sapiens 75-79 9848777-9 1998 In conclusion, lovastatin inhibited mesangial proliferation via translational upregulation or impairment of p27Kip1 protein degradation. Lovastatin 15-25 cyclin dependent kinase inhibitor 1B Homo sapiens 108-115 9806908-6 1998 Lack of 25-hydroxycholesterol activation of SM synthesis in cholesterol-starved SRD 6 and lovastatin-treated CHO-K1 cells was correlated with dephosphorylation of OSBP. Lovastatin 90-100 LOW QUALITY PROTEIN: oxysterol-binding protein 1 Cricetulus griseus 163-167 9811471-0 1998 Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53. Lovastatin 0-10 cyclin dependent kinase 2 Homo sapiens 88-92 9811471-0 1998 Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 124-127 9811471-0 1998 Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53. Lovastatin 0-10 interferon alpha inducible protein 27 Homo sapiens 132-135 9811471-2 1998 In the present study we have investigated the nature of the CKIs (p21 and p27) alterations resulting in G1 arrest in both normal and tumor breast cell lines by lovastatin. Lovastatin 160-170 H3 histone pseudogene 16 Homo sapiens 66-69 9811471-2 1998 In the present study we have investigated the nature of the CKIs (p21 and p27) alterations resulting in G1 arrest in both normal and tumor breast cell lines by lovastatin. Lovastatin 160-170 interferon alpha inducible protein 27 Homo sapiens 74-77 9811471-3 1998 We show that even though lovastatin treatment causes G1 arrest in a wide variety of normal and tumor breast cells irrespective of their p53 or pRb status, the p21 and p27 protein levels are not increased in all cell lines treated suggesting that the increase in p21 and p27 protein expression per se is not necessary for lovastatin mediated G1 arrest. Lovastatin 25-35 H3 histone pseudogene 16 Homo sapiens 262-265 9811471-3 1998 We show that even though lovastatin treatment causes G1 arrest in a wide variety of normal and tumor breast cells irrespective of their p53 or pRb status, the p21 and p27 protein levels are not increased in all cell lines treated suggesting that the increase in p21 and p27 protein expression per se is not necessary for lovastatin mediated G1 arrest. Lovastatin 25-35 interferon alpha inducible protein 27 Homo sapiens 270-273 9758637-5 1998 Aortas isolated from rats treated for 2 days with lovastatin (4 mg/kg body wt per day) showed a 3-fold increase in tissue plasminogen activator (tPA) activity. Lovastatin 50-60 plasminogen activator, tissue type Rattus norvegicus 115-143 9799039-7 1998 Renal arterioles isolated from lovastatin-treated SHR were significantly less responsive to norepinephrine and vasopressin than those obtained from vehicle-treated rats (ED50: 5.0 v 1.8 x 10(-7) mol/L for norepinephrine, and 8.0 v 5.2 x 10(-10) mol/L for vasopressin). Lovastatin 31-41 arginine vasopressin Rattus norvegicus 111-122 9799039-7 1998 Renal arterioles isolated from lovastatin-treated SHR were significantly less responsive to norepinephrine and vasopressin than those obtained from vehicle-treated rats (ED50: 5.0 v 1.8 x 10(-7) mol/L for norepinephrine, and 8.0 v 5.2 x 10(-10) mol/L for vasopressin). Lovastatin 31-41 arginine vasopressin Rattus norvegicus 255-266 9793596-12 1998 In comparison, currently available HMG-CoA reductase inhibitors (lovastatin, simvastatin, pravastatin, fluvastatin, cerivastatin) lower LDL-C concentrations by approximately 20-40% and TG concentrations by approximately 10-30%. Lovastatin 65-75 component of oligomeric golgi complex 2 Homo sapiens 136-141 9807971-6 1998 After 12 weeks of treatment with lovastatin alone, improvement was observed in total cholesterol (21% reduction), triglyceride (32% reduction), low-density lipoprotein (LDL) cholesterol (5.5% reduction), HDL cholesterol (11.6% elevation), apolipoprotein A-I (4.6% elevation), and apolipoprotein B (20.5% reduction). Lovastatin 33-43 apolipoprotein A1 Homo sapiens 239-257 9807971-6 1998 After 12 weeks of treatment with lovastatin alone, improvement was observed in total cholesterol (21% reduction), triglyceride (32% reduction), low-density lipoprotein (LDL) cholesterol (5.5% reduction), HDL cholesterol (11.6% elevation), apolipoprotein A-I (4.6% elevation), and apolipoprotein B (20.5% reduction). Lovastatin 33-43 apolipoprotein B Homo sapiens 280-296 9807971-7 1998 The addition of acipimox to lovastatin for an additional 12 weeks further reduced serum total cholesterol, triglyceride, LDL cholesterol, and apolipoprotein B, but this additional decrease was not statistically significant. Lovastatin 28-38 apolipoprotein B Homo sapiens 142-158 9807971-11 1998 Combination treatment with lovastatin and acipimox appears to be a safe and effective therapy in patients with type 2 diabetes and mixed dyslipidemia, and has particular benefit in elevating serum HDL cholesterol and apolipoprotein A-I levels. Lovastatin 27-37 apolipoprotein A1 Homo sapiens 217-235 9804052-3 1998 Pharmacokinetic interaction with some of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, specifically lovastatin and simvastatin, leads to an increased incidence of muscle skeletal toxicity in transplant patients. Lovastatin 118-128 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 45-92 9726984-10 1998 Lovastatin and simvastatin, inhibitors of HMG-CoA reductase, strongly suppressed cholesterol synthesis while having no effect on autophagic activity, suggesting that AMPK inhibits autophagy independently of its effects on HMG-CoA reductase and cholesterol metabolism. Lovastatin 0-10 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 166-170 16674346-4 1998 Later in the decade, the introduction of lovastatin, the first 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (or "statin"), revolutionized the treatment of hypercholesterolemia, as it was significantly more effective than earlier agents (as were the other statins that followed it). Lovastatin 41-51 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-120 9714140-7 1998 Apolipoprotein (apo) E mRNA levels increased but apoE secretion into the medium decreased with lovastatin treatment in both cholesterol-loaded and nonloaded cells. Lovastatin 95-105 apolipoprotein E Homo sapiens 0-22 9714140-7 1998 Apolipoprotein (apo) E mRNA levels increased but apoE secretion into the medium decreased with lovastatin treatment in both cholesterol-loaded and nonloaded cells. Lovastatin 95-105 apolipoprotein E Homo sapiens 49-53 9697659-5 1998 Incubation with lovastatin (5 microM) of proximal tubules isolated from untreated rats induced an increase in tPA and uPA and a decrease in plasminogen activator inhibitor-1 (PAI-1) activities. Lovastatin 16-26 plasminogen activator, tissue type Rattus norvegicus 110-113 9697659-5 1998 Incubation with lovastatin (5 microM) of proximal tubules isolated from untreated rats induced an increase in tPA and uPA and a decrease in plasminogen activator inhibitor-1 (PAI-1) activities. Lovastatin 16-26 plasminogen activator, urokinase Rattus norvegicus 118-121 9697659-5 1998 Incubation with lovastatin (5 microM) of proximal tubules isolated from untreated rats induced an increase in tPA and uPA and a decrease in plasminogen activator inhibitor-1 (PAI-1) activities. Lovastatin 16-26 serpin family E member 1 Rattus norvegicus 140-173 9697659-5 1998 Incubation with lovastatin (5 microM) of proximal tubules isolated from untreated rats induced an increase in tPA and uPA and a decrease in plasminogen activator inhibitor-1 (PAI-1) activities. Lovastatin 16-26 serpin family E member 1 Rattus norvegicus 175-180 9697659-6 1998 In vitro, supernatants, cytosols, and membranes of renal proximal tubular cells in primary cultures had no detectable uPA activity, and lovastatin (0.1 to 10 microM) induced an increase in tPA and a decrease in PAI-1 activities and antigens. Lovastatin 136-146 plasminogen activator, tissue type Rattus norvegicus 189-192 9697659-6 1998 In vitro, supernatants, cytosols, and membranes of renal proximal tubular cells in primary cultures had no detectable uPA activity, and lovastatin (0.1 to 10 microM) induced an increase in tPA and a decrease in PAI-1 activities and antigens. Lovastatin 136-146 serpin family E member 1 Rattus norvegicus 211-216 9697659-8 1998 C3 exoenzyme, an inhibitor of the geranylgeranylated-activated Rho protein, reproduced the effect of lovastatin on tPA and PAI- activity and blocked its reversion by GGPP. Lovastatin 101-111 plasminogen activator, tissue type Rattus norvegicus 115-118 9697659-8 1998 C3 exoenzyme, an inhibitor of the geranylgeranylated-activated Rho protein, reproduced the effect of lovastatin on tPA and PAI- activity and blocked its reversion by GGPP. Lovastatin 101-111 serpin family E member 1 Rattus norvegicus 123-126 9882513-1 1999 The Ewing"s sarcoma cell line RD-ES, which carries the EWS/FLI-1 fusion gene, responded to the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin with growth arrest. Lovastatin 163-173 EWS RNA binding protein 1 Homo sapiens 55-58 9882513-1 1999 The Ewing"s sarcoma cell line RD-ES, which carries the EWS/FLI-1 fusion gene, responded to the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin with growth arrest. Lovastatin 163-173 Fli-1 proto-oncogene, ETS transcription factor Homo sapiens 59-64 9758637-5 1998 Aortas isolated from rats treated for 2 days with lovastatin (4 mg/kg body wt per day) showed a 3-fold increase in tissue plasminogen activator (tPA) activity. Lovastatin 50-60 plasminogen activator, tissue type Rattus norvegicus 145-148 9758637-11 1998 C3 exoenzyme, an inhibitor of the geranylgeranylated-activated Rho protein, reproduced the effect of lovastatin on tPA and plasminogen activator inhibitor-1 activity and blocked its reversal by geranylgeranyl pyrophosphate. Lovastatin 101-111 plasminogen activator, tissue type Rattus norvegicus 115-118 9758637-11 1998 C3 exoenzyme, an inhibitor of the geranylgeranylated-activated Rho protein, reproduced the effect of lovastatin on tPA and plasminogen activator inhibitor-1 activity and blocked its reversal by geranylgeranyl pyrophosphate. Lovastatin 101-111 serpin family E member 1 Rattus norvegicus 123-156 9758637-13 1998 A disrupter of actin filaments, cytochalasin D, induced the same effect as lovastatin on tPA, whereas a disrupter of microtubules, nocodazole, did not. Lovastatin 75-85 plasminogen activator, tissue type Rattus norvegicus 89-92 9811471-4 1998 However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1. Lovastatin 102-112 interferon alpha inducible protein 27 Homo sapiens 32-35 9811471-4 1998 However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1. Lovastatin 102-112 cyclin dependent kinase 2 Homo sapiens 39-43 9811471-4 1998 However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1. Lovastatin 102-112 cyclin dependent kinase 2 Homo sapiens 138-142 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 choline kinase alpha Homo sapiens 14-17 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 cyclin dependent kinase 2 Homo sapiens 29-33 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 H3 histone pseudogene 16 Homo sapiens 76-79 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 interferon alpha inducible protein 27 Homo sapiens 84-87 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 cyclin dependent kinase 4 Homo sapiens 93-97 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 cyclin dependent kinase 2 Homo sapiens 101-105 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 cyclin dependent kinase 4 Homo sapiens 143-147 9811471-5 1998 The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment. Lovastatin 183-193 cyclin D3 Homo sapiens 152-161 9811471-6 1998 Lastly, we show that lovastatin treatment of 76N-E6 breast cell line with an altered p53 pathway also results in G1 arrest and similar redistribution of CKIs from CDK4 to CDK2 as observed in other breast cell lines examined. Lovastatin 21-31 tumor protein p53 Homo sapiens 85-88 9811471-6 1998 Lastly, we show that lovastatin treatment of 76N-E6 breast cell line with an altered p53 pathway also results in G1 arrest and similar redistribution of CKIs from CDK4 to CDK2 as observed in other breast cell lines examined. Lovastatin 21-31 cyclin dependent kinase 4 Homo sapiens 163-167 9811471-6 1998 Lastly, we show that lovastatin treatment of 76N-E6 breast cell line with an altered p53 pathway also results in G1 arrest and similar redistribution of CKIs from CDK4 to CDK2 as observed in other breast cell lines examined. Lovastatin 21-31 cyclin dependent kinase 2 Homo sapiens 171-175 9811471-7 1998 These observations suggest that lovastatin induced G1 arrest of breast cell lines is through a p53 independent pathway and is mediated by decreased CDK2 activity through redistribution of CKIs from CDK4 to CDK2. Lovastatin 32-42 tumor protein p53 Homo sapiens 95-98 9811471-7 1998 These observations suggest that lovastatin induced G1 arrest of breast cell lines is through a p53 independent pathway and is mediated by decreased CDK2 activity through redistribution of CKIs from CDK4 to CDK2. Lovastatin 32-42 cyclin dependent kinase 2 Homo sapiens 148-152 9811471-7 1998 These observations suggest that lovastatin induced G1 arrest of breast cell lines is through a p53 independent pathway and is mediated by decreased CDK2 activity through redistribution of CKIs from CDK4 to CDK2. Lovastatin 32-42 cyclin dependent kinase 4 Homo sapiens 198-202 9811471-7 1998 These observations suggest that lovastatin induced G1 arrest of breast cell lines is through a p53 independent pathway and is mediated by decreased CDK2 activity through redistribution of CKIs from CDK4 to CDK2. Lovastatin 32-42 cyclin dependent kinase 2 Homo sapiens 206-210 9703948-3 1998 Here we report that depletion of intracellular mevalonate by lovastatin in FRTL-5 thyroid cells specifically resulted in a four-fold increase of Rab5 and Rab7 protein levels. Lovastatin 61-71 RAB7A, member RAS oncogene family Rattus norvegicus 154-158 9802623-1 1998 Lovastatin, a fungal antibiotic used in the treatment of hypercholesterolemia, is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the key regulatory enzyme in the mevalonate pathway of cholesterol synthesis. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 98-145 9658178-8 1998 Indeed, blocking the activity of G-proteins using the general inhibitor lovastatin, or more specific antagonists of Rho proteins such as C3-transferase or dominant negative RhoA protein, resulted in a dramatic decrease of MyoD protein levels and promoter activity without any effects on Myf5 expression. Lovastatin 72-82 myogenic differentiation 1 Mus musculus 222-226 9661807-2 1998 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, such as lovastatin, prevent farnesylation of the Ras protein, which is critical for Ras"s membrane localization and function. Lovastatin 78-88 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 0-57 9661807-10 1998 Lovastatin as well as calphostin C partially but significantly inhibited the stretch-induced increases in MAP kinase activity, c-fos mRNA expression, and protein synthesis. Lovastatin 0-10 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 127-132 9600988-4 1998 By reducing the cellular cholesterol level of living hippocampal neurons by 70% with lovastatin and methyl-beta-cyclodextrin, we show that the formation of Abeta is completely inhibited while the generation of APPsec is unperturbed. Lovastatin 85-95 amyloid beta precursor protein Homo sapiens 156-161 9603146-2 1998 We report that pharmacologic concentrations of lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor, induced apoptosis in human malignant mesothelioma cell lines. Lovastatin 47-57 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 61-118 9591747-4 1998 We investigated the effect of apoE polymorphism on the serum lipid response to the hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin and the fibric acid derivative gemfibrozil. Lovastatin 155-165 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 91-144 9678770-5 1998 Lovastatin supplementation of the atherogenic diet induced significant upregulation of both LDL receptor and HMG CoA reductase message levels in liver and intestine compared to the chow and atherogenic diet fed groups. Lovastatin 0-10 low density lipoprotein receptor Homo sapiens 92-104 9678770-5 1998 Lovastatin supplementation of the atherogenic diet induced significant upregulation of both LDL receptor and HMG CoA reductase message levels in liver and intestine compared to the chow and atherogenic diet fed groups. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 109-126 9678770-6 1998 These data demonstrate that lovastatin supplementation of an atherogenic diet decreases foam cell accumulation and induces upregulation of hepatic and intestinal LDL receptor and HMG CoA reductase mRNA levels. Lovastatin 28-38 low density lipoprotein receptor Homo sapiens 162-174 9678770-6 1998 These data demonstrate that lovastatin supplementation of an atherogenic diet decreases foam cell accumulation and induces upregulation of hepatic and intestinal LDL receptor and HMG CoA reductase mRNA levels. Lovastatin 28-38 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 179-196 9525472-2 1998 The objective of this study was to determine the effect of IGF-I on cell death induced by cytotoxic agents actinomycin D (Act-D), lovastatin (LOV), and doxorubicin (DOX) in the MCLM mouse colon cancer cell line, and the mechanisms involved. Lovastatin 130-140 insulin-like growth factor 1 Mus musculus 59-64 9525472-2 1998 The objective of this study was to determine the effect of IGF-I on cell death induced by cytotoxic agents actinomycin D (Act-D), lovastatin (LOV), and doxorubicin (DOX) in the MCLM mouse colon cancer cell line, and the mechanisms involved. Lovastatin 142-145 insulin-like growth factor 1 Mus musculus 59-64 9555954-0 1998 Three-fold effect of lovastatin treatment on low density lipoprotein metabolism in subjects with hyperlipidemia: increase in receptor activity, decrease in apoB production, and decrease in particle affinity for the receptor. Lovastatin 21-31 apolipoprotein B Homo sapiens 156-160 17165328-5 1998 Cost-effectiveness analysis of cholesterol-lowering drugs indicated that lovastatin (HMG-CoA reductase inhibitor) was more cost effective than cholestyramine (bile acid sequestrant) and gemfibrozil (fibrate). Lovastatin 73-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 85-102 9553123-2 1998 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin induces growth arrest and cell death in certain cancer cell types. Lovastatin 72-82 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-61 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 96-99 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 100-109 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 133-136 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase 2 Homo sapiens 142-146 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase 2 Homo sapiens 181-185 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 E2F transcription factor 1 Homo sapiens 333-338 9553123-4 1998 Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct. Lovastatin 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 133-136 9553123-5 1998 By using p21 promoter deletion constructs, the lovastatin-responsive element was mapped to a region between -93 and -64 relative to the transcription start site. Lovastatin 47-57 cyclin dependent kinase inhibitor 1A Homo sapiens 9-12 9650858-3 1998 Further, we assessed the effect of lovastatin, an 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on hypertrophy of cultured vascular smooth muscle cells as defined by the increased incorporation of [14C]leucine caused by phenylephrine. Lovastatin 35-45 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 50-107 9555954-8 1998 The results demonstrate three important outcomes of lovastatin treatment in these subjects: LDL receptor activity increased by 49% (P < 0.02); LDL apoB production rate decreased by 17% (P < 0.03), and LDL particle in vivo affinity for the LDL receptor decreased by 15% (P < 0.01). Lovastatin 52-62 low density lipoprotein receptor Homo sapiens 92-104 9555954-8 1998 The results demonstrate three important outcomes of lovastatin treatment in these subjects: LDL receptor activity increased by 49% (P < 0.02); LDL apoB production rate decreased by 17% (P < 0.03), and LDL particle in vivo affinity for the LDL receptor decreased by 15% (P < 0.01). Lovastatin 52-62 apolipoprotein B Homo sapiens 150-154 9555954-8 1998 The results demonstrate three important outcomes of lovastatin treatment in these subjects: LDL receptor activity increased by 49% (P < 0.02); LDL apoB production rate decreased by 17% (P < 0.03), and LDL particle in vivo affinity for the LDL receptor decreased by 15% (P < 0.01). Lovastatin 52-62 low density lipoprotein receptor Homo sapiens 245-257 9510082-2 1998 Lovastatin (1, 1.5, and 2 mg/kg) decreased systolic (SBP) and diastolic blood pressure (DBP) in spontaneously hypertensive rats (SHRs) and did not modify the basal values of blood pressure in normotensive rats. Lovastatin 0-10 spermine binding protein Rattus norvegicus 53-56 9697659-4 1998 Proximal tubules freshly isolated from rats treated for 2 d with lovastatin (4 mg/kg per d) showed increased tissue-type plasminogen activator (tPA) and urokinase (uPA) activities and antigens. Lovastatin 65-75 plasminogen activator, tissue type Rattus norvegicus 144-147 9697659-4 1998 Proximal tubules freshly isolated from rats treated for 2 d with lovastatin (4 mg/kg per d) showed increased tissue-type plasminogen activator (tPA) and urokinase (uPA) activities and antigens. Lovastatin 65-75 plasminogen activator, urokinase Rattus norvegicus 164-167 9537338-5 1998 Both simvastatin (1 micromol/L) and lovastatin (10 micromol/L) upregulated ecNOS expression by 3.8-fold and 3.6-fold, respectively, and completely prevented its downregulation by ox-LDL. Lovastatin 36-46 nitric oxide synthase 3 Homo sapiens 75-80 9428473-0 1998 Lovastatin reduces glomerular macrophage influx and expression of monocyte chemoattractant protein-1 mRNA in nephrotic rats. Lovastatin 0-10 C-C motif chemokine ligand 2 Rattus norvegicus 66-100 9487235-2 1998 OBJECTIVE: To compare the average and marginal life-time cost-effectiveness of increasing dosages of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, such as lovastatin, for the primary prevention of coronary heart disease (CHD). Lovastatin 179-189 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 101-158 9472115-0 1998 Lovastatin inhibits proliferation of pancreatic cancer cell lines with mutant as well as with wild-type K-ras oncogene but has different effects on protein phosphorylation and induction of apoptosis. Lovastatin 0-10 KRAS proto-oncogene, GTPase Homo sapiens 104-109 9472115-1 1998 Besides its pharmacological effect on cholesterol biosynthesis, lovastatin inhibits p21ras proteins by substrate depletion for post-translational protein farnesylation and geranylation. Lovastatin 64-74 HRas proto-oncogene, GTPase Homo sapiens 84-90 9472115-9 1998 However, after 72 h of drug exposure, lovastatin significantly decreased protein phosphorylation on tyrosine, serine and threonine residues in A818-4 (p21ras-M) cells. Lovastatin 38-48 HRas proto-oncogene, GTPase Homo sapiens 151-157 9428473-2 1998 Previous studies have shown that lovastatin ameliorates experimental renal disease and reduces MCP-1 expression in serum-stimulated, cultured mesangial cells. Lovastatin 33-43 C-C motif chemokine ligand 2 Rattus norvegicus 95-100 9555564-4 1998 Lovastatin, an inhibitor of hydroxymethylglutaryl coenzyme A, antagonized both the basal proliferation and the growth factor-stimulated proliferation of human prostate epithelium (EGF, mean inhibition approximately 80-95%; b-FGF, mean inhibition approximately 40-90%). Lovastatin 0-10 fibroblast growth factor 2 Homo sapiens 223-228 9426061-0 1998 Caspase-7 is activated during lovastatin-induced apoptosis of the prostate cancer cell line LNCaP. Lovastatin 30-40 caspase 7 Homo sapiens 0-9 9426061-7 1998 Lovastatin induced a proteolytic activity that was able to cleave the enzyme poly(ADP-ribose) polymerase and the substrate Z-DEVD-AFC, which is modeled after the P1-P4 amino acids of the poly(ADP-ribose) polymerase cleavage site. Lovastatin 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 77-104 9426061-7 1998 Lovastatin induced a proteolytic activity that was able to cleave the enzyme poly(ADP-ribose) polymerase and the substrate Z-DEVD-AFC, which is modeled after the P1-P4 amino acids of the poly(ADP-ribose) polymerase cleavage site. Lovastatin 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 187-214 9426061-8 1998 Caspase-7, but not caspase-3, underwent proteolytic activation during lovastatin-induced apoptosis, an effect prevented by mevalonate. Lovastatin 70-80 caspase 7 Homo sapiens 0-9 9426061-9 1998 Caspase-7 was the only detected interleukin 1beta converting enzyme family protease with DEVD cleavage activity that exhibited lovastatin-induced mRNA up-regulation. Lovastatin 127-137 caspase 7 Homo sapiens 0-9 9426061-14 1998 Of the caspases tested, only caspase-7 underwent proteolytic activation after stimulation with lovastatin. Lovastatin 95-105 caspase 7 Homo sapiens 29-38 9426061-15 1998 Identification of caspase-7 as a potential mediator of lovastatin-induced apoptosis broadens our knowledge of the molecular events associated with programmed cell death in a cell line derived from prostatic epithelium. Lovastatin 55-65 caspase 7 Homo sapiens 18-27 9509899-1 1998 The recent development of specific competitive inhibitors of the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase such as lovastatin, simvastatin, pravastatin and fluvastatin has provided an important new and effective approach to the treatment of hyperlipidaemia and atherosclerosis. Lovastatin 126-136 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 65-117 9430371-3 1997 The present study addressed the question whether the inhibitory effect of lovastatin on premitotic DNA synthesis correlates with a downregulation of c-fos mRNA levels, a marker of signaling efficiency, in human SMC. Lovastatin 74-84 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 149-154 9395516-5 1997 In a concentration-dependent manner, simvastatin, and to a lesser extent, lovastatin, prevented the down-regulation of ecNOS expression by hypoxia. Lovastatin 74-84 nitric oxide synthase 3 Homo sapiens 119-124 9430371-6 1997 Lovastatin efficiently inhibited [3H]thymidine uptake promoted by all mitogens tested (76-87%); however, it significantly inhibited upregulation of c-fos mRNA levels induced only by insulin (33-67%, P < 0.05) and IGF-I (31 57%, P < 0.05). Lovastatin 0-10 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 148-153 9430371-6 1997 Lovastatin efficiently inhibited [3H]thymidine uptake promoted by all mitogens tested (76-87%); however, it significantly inhibited upregulation of c-fos mRNA levels induced only by insulin (33-67%, P < 0.05) and IGF-I (31 57%, P < 0.05). Lovastatin 0-10 insulin Homo sapiens 182-189 9430371-6 1997 Lovastatin efficiently inhibited [3H]thymidine uptake promoted by all mitogens tested (76-87%); however, it significantly inhibited upregulation of c-fos mRNA levels induced only by insulin (33-67%, P < 0.05) and IGF-I (31 57%, P < 0.05). Lovastatin 0-10 insulin like growth factor 1 Homo sapiens 216-221 9389730-2 1997 Lovastatin and sodium phenylacetate (NaPA) were found to inhibit LPS- and cytokine-mediated production of NO and expression of iNOS in rat primary astrocytes; this inhibition was not due to depletion of end products of mevalonate pathway (e.g., cholesterol and ubiquinone). Lovastatin 0-10 nitric oxide synthase 2 Rattus norvegicus 127-131 9389730-3 1997 Reversal of the inhibitory effect of lovastatin on LPS-induced iNOS expression by mevalonate and farnesyl pyrophosphate and reversal of the inhibitory effect of NaPA on LPS-induced iNOS expression by farnesyl pyrophosphate, however, suggests a role of farnesylation in the LPS-mediated induction of iNOS. Lovastatin 37-47 nitric oxide synthase 2 Rattus norvegicus 63-67 9389730-5 1997 Inhibition of LPS-mediated activation of NF-kbeta by lovastatin, NaPA, and FPT inhibitor II in astrocytes indicates that the observed inhibition of iNOS expression is mediated via inhibition of NF-kbeta activation. Lovastatin 53-63 nitric oxide synthase 2 Rattus norvegicus 148-152 9389730-6 1997 In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages. Lovastatin 21-31 tumor necrosis factor Rattus norvegicus 82-91 9356453-9 1997 Treatment with lovastatin and Colestipol, which increases hepatic demands for cholesterol, increased the amount of SREBP-2 mRNA as well as the precursor and nuclear forms of the protein. Lovastatin 15-25 sterol regulatory element binding transcription factor 2 Homo sapiens 115-122 9389730-6 1997 In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages. Lovastatin 21-31 interleukin 1 beta Rattus norvegicus 93-101 9389730-6 1997 In addition to iNOS, lovastatin and NaPA also inhibited LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages. Lovastatin 21-31 interleukin 6 Rattus norvegicus 107-111 9421099-1 1997 Itraconazole strongly interacts with some drugs metabolized by cytochrome P450 3A4, for example, felodipine and lovastatin, by inhibiting their metabolism. Lovastatin 112-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 9353308-5 1997 Actinomycin D and lovastatin induced rapid loss of cyclin D1 in prostate and breast cancer cells that was reversible by calpain inhibitors and not by phenylmethylsulfonyl fluoride, caspase inhibitors, or lactacystin, a specific inhibitor of the 26 S proteasome. Lovastatin 18-28 cyclin D1 Mus musculus 51-60 9459136-19 1997 Also, plasma acetylhydrolase activity significantly correlated with fasting plasma insulin levels before lovastatin therapy but not after. Lovastatin 105-115 insulin Homo sapiens 83-90 9350917-6 1997 Treatment of monocytes with lovastatin in vitro slightly and dose dependently reduced surface expression of CD11b on monocytes. Lovastatin 28-38 integrin subunit alpha M Homo sapiens 108-113 9350917-7 1997 Moreover, lovastatin inhibited CD11b-dependent adhesiveness to fixed endothelium of unstimulated monocytes or monocytes stimulated with monocyte chemotactic protein 1. Lovastatin 10-20 integrin subunit alpha M Homo sapiens 31-36 9350917-7 1997 Moreover, lovastatin inhibited CD11b-dependent adhesiveness to fixed endothelium of unstimulated monocytes or monocytes stimulated with monocyte chemotactic protein 1. Lovastatin 10-20 C-C motif chemokine ligand 2 Homo sapiens 136-166 9350917-10 1997 Treatment of these patients with the HMG-CoA reductase inhibitors lovastatin or simvastatin (20 to 40 mg/day) for 6 weeks slightly decreased total and LDL cholesterol plasma levels and monocyte CD11b surface expression but resulted in a significant reduction of monocyte adhesion to endothelium (p < 0.01, n = 7). Lovastatin 66-76 integrin subunit alpha M Homo sapiens 194-199 9392426-5 1997 Among normolipidemic individuals, plasma PAF-AH activity was strongly correlated with the plasma concentration of low density lipoprotein cholesterol (LDL-C), and treatment with lovastatin resulted in proportional decreases in plasma PAF-AH activity and LDL-C concentrations. Lovastatin 178-188 phospholipase A2 group VII Homo sapiens 41-47 9392426-5 1997 Among normolipidemic individuals, plasma PAF-AH activity was strongly correlated with the plasma concentration of low density lipoprotein cholesterol (LDL-C), and treatment with lovastatin resulted in proportional decreases in plasma PAF-AH activity and LDL-C concentrations. Lovastatin 178-188 phospholipase A2 group VII Homo sapiens 234-240 9398081-9 1997 The small GTP-binding protein RhoA, which may be important for cell spreading and cytokinesis, accumulated in the cytosol following treatment with lovastatin, suggestive of its inactivation. Lovastatin 147-157 ras homolog family member A Homo sapiens 30-34 9353412-10 1997 On the contrary, lovastatin-treated, round Swiss 3T3 cells reverted to a flat morphology when microinjected with dominant active RhoA (Val14RhoA). Lovastatin 17-27 ras homolog family member A Mus musculus 129-133 9351353-0 1997 Lovastatin decreases de novo cholesterol synthesis and LDL Apo B-100 production rates in combined-hyperlipidemic males. Lovastatin 0-10 apolipoprotein B Homo sapiens 59-68 9351353-8 1997 Comparing the kinetic data of these patients with those of 10 normolipidemic control subjects indicates that lovastatin treatment normalized apoB-100 IDL and LDL PR. Lovastatin 109-119 apolipoprotein B Homo sapiens 141-149 9351353-9 1997 The results of these studies suggest that the declines in plasma lipid levels observed after treatment of combined hyperlipidemic patients with lovastatin are attributable to reductions in the C-FSR and C-PR of de novo cholesterol synthesis and the PR of apoB-100 containing lipoproteins. Lovastatin 144-154 cytochrome p450 oxidoreductase Homo sapiens 203-207 9351353-9 1997 The results of these studies suggest that the declines in plasma lipid levels observed after treatment of combined hyperlipidemic patients with lovastatin are attributable to reductions in the C-FSR and C-PR of de novo cholesterol synthesis and the PR of apoB-100 containing lipoproteins. Lovastatin 144-154 apolipoprotein B Homo sapiens 255-263 9410880-7 1997 When membrane localization of RhoA is prevented by lovastatin, an inhibitor of protein isoprenylation, or by CAAX motif mutation, cytoskeletal contraction is blocked. Lovastatin 51-61 ras homolog family member A Mus musculus 30-34 9381994-0 1997 Comparison of bezafibrate versus lovastatin for lowering plasma insulin, fibrinogen, and plasminogen activator inhibitor-1 concentrations in hyperlipemic heart transplant patients. Lovastatin 33-43 insulin Homo sapiens 64-71 9381994-0 1997 Comparison of bezafibrate versus lovastatin for lowering plasma insulin, fibrinogen, and plasminogen activator inhibitor-1 concentrations in hyperlipemic heart transplant patients. Lovastatin 33-43 serpin family E member 1 Homo sapiens 89-122 9344354-5 1997 RESULTS: Rat lenses organ cultured for 7 days with lovastatin, a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, developed frank subcapsular opacity. Lovastatin 51-61 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 65-105 9316617-0 1997 Lovastatin inhibits prolactin-induced Nb2 cell mitogenesis and milk product synthesis in mouse mammary gland explants. Lovastatin 0-10 prolactin Mus musculus 20-29 9365051-9 1997 We conclude that in two siblings with a novel LAL variant and mild phenotype of CESD, lovastatin decreased both serum lipid concentrations and hepatocellular lysosomal content. Lovastatin 86-96 lipase A, lysosomal acid type Homo sapiens 46-49 9316617-4 1997 Lovastatin completely inhibited PRL-induced Nb2 cell mitogenesis at 1 micron. Lovastatin 0-10 prolactin Mus musculus 32-35 9316617-5 1997 In the mammary gland, lovastatin at 0.1 micron inhibited the PRL stimulation of lipid and lactose synthesis; at 2 microns, lovastatin abolished the PRL stimulation of casein production. Lovastatin 22-32 prolactin Mus musculus 61-64 9316617-5 1997 In the mammary gland, lovastatin at 0.1 micron inhibited the PRL stimulation of lipid and lactose synthesis; at 2 microns, lovastatin abolished the PRL stimulation of casein production. Lovastatin 123-133 prolactin Mus musculus 148-151 9316617-6 1997 When p21ras was immunoprecipitated from lovastatin (25 microns)-treated Nb2 cells and mammary gland explants, the unfarnesylated (inactive) form of ras was shown to be redistributed from the cell membrane to the cytosolic compartment of the cell. Lovastatin 40-50 Harvey rat sarcoma virus oncogene Mus musculus 5-11 9244400-9 1997 In contrast, feeding 2% cholesterol to rats fed a diet supplemented with 0.04% lovastatin significantly decreased hepatic LDL receptor mRNA levels and transcription rates. Lovastatin 79-89 low density lipoprotein receptor Rattus norvegicus 122-134 9328940-0 1997 Lovastatin-induced inhibition of renal epithelial tubular cell proliferation involves a p21ras activated, AP-1-dependent pathway. Lovastatin 0-10 HRas proto-oncogene, GTPase Rattus norvegicus 88-94 9328940-0 1997 Lovastatin-induced inhibition of renal epithelial tubular cell proliferation involves a p21ras activated, AP-1-dependent pathway. Lovastatin 0-10 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 106-110 9328940-4 1997 The proliferative effect of epidermal growth factor (EGF) was similarly abolished by lovastatin. Lovastatin 85-95 epidermal growth factor like 1 Rattus norvegicus 28-51 9328940-4 1997 The proliferative effect of epidermal growth factor (EGF) was similarly abolished by lovastatin. Lovastatin 85-95 epidermal growth factor like 1 Rattus norvegicus 53-56 9328940-6 1997 Immunoblot analysis showed that lovastatin decreased membrane-bound p21ras and inhibited FCS-induced c-fos and c-jun protein expression. Lovastatin 32-42 HRas proto-oncogene, GTPase Rattus norvegicus 68-74 9328940-6 1997 Immunoblot analysis showed that lovastatin decreased membrane-bound p21ras and inhibited FCS-induced c-fos and c-jun protein expression. Lovastatin 32-42 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 101-106 9328940-7 1997 Furthermore, electrophoretic mobility shift assay demonstrated the functional impairement of AP-1 DNA binding activity in lovastatin-treated cells. Lovastatin 122-132 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 93-97 9252408-7 1997 Our observations support the role of a prenylated protein, such as the geranylgeranylated small G protein Rab6, in the retrograde transport from the Golgi apparatus to the ER, since lovastatin acts by inhibiting its prenylation. Lovastatin 182-192 RAB6A, member RAS oncogene family Homo sapiens 106-110 9244400-10 1997 These results suggest that lovastatin unmasks transcriptional regulation of the hepatic LDL receptor by dietary cholesterol. Lovastatin 27-37 low density lipoprotein receptor Rattus norvegicus 88-100 9300777-4 1997 HSL transfectants expressed 20-60% fewer LDL receptors than control cells when grown in lipid-depleted media or in the presence of mevinolin, as assessed by binding and degradation of LDL and immunoblotting of LDL receptors. Lovastatin 131-140 hormone-sensitive lipase Cricetulus griseus 0-3 9283719-2 1997 In this study the effect of lovastatin, an inhibitor of cholesterol and isoprenoid synthesis, on the rises in intracellular calcium concentration ([Ca2+]i) induced by platelet derived growth factor BB (PDGF-BB), angiotensin II (AII), low density lipoproteins (LDL) and foetal calf serum (FCS) was examined in human cultured vascular smooth muscle cells (VSMC) from saphenous vein. Lovastatin 28-38 angiotensinogen Homo sapiens 212-226 9283719-2 1997 In this study the effect of lovastatin, an inhibitor of cholesterol and isoprenoid synthesis, on the rises in intracellular calcium concentration ([Ca2+]i) induced by platelet derived growth factor BB (PDGF-BB), angiotensin II (AII), low density lipoproteins (LDL) and foetal calf serum (FCS) was examined in human cultured vascular smooth muscle cells (VSMC) from saphenous vein. Lovastatin 28-38 angiotensinogen Homo sapiens 228-231 9283719-5 1997 Incubation with lovastatin for 24-26 h markedly reduced the peak rise and sustained phase of [Ca2+]i elevation in response to PDGF-BB but the responses to AII, LDL and FCS were unaffected. Lovastatin 16-26 angiotensinogen Homo sapiens 155-158 9247534-1 1997 OBJECTIVES: We sought to document the common mechanisms of the antiatherogenic effects of the cholesterol-lowering hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin, the dihydropyridine Ca2+ blocker amlodipine and the antioxidant vitamin E. Lovastatin 179-189 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 115-168 9377621-7 1997 Lovastatin 20 mg/d reduced LDL-C levels by 24.9% and total-C levels by 17.7%; lovastatin 80 mg/d reduced these levels by 39.8% and 29.2%, respectively. Lovastatin 0-10 component of oligomeric golgi complex 2 Homo sapiens 27-32 9210653-1 1997 The possibility that potent inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase may alter the mechanisms by which dietary cholesterol and farnesol regulate this gene was investigated by comparing the regulatory responses of rats maintained on diets with or without 0.04% Lovastatin supplementation to dietary cholesterol. Lovastatin 291-301 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 42-99 9220025-0 1997 Lovastatin decreases prolactin and growth hormone gene expression in GH4C1 cells through a cAMP dependent mechanism. Lovastatin 0-10 prolactin Rattus norvegicus 21-30 9237866-4 1997 Mevalonate derived nonsterols were additionally restricted by inhibition of HMGR activity with lovastatin. Lovastatin 95-105 high mobility group AT-hook 1 Homo sapiens 76-80 9221829-0 1997 HMG CoA reductase inhibitor-induced myotoxicity: pravastatin and lovastatin inhibit the geranylgeranylation of low-molecular-weight proteins in neonatal rat muscle cell culture. Lovastatin 65-75 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 0-17 9237640-2 1997 During the 6-week treatment period lovastatin (60 mg/day) decreased fasting serum LDL cholesterol by 45%, LDL phosphorus by 38% and apoB by 33%. Lovastatin 35-45 apolipoprotein B Homo sapiens 132-136 9220025-10 1997 Moreover the effects of lovastatin may be taken into account in the study of constitutively endocrine disorders associated with an increased secretion of either PRL or GH. Lovastatin 24-34 prolactin Rattus norvegicus 161-164 9220025-10 1997 Moreover the effects of lovastatin may be taken into account in the study of constitutively endocrine disorders associated with an increased secretion of either PRL or GH. Lovastatin 24-34 gonadotropin releasing hormone receptor Rattus norvegicus 168-170 9254045-5 1997 We found that mevalonate depletion due to treatment with 3 microM lovastatin for 24 h, which efficiently growth-arrested the cells, hardly at all affected the expression of c-myc, and although Ras prenylation was inhibited by 50%, the most pronounced effect of lovastatin was seen on N-linked glycosylation of IGF-1 receptors, which was inhibited by more than 95%. Lovastatin 66-76 insulin like growth factor 1 Homo sapiens 310-315 9220025-0 1997 Lovastatin decreases prolactin and growth hormone gene expression in GH4C1 cells through a cAMP dependent mechanism. Lovastatin 0-10 gonadotropin releasing hormone receptor Rattus norvegicus 35-49 9220025-0 1997 Lovastatin decreases prolactin and growth hormone gene expression in GH4C1 cells through a cAMP dependent mechanism. Lovastatin 0-10 gonadotropin releasing hormone receptor Rattus norvegicus 69-71 9220025-4 1997 Since the regulation of these two genes is dependent on the pituitary specific transcription factor Pit-1, the effect of lovastatin on the expression of Pit-1-CAT constructions was also studied. Lovastatin 121-131 POU class 1 homeobox 1 Rattus norvegicus 153-158 9220025-6 1997 This effect of lovastatin on the promoter activities of the transfected constructions was also observed in PRL and GH secretion to the medium, suggesting that this drug produces similar changes in the endogenous promoters of both hormones. Lovastatin 15-25 prolactin Rattus norvegicus 107-110 9220025-6 1997 This effect of lovastatin on the promoter activities of the transfected constructions was also observed in PRL and GH secretion to the medium, suggesting that this drug produces similar changes in the endogenous promoters of both hormones. Lovastatin 15-25 gonadotropin releasing hormone receptor Rattus norvegicus 115-117 9220025-8 1997 In conclusion, our data indicate that lovastatin decreases the basal expression of Pit-1 and consequently of both GH and PRL genes through a mechanism probably mediated by the decrease of G alpha s levels in the cell membrane. Lovastatin 38-48 POU class 1 homeobox 1 Rattus norvegicus 83-88 9220025-8 1997 In conclusion, our data indicate that lovastatin decreases the basal expression of Pit-1 and consequently of both GH and PRL genes through a mechanism probably mediated by the decrease of G alpha s levels in the cell membrane. Lovastatin 38-48 gonadotropin releasing hormone receptor Rattus norvegicus 114-116 9220025-8 1997 In conclusion, our data indicate that lovastatin decreases the basal expression of Pit-1 and consequently of both GH and PRL genes through a mechanism probably mediated by the decrease of G alpha s levels in the cell membrane. Lovastatin 38-48 prolactin Rattus norvegicus 121-124 9199496-3 1997 In this study we show that lovastatin-mediated inhibition of G gamma subunits isoprenylation in HEK-293 cells stably transfected with beta ARK1 leads to a significant release of G beta subunits to the cytosol without causing changes in total particulate beta ARK or in the association of this kinase to plasma or microsomal membrane fractions. Lovastatin 27-37 G protein-coupled receptor kinase 2 Homo sapiens 134-143 9199267-8 1997 LDL and lovastatin modulated the LDL-R expression without affecting SI. Lovastatin 8-18 low density lipoprotein receptor Homo sapiens 33-38 9184709-11 1997 CONCLUSIONS: Lovastatin 20 mg every other day may effectively lower LDL-C in some elderly men, and target LDL-C concentrations may be obtained in some patients. Lovastatin 13-23 component of oligomeric golgi complex 2 Homo sapiens 68-73 9141529-6 1997 After cells achieved confluence, we induced apoptosis with the HMGCoA reductase inhibitor, lovastatin (30 micromol/L). Lovastatin 91-101 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-79 9153192-8 1997 Pretreatment with lovastatin, an inhibitor of protein prenylation, resulted in superinduction of NOS-2. Lovastatin 18-28 nitric oxide synthase 2 Rattus norvegicus 97-102 9108785-2 1997 This differential effect of lovastatin on apoB-containing lipoprotein families offered the opportunity to determine in the same subset of MARS subjects the independent relationship of LpB and LpBc with the progression of coronary artery disease. Lovastatin 28-38 apolipoprotein B Homo sapiens 42-46 9108785-7 1997 In the placebo- and lovastatin-treated groups combined, progressors had significantly higher on-trial levels of triglycerides (P = .003), VLDL cholesterol (P = .005), apoC-III in VLDL + LDL (P = .008), apoC-III (P = .01), apoB (P = .03), and total cholesterol (P = .04) than nonprogressors. Lovastatin 20-30 apolipoprotein C3 Homo sapiens 167-175 9108785-7 1997 In the placebo- and lovastatin-treated groups combined, progressors had significantly higher on-trial levels of triglycerides (P = .003), VLDL cholesterol (P = .005), apoC-III in VLDL + LDL (P = .008), apoC-III (P = .01), apoB (P = .03), and total cholesterol (P = .04) than nonprogressors. Lovastatin 20-30 apolipoprotein C3 Homo sapiens 202-210 9108785-7 1997 In the placebo- and lovastatin-treated groups combined, progressors had significantly higher on-trial levels of triglycerides (P = .003), VLDL cholesterol (P = .005), apoC-III in VLDL + LDL (P = .008), apoC-III (P = .01), apoB (P = .03), and total cholesterol (P = .04) than nonprogressors. Lovastatin 20-30 apolipoprotein B Homo sapiens 222-226 9108785-8 1997 Even after adjustment for treatment group, progressors in the combined placebo- and lovastatin-treated groups had significantly higher levels of LpBc, LpA-II:B:C:D:E, triglycerides, and apoC-III in VLDL + LDL than nonprogressors. Lovastatin 84-94 apolipoprotein C3 Homo sapiens 186-194 9497506-6 1997 Lovastatin reduced TC (-29%), LDL-C (-37%) and TG (-25%) (p < 0.001) however, it did not affect Lp(a). Lovastatin 0-10 component of oligomeric golgi complex 2 Homo sapiens 30-35 9108785-9 1997 Progressors in the placebo-treated, lovastatin-treated, and combined treatment groups had lower levels of LpA-1 but not LpA-I:A-II than non-progressors, and this difference reached statistical significance (P = .047) in the combined sample adjusted for treatment group. Lovastatin 36-46 lysophosphatidic acid receptor 1 Homo sapiens 106-111 8954966-6 1996 The effect of lovastatin and (alpha-hydroxyfarnesyl) phosphonic acid is specifically due to their ability to inhibit p21(ras) activity. Lovastatin 14-24 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 117-120 18975195-1 1997 New HMG-CoA reductase inhibitors, in which 3-substituted 4,5-polymethylenepyrazoles are employed as a hydrophobic anchor connected to tetrahydro-4-hydroxy-2H-pyran-2-one by a two-carbon bridge, were designed and synthesized to exhibit significant inhibitory activity comparable to mevinolin. Lovastatin 281-290 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-21 18975195-2 1997 The most potent enzyme inhibitor (11cc, IC(50)=0.01 muM) is 4-fold more potent than lovastatin. Lovastatin 84-94 latexin Homo sapiens 52-55 9129558-2 1997 Itraconazole strongly interacts with some of the substrates of CYP3A4 (e.g., terfenadine, triazolam and lovastatin); hence it is important to uncover the possible interaction of itraconazole with felodipine. Lovastatin 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 9070894-5 1997 RTAC cells pretreated with lovastatin and labeled with either [3H]geranylgeranyl-pyrophosphate or [3H]farnesyl-pyrophosphate incorporated also radioactivity into Ras p21. Lovastatin 27-37 KRAS proto-oncogene, GTPase Rattus norvegicus 166-169 9044834-5 1997 Synchronization of tumor cells by lovastatin, which arrests cells in G1, resulted in increased levels of p21 and p27 with a concomitant decrease in cyclin-dependent kinase 2-associated kinase activity. Lovastatin 34-44 cyclin dependent kinase inhibitor 1A Homo sapiens 105-108 9044834-5 1997 Synchronization of tumor cells by lovastatin, which arrests cells in G1, resulted in increased levels of p21 and p27 with a concomitant decrease in cyclin-dependent kinase 2-associated kinase activity. Lovastatin 34-44 interferon alpha inducible protein 27 Homo sapiens 113-116 9044834-7 1997 These observations suggest that lovastatin causes a profound cell cycle-independent alteration of CKI expression which is distinct from growth factor deprivation or thymidine block. Lovastatin 32-42 choline kinase alpha Homo sapiens 98-101 9018116-0 1997 Geranylgeraniol potentiates lovastatin inhibition of oncogenic H-Ras processing and signaling while preventing cytotoxicity. Lovastatin 28-38 HRas proto-oncogene, GTPase Homo sapiens 63-68 9018116-4 1997 In this report, we describe a novel approach utilizing a combination of lovastatin and geranylgeraniol (GGOH) to potentiate the ability of lovastatin to block oncogenic H-Ras signaling and concomitantly rescue lovastatin toxicity. Lovastatin 72-82 HRas proto-oncogene, GTPase Homo sapiens 169-174 9018116-4 1997 In this report, we describe a novel approach utilizing a combination of lovastatin and geranylgeraniol (GGOH) to potentiate the ability of lovastatin to block oncogenic H-Ras signaling and concomitantly rescue lovastatin toxicity. Lovastatin 139-149 HRas proto-oncogene, GTPase Homo sapiens 169-174 9018116-4 1997 In this report, we describe a novel approach utilizing a combination of lovastatin and geranylgeraniol (GGOH) to potentiate the ability of lovastatin to block oncogenic H-Ras signaling and concomitantly rescue lovastatin toxicity. Lovastatin 139-149 HRas proto-oncogene, GTPase Homo sapiens 169-174 9018116-5 1997 GGOH co-treatment with lovastatin enhances inhibition of oncogenic H-Ras processing and constitutive activation of mitogen-activated protein kinase (MAPK), and preserves the processing of geranylgeranyltransferase (GGTase) I and GGTase II protein substrates. Lovastatin 23-33 HRas proto-oncogene, GTPase Homo sapiens 67-72 9605009-0 1997 Human multidrug-resistant (MRP,p190) myeloid leukemia HL-60/ADR cells in vitro: resistance to the mevalonate pathway inhibitor lovastatin. Lovastatin 127-137 ATP binding cassette subfamily C member 1 Homo sapiens 27-30 9605009-0 1997 Human multidrug-resistant (MRP,p190) myeloid leukemia HL-60/ADR cells in vitro: resistance to the mevalonate pathway inhibitor lovastatin. Lovastatin 127-137 contactin associated protein 1 Homo sapiens 31-35 9605009-1 1997 Mevalonate pathway inhibitor lovastatin inhibited proliferation of human multidrug-resistant promyelocytic leukemia HL-60/ADR cells in vitro, with MRP-gene coded p190 mediated drug resistance, to a markedly lesser extent than that of the parental drug sensitive HL-60 cells and also that of the other human multidrug resistant (MDR-1, P-glycoprotein) myeloid leukemia cell line HL-60/VCR. Lovastatin 29-39 ATP binding cassette subfamily C member 1 Homo sapiens 147-150 9605009-1 1997 Mevalonate pathway inhibitor lovastatin inhibited proliferation of human multidrug-resistant promyelocytic leukemia HL-60/ADR cells in vitro, with MRP-gene coded p190 mediated drug resistance, to a markedly lesser extent than that of the parental drug sensitive HL-60 cells and also that of the other human multidrug resistant (MDR-1, P-glycoprotein) myeloid leukemia cell line HL-60/VCR. Lovastatin 29-39 contactin associated protein 1 Homo sapiens 162-166 9605009-1 1997 Mevalonate pathway inhibitor lovastatin inhibited proliferation of human multidrug-resistant promyelocytic leukemia HL-60/ADR cells in vitro, with MRP-gene coded p190 mediated drug resistance, to a markedly lesser extent than that of the parental drug sensitive HL-60 cells and also that of the other human multidrug resistant (MDR-1, P-glycoprotein) myeloid leukemia cell line HL-60/VCR. Lovastatin 29-39 ATP binding cassette subfamily B member 1 Homo sapiens 328-333 9221828-1 1997 The cholesterol-lowering HMG CoA reductase inhibitors (HMGRI), pravastatin and lovastatin, have been associated with skeletal myopathy in humans and in rats. Lovastatin 79-89 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 25-42 8954966-7 1996 In fact, inhibition of p21(ras) by transfecting E32-4-2 cells with the transdominant negative mutant of H-ras (L61, S186) led, analogously to lovastatin or (alpha-hydroxyfarnesyl) phosphonic acid treatment, to a strong increase of stress-induced ROS levels. Lovastatin 142-152 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 23-26 8954966-7 1996 In fact, inhibition of p21(ras) by transfecting E32-4-2 cells with the transdominant negative mutant of H-ras (L61, S186) led, analogously to lovastatin or (alpha-hydroxyfarnesyl) phosphonic acid treatment, to a strong increase of stress-induced ROS levels. Lovastatin 142-152 Harvey rat sarcoma virus oncogene Mus musculus 104-109 8977253-0 1996 Lovastatin inhibits T-cell antigen receptor signaling independent of its effects on ras. Lovastatin 0-10 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 20-43 8977253-2 1996 We examined the effects of lovastatin on signal transduction via the T-cell antigen receptor (TCR). Lovastatin 27-37 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 69-92 8977253-2 1996 We examined the effects of lovastatin on signal transduction via the T-cell antigen receptor (TCR). Lovastatin 27-37 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 94-97 8977253-3 1996 Lovastatin inhibited both proximal and distal TCR-mediated signaling events in a time- and concentration-dependent manner in the human Jurkat T-cell line. Lovastatin 0-10 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 46-49 8977253-4 1996 Upregulation of CD69 surface expression after TCR stimulation was blocked by lovastatin, although no inhibition of phorbol ester-induced CD69 expression was noted. Lovastatin 77-87 CD69 molecule Homo sapiens 16-20 8977253-4 1996 Upregulation of CD69 surface expression after TCR stimulation was blocked by lovastatin, although no inhibition of phorbol ester-induced CD69 expression was noted. Lovastatin 77-87 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 46-49 8977253-5 1996 Proximal TCR-mediated signaling events, including intracellular calcium mobilization, inositol phosphate production, and tyrosine phosphorylation of phospholipase Cgamma1, were similarly inhibited by lovastatin, although global protein tyrosine kinase activity remained intact. Lovastatin 200-210 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 9-12 8977253-6 1996 In a Jurkat variant transfected with the human type-1 muscarinic receptor, lovastatin also inhibited TCR-mediated calcium mobilization and inositol phosphate production but failed to affect muscarinic receptor-induced responses. Lovastatin 75-85 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 101-104 8977253-7 1996 Lovastatin, at similar doses, also disrupted post-translational processing of ras and inhibited ras-dependent signals, including phosphorylation and activation of mitogen-associated protein kinase after TCR stimulation. Lovastatin 0-10 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 203-206 9007143-2 1996 The compounds examined included: lovastatin, an inhibitor of HMG-CoA reductase, which interferes with membrane localization of p21 ras protein; H-7, a classic inhibitor of protein kinase C; and tiazofurin, a GTP depleting agent, that might affect the GTP/GDP ratio on p21ras. Lovastatin 33-43 Harvey rat sarcoma virus oncogene Mus musculus 127-134 9007143-5 1996 Lovastatin and H-7 altered p21 subcellular localization. Lovastatin 0-10 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 27-30 8943347-4 1996 Combined microinjection and biochemical approaches showed that whereas these three mitogenic cascades are sensitive to the p16 inhibitor of cdk4/6 and/or cyclin D1-neutralizing antibody and able to induce pRb kinase activity, their upstream biochemical routes are distinct as demonstrated by their differential sensitivity to lovastatin and requirements for mitogen-activated protein kinases whose sustained activation is seen only in the growth factor-dependent pathway. Lovastatin 326-336 cyclin dependent kinase inhibitor 2A Homo sapiens 123-126 8943347-4 1996 Combined microinjection and biochemical approaches showed that whereas these three mitogenic cascades are sensitive to the p16 inhibitor of cdk4/6 and/or cyclin D1-neutralizing antibody and able to induce pRb kinase activity, their upstream biochemical routes are distinct as demonstrated by their differential sensitivity to lovastatin and requirements for mitogen-activated protein kinases whose sustained activation is seen only in the growth factor-dependent pathway. Lovastatin 326-336 cyclin dependent kinase 4 Homo sapiens 140-146 8943347-4 1996 Combined microinjection and biochemical approaches showed that whereas these three mitogenic cascades are sensitive to the p16 inhibitor of cdk4/6 and/or cyclin D1-neutralizing antibody and able to induce pRb kinase activity, their upstream biochemical routes are distinct as demonstrated by their differential sensitivity to lovastatin and requirements for mitogen-activated protein kinases whose sustained activation is seen only in the growth factor-dependent pathway. Lovastatin 326-336 cyclin D1 Homo sapiens 154-163 8943347-4 1996 Combined microinjection and biochemical approaches showed that whereas these three mitogenic cascades are sensitive to the p16 inhibitor of cdk4/6 and/or cyclin D1-neutralizing antibody and able to induce pRb kinase activity, their upstream biochemical routes are distinct as demonstrated by their differential sensitivity to lovastatin and requirements for mitogen-activated protein kinases whose sustained activation is seen only in the growth factor-dependent pathway. Lovastatin 326-336 RB transcriptional corepressor 1 Homo sapiens 205-208 8940037-3 1996 Inhibition of Ras farnesylation with lovastatin blocked activation of p21(ras) and Raf-1 kinase in both 3T3-L1 fibroblasts and 3T3-L1 adipocytes. Lovastatin 37-47 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 70-73 8940037-3 1996 Inhibition of Ras farnesylation with lovastatin blocked activation of p21(ras) and Raf-1 kinase in both 3T3-L1 fibroblasts and 3T3-L1 adipocytes. Lovastatin 37-47 v-raf-leukemia viral oncogene 1 Mus musculus 83-88 8940037-5 1996 In contrast, in 3T3-L1 adipocytes, despite an inhibition of activation of p21(ras) and Raf-1 by lovastatin, insulin continued to stimulate MAP kinase activity. Lovastatin 96-106 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 74-77 8940037-5 1996 In contrast, in 3T3-L1 adipocytes, despite an inhibition of activation of p21(ras) and Raf-1 by lovastatin, insulin continued to stimulate MAP kinase activity. Lovastatin 96-106 v-raf-leukemia viral oncogene 1 Mus musculus 87-92 8940037-6 1996 Fractionation of the cell lysates on the FPLC Mono-Q column revealed that lovastatin inhibited insulin stimulation of ERK2 (and, to a lesser extent, ERK1) in 3T3-L1 fibroblasts and had no effect on the insulin-stimulated ERK2 in 3T3-L1 adipocytes. Lovastatin 74-84 mitogen-activated protein kinase 1 Mus musculus 118-122 8940037-6 1996 Fractionation of the cell lysates on the FPLC Mono-Q column revealed that lovastatin inhibited insulin stimulation of ERK2 (and, to a lesser extent, ERK1) in 3T3-L1 fibroblasts and had no effect on the insulin-stimulated ERK2 in 3T3-L1 adipocytes. Lovastatin 74-84 mitogen-activated protein kinase 3 Mus musculus 149-153 8940037-6 1996 Fractionation of the cell lysates on the FPLC Mono-Q column revealed that lovastatin inhibited insulin stimulation of ERK2 (and, to a lesser extent, ERK1) in 3T3-L1 fibroblasts and had no effect on the insulin-stimulated ERK2 in 3T3-L1 adipocytes. Lovastatin 74-84 mitogen-activated protein kinase 1 Mus musculus 221-225 8663292-4 1996 Up-regulation of LDL receptors by lovastatin treatment of normal human foreskin fibroblasts (FSF cells) resulted in an increase in LPL-induced VLDL binding and catabolism to a level that was 10-15-fold greater than in LDL receptor-negative fibroblasts, despite similar LRP activity in both cell lines. Lovastatin 34-44 CD320 antigen Mus musculus 143-147 8937853-1 1996 It was previously demonstrated that treatment of primary cultured rat hepatocytes with lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, induced the mRNAs for several cytochromes P450 (P450s), including CYP2B1/2, CYP3A1/2, and CYP4A. Lovastatin 87-97 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 115-165 8937853-1 1996 It was previously demonstrated that treatment of primary cultured rat hepatocytes with lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, induced the mRNAs for several cytochromes P450 (P450s), including CYP2B1/2, CYP3A1/2, and CYP4A. Lovastatin 87-97 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 233-239 8937853-1 1996 It was previously demonstrated that treatment of primary cultured rat hepatocytes with lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, induced the mRNAs for several cytochromes P450 (P450s), including CYP2B1/2, CYP3A1/2, and CYP4A. Lovastatin 87-97 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 243-251 8937853-3 1996 Treatment of cultured hepatocytes with lovastatin, simvastatin, or fluvastatin increased CYP2B1/2, CYP3A1/2, and CYP4A mRNA and immunoreactive protein levels over the dose range (3 x 10(-6) to 3 x 10(-5) M) required to increase the amount of HMG-CoA reductase mRNA. Lovastatin 39-49 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 89-95 8937853-3 1996 Treatment of cultured hepatocytes with lovastatin, simvastatin, or fluvastatin increased CYP2B1/2, CYP3A1/2, and CYP4A mRNA and immunoreactive protein levels over the dose range (3 x 10(-6) to 3 x 10(-5) M) required to increase the amount of HMG-CoA reductase mRNA. Lovastatin 39-49 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 99-107 8937853-4 1996 The increases in CYP2B1/2 levels produced by 3 x 10(-5) M fluvastatin treatment were larger than those produced by lovastatin or simvastatin treatment or by treatment with 10(-4) M phenobarbital. Lovastatin 115-125 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 17-23 8937853-5 1996 In contrast, treatment of cultured hepatocytes with 3 x 10(-5) M lovastatin, simvastatin, or fluvastatin increased CYP3A1/2 and CYP4A mRNA and immunoreactive protein to lower levels than those produced by treatment with 10(-5) M dexamethasone or 10(-4) M ciprofibrate. Lovastatin 65-75 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 115-121 8896278-3 1996 Specifically, hmgl+ was isolated on the basis of its ability to confer resistance to lovastatin, a competitive inhibitor of HMG-CoA reductase. Lovastatin 85-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 124-141 8896278-8 1996 A previously undescribed "feed-forward" regulation was observed in which elevated levels of HMG-CoA synthase, the enzyme catalysing the synthesis of the HMG-CoA reductase substrate, induced elevated levels of hmgl+ protein in the cell and conferred partial resistance to lovastatin. Lovastatin 271-281 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 153-170 8880225-1 1996 It has been shown previously that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA RIs) such as compactin and lovastatin suppress human lymphocyte functions in vitro (Cuthbert and Lipsky, 1981; Cutts and Bankhurst, 1989). Lovastatin 129-139 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 34-81 8663239-2 1996 Depletion of mevalonic acid (MVA), obtained by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase using lovastatin, depressed the biosynthesis of dolichyl-phosphate and the rate of N-linked glycosylation and caused growth arrest in the melanoma cell line SK-MEL-2. Lovastatin 125-135 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 61-118 8908154-0 1996 Lovastatin inhibits gene expression of type-I scavenger receptor in THP-1 human macrophages. Lovastatin 0-10 GLI family zinc finger 2 Homo sapiens 68-73 8908154-1 1996 Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, inhibits the synthesis of mevalonic acid and is widely used as an anti-atherosclerotic drug. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 28-85 8908154-4 1996 Accordingly, we examined whether lovastatin alters the gene expression of SCRs in THP-1 cell derived human macrophages. Lovastatin 33-43 GLI family zinc finger 2 Homo sapiens 82-87 8908154-5 1996 Lovastatin (5-15 microM) caused a significant dose-related reduction in steady state levels of type-I SCR mRNA in phorbol 12-myristate 13-acetate (PMA)-treated THP-1 cells. Lovastatin 0-10 GLI family zinc finger 2 Homo sapiens 160-165 8908154-10 1996 These results suggest that lovastatin inhibits the transcription of type-I SCR gene by affecting mevalonate metabolism, possibly through the farnesyl-pyrophosphate related end-product(s) in the THP-1-derived macrophages. Lovastatin 27-37 GLI family zinc finger 2 Homo sapiens 194-199 8904621-3 1996 It has been suggested that lipophilic HMG CoA reductase inhibitors, like lovastatin and simvastatin, may cause sleep disturbance. Lovastatin 73-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-55 8765518-3 1996 Mevinolin (lovastatin) was found to increase the LDL receptor expression by 70% at the same concentration. Lovastatin 0-9 low density lipoprotein receptor Homo sapiens 49-61 8765518-3 1996 Mevinolin (lovastatin) was found to increase the LDL receptor expression by 70% at the same concentration. Lovastatin 11-21 low density lipoprotein receptor Homo sapiens 49-61 8862469-2 1996 Here, the suppression of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase activity by lovastatin was studied both in dermal fibroblasts from patients with different peroxisomal defects and in a Chinese hamster ovary (CHO) cell line lacking morphologically intact peroxisomes. Lovastatin 95-105 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 25-82 8663292-4 1996 Up-regulation of LDL receptors by lovastatin treatment of normal human foreskin fibroblasts (FSF cells) resulted in an increase in LPL-induced VLDL binding and catabolism to a level that was 10-15-fold greater than in LDL receptor-negative fibroblasts, despite similar LRP activity in both cell lines. Lovastatin 34-44 low density lipoprotein receptor Homo sapiens 17-29 8663292-4 1996 Up-regulation of LDL receptors by lovastatin treatment of normal human foreskin fibroblasts (FSF cells) resulted in an increase in LPL-induced VLDL binding and catabolism to a level that was 10-15-fold greater than in LDL receptor-negative fibroblasts, despite similar LRP activity in both cell lines. Lovastatin 34-44 LDL receptor related protein 1 Homo sapiens 269-272 8656610-1 1996 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has been shown to inhibit the in vitro and in vivo growth of a number of different cell lines. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 14-61 8663599-5 1996 Analysis of transcripts from human lymphoblasts subcultured in lipid-depleted sera (LDS) and LDS supplemented with lovastatin indicated that PMKase gene expression is subject to regulation by sterol at the level of transcription. Lovastatin 115-125 phosphomevalonate kinase Homo sapiens 141-147 8671958-0 1996 Lovastatin inhibits lipopolysaccharide-induced NF-kappaB activation in human mesangial cells. Lovastatin 0-10 nuclear factor kappa B subunit 1 Homo sapiens 47-56 8671958-3 1996 We therefore examined the effects of the HMG-CoA reductase inhibitor lovastatin on NFkappaB activation in human mesangial cells. Lovastatin 69-79 nuclear factor kappa B subunit 1 Homo sapiens 83-91 8671958-8 1996 In the presence of either mevalonate or the mevalonate metabolite farnesyl pyrophosphate, the lovastatin inhibition of NF-kappaB activation was substantially reversed, supporting a role for mevalonate metabolites in LPS-induced mesangial cell NF-kappaB activation. Lovastatin 94-104 nuclear factor kappa B subunit 1 Homo sapiens 119-128 8671958-8 1996 In the presence of either mevalonate or the mevalonate metabolite farnesyl pyrophosphate, the lovastatin inhibition of NF-kappaB activation was substantially reversed, supporting a role for mevalonate metabolites in LPS-induced mesangial cell NF-kappaB activation. Lovastatin 94-104 nuclear factor kappa B subunit 1 Homo sapiens 243-252 8628597-5 1996 Therefore, our objectives were to determine the efficacy, safety, and tolerance of the short-term use of lovastatin, a 3-hydroxy 3-methylglutaryl coenzyme A reductase inhibitor, in the control of severe FH in a male pediatric population and to evaluate the dose-response relationship. Lovastatin 105-115 low density lipoprotein receptor Homo sapiens 203-205 8628597-10 1996 RESULTS: All lovastatin doses reduced total cholesterol (-17% to -29%), low density lipoprotein cholesterol (-21% to -36%), and ApoB (-19% to -28%) concentrations. Lovastatin 13-23 apolipoprotein B Homo sapiens 128-132 8773465-1 1996 Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, inhibits the synthesis of mevalonic acid. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 14-61 8709977-9 1996 Results demonstrate that lovastatin specifically increases the expression of a 24 kDa GTP-binding protein in HEL cells and that, isoprenylation of low molecular mass GTP-binding protein(s) may have function(s) in addition to its role in the targetting of these proteins to cell membrane. Lovastatin 25-35 hydroxycarboxylic acid receptor 3 Homo sapiens 86-105 8800498-5 1996 We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. Lovastatin 111-121 low density lipoprotein receptor Homo sapiens 30-35 8800498-5 1996 We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. Lovastatin 111-121 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 40-57 8800498-5 1996 We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. Lovastatin 111-121 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 83-100 8800498-8 1996 Control subjects exhibited coordinate regulation of the LDL-R and HMG CoA reductase genes in response to lovastatin, 0.1-25 microM, for 0-24 h. Correlation coefficients between mRNA levels of both genes were > 0.9 in controls and FH subjects. Lovastatin 105-115 low density lipoprotein receptor Homo sapiens 56-61 8800498-8 1996 Control subjects exhibited coordinate regulation of the LDL-R and HMG CoA reductase genes in response to lovastatin, 0.1-25 microM, for 0-24 h. Correlation coefficients between mRNA levels of both genes were > 0.9 in controls and FH subjects. Lovastatin 105-115 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 66-83 8800498-13 1996 Some subjects, with FH caused by the > 10-kb deletion of the LDL-R gene, who fail to respond to HMG CoA reductase inhibitors have abnormal LDL receptor binding activity at the cell surface in response to lovastatin in vitro. Lovastatin 207-217 low density lipoprotein receptor Homo sapiens 64-69 8800498-13 1996 Some subjects, with FH caused by the > 10-kb deletion of the LDL-R gene, who fail to respond to HMG CoA reductase inhibitors have abnormal LDL receptor binding activity at the cell surface in response to lovastatin in vitro. Lovastatin 207-217 low density lipoprotein receptor Homo sapiens 142-154 8689812-3 1996 Lovastatin is metabolized by CYP3A4. Lovastatin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 8689812-13 1996 Inhibition of CYP3A4-mediated metabolism probably explains the increased toxicity of lovastatin caused not only by itraconazole but also by cyclosporine, erythromycin, and other inhibitors of CYP3A4. Lovastatin 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 8689812-13 1996 Inhibition of CYP3A4-mediated metabolism probably explains the increased toxicity of lovastatin caused not only by itraconazole but also by cyclosporine, erythromycin, and other inhibitors of CYP3A4. Lovastatin 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 17180086-1 1996 Lovastatin is a very specific and potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which regulates a rate-limiting step in the cellular synthesis of isoprenoid and cholesterol. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 54-111 8709977-0 1996 Expression of a 24 kDa GTP-binding protein (Gn24) is increased in lovastatin treated human erythroleukemia cells. Lovastatin 66-76 hydroxycarboxylic acid receptor 3 Homo sapiens 23-42 8709977-4 1996 Addition of cycloheximide plus lovastatin to cells in culture abolished the observed increase in 24 kDa GTP-binding protein. Lovastatin 31-41 hydroxycarboxylic acid receptor 3 Homo sapiens 104-123 8709977-6 1996 The mobility of this 24 kDa isoprenylated protein on SDS-PAGE was identical to that of the GTP-binding protein increased in response to lovastatin. Lovastatin 136-146 hydroxycarboxylic acid receptor 3 Homo sapiens 91-110 8612233-0 1996 HMG-CoA reductase mediates the biological effects of retinoic acid on human neuroblastoma cells: lovastatin specifically targets P-glycoprotein-expressing cells. Lovastatin 97-107 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-17 8612233-0 1996 HMG-CoA reductase mediates the biological effects of retinoic acid on human neuroblastoma cells: lovastatin specifically targets P-glycoprotein-expressing cells. Lovastatin 97-107 ATP binding cassette subfamily B member 1 Homo sapiens 129-143 8612233-2 1996 Lovastatin, a nonreversible inhibitor of HMG-CoA reductase, induced extensive cytotoxicity that was restricted to drug-resistant P-glycoprotein-expressing neuroblastoma cell lines. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 41-58 8612233-2 1996 Lovastatin, a nonreversible inhibitor of HMG-CoA reductase, induced extensive cytotoxicity that was restricted to drug-resistant P-glycoprotein-expressing neuroblastoma cell lines. Lovastatin 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 129-143 8935222-0 1996 Lovastatin lowers serum cholesterol levels in non-insulin-dependent diabetes mellitus patients without altering their insulin sensitivity. Lovastatin 0-10 insulin Homo sapiens 50-57 8561503-3 1996 We found that administration of inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase such as lovastatin, pravastatin, fluvastatin, and rivastatin resulted in increased hepatic LDL receptor mRNA levels. Lovastatin 102-112 low density lipoprotein receptor Rattus norvegicus 185-197 8935222-1 1996 BACKGROUND: Lovastatin, a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, has been widely used in the treatment of hypercholesterolemia. Lovastatin 12-22 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 33-90 8935222-3 1996 The influence of lovastatin on insulin sensitivity was evaluated in twelve Chinese non-insulin-dependent diabetes mellitus (NIDDM) patients with hypercholesterolemia. Lovastatin 17-27 insulin Homo sapiens 31-38 8935222-14 1996 A significant reduction of serum apolipoprotein B concentrations was also noted in lovastatin period. Lovastatin 83-93 apolipoprotein B Homo sapiens 33-49 8611028-8 1996 Furthermore, immunodetection of the beta-subunit of the insulin receptor in anti-phosphotyrosine immunoprecipitates revealed that treatment with lovastatin reduced the tyrosine phosphorylation levels of the receptor. Lovastatin 145-155 insulin receptor Rattus norvegicus 56-72 8611028-11 1996 It is concluded that, in addition to inhibition of Ras farnesylation, lovastatin reduces receptor tyrosine phosphorylation levels which also contributes to the blockade of MAPK activation by the insulin receptor. Lovastatin 70-80 insulin receptor Rattus norvegicus 195-211 8592143-2 1996 Human glioblastoma cells were found to be uniquely vulnerable to growth arrest by lovastatin, a competitive inhibitor of the enzyme regulating MVA synthesis, 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 82-92 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 158-205 8729584-2 1996 It is structurally distinct from the other currently available HMGCoA reductase inhibitors (lovastatin, simvastatin, and pravastatin), leading to unique biopharmaceutical properties relative to the other agents of this class. Lovastatin 92-102 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-79 8737761-7 1996 As already reported for lovastatin and simvastatin, in vivo drug interactions by inhibition of liver oxidation of CYP2C9 substrates (e.g. hypoglyceamic sulphonylureas and oral anticoagulants) may be expected. Lovastatin 24-34 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 114-120 8737761-1 1996 OBJECTIVE: The affinity of (+)-, (-)- and (+/-)- fluvastatin, a new synthetic HMG-CoA reductase inhibitor developed as a racemate, for specific human P450 monooxygenases in liver microsomes was compared with that of the pharmacologically active acidic forms of lovastatin, pravastatin and simvastatin. Lovastatin 261-271 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 150-154 8565148-1 1995 The proliferation of human monocytic Mono Mac 6 cells was significantly retarded by treatment with lovastatin (LOV, 10 microM) for 72 h. Treatment of Mono Mac 6 cells with LOV increased surface protein expression of monocyte-associated CD14 and the integrin-chain CD11b towards levels found in isolated human blood monocytes. Lovastatin 99-109 CD14 molecule Homo sapiens 236-240 8565148-1 1995 The proliferation of human monocytic Mono Mac 6 cells was significantly retarded by treatment with lovastatin (LOV, 10 microM) for 72 h. Treatment of Mono Mac 6 cells with LOV increased surface protein expression of monocyte-associated CD14 and the integrin-chain CD11b towards levels found in isolated human blood monocytes. Lovastatin 99-109 integrin subunit alpha M Homo sapiens 264-269 8565148-1 1995 The proliferation of human monocytic Mono Mac 6 cells was significantly retarded by treatment with lovastatin (LOV, 10 microM) for 72 h. Treatment of Mono Mac 6 cells with LOV increased surface protein expression of monocyte-associated CD14 and the integrin-chain CD11b towards levels found in isolated human blood monocytes. Lovastatin 111-114 CD14 molecule Homo sapiens 236-240 8565148-1 1995 The proliferation of human monocytic Mono Mac 6 cells was significantly retarded by treatment with lovastatin (LOV, 10 microM) for 72 h. Treatment of Mono Mac 6 cells with LOV increased surface protein expression of monocyte-associated CD14 and the integrin-chain CD11b towards levels found in isolated human blood monocytes. Lovastatin 111-114 integrin subunit alpha M Homo sapiens 264-269 9072409-0 1995 Effect of lovastatin and fluoromevalonate on phosphatidylinositol 3-kinase activity stimulated with PDGF. Lovastatin 10-20 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 45-74 12013483-13 1996 Simvastatin, lovastatin and mevastatin significantly reduced the angiotensin II-induced calcium mobilization. Lovastatin 13-23 angiotensinogen Rattus norvegicus 65-79 8676808-5 1996 In vitro, lovastatin has been shown to downregulate mesangial cell production of monocyte chemoattractant protein-1 and colony-stimulating factor. Lovastatin 10-20 C-C motif chemokine ligand 2 Homo sapiens 81-115 8773342-6 1996 After 12 months of lovastatin treatment, a significant decrease in the concentration of cholesterol, LDL C, VLDL C and apo B was observed, but neither the basal testosterone concentration nor the response to gonadorelin stimulation was modified. Lovastatin 19-29 component of oligomeric golgi complex 2 Homo sapiens 101-106 8719939-0 1995 Is responsiveness to lovastatin in familial hypercholesterolaemia heterozygotes influenced by the specific mutation in the low-density lipoprotein receptor gene? Lovastatin 21-31 low density lipoprotein receptor Homo sapiens 123-155 7580288-1 1995 The hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin is used to treat hyperlipidaemia. Lovastatin 67-77 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 4-56 7559642-0 1995 Effects of lovastatin on trafficking of cystic fibrosis transmembrane conductance regulator in human tracheal epithelium. Lovastatin 11-21 CF transmembrane conductance regulator Homo sapiens 40-91 8672984-4 1995 Also, agents such as perillyl alcohol and lovastatin that interfere with protein isoprenylation and, hence, inhibit oncogene activation may protect against aberrant K-ras expression. Lovastatin 42-52 KRAS proto-oncogene, GTPase Homo sapiens 165-170 7559642-5 1995 Lovastatin, an inhibitor of isoprenyl lipid biosynthesis, markedly inhibited all measures of CFTR function. Lovastatin 0-10 CF transmembrane conductance regulator Homo sapiens 93-97 7559642-6 1995 The lovastatin-induced declines in CFTR function were corrected by the simultaneous addition of mevalonate or the isoprenyl lipids geranylgeranyl and farnesyl but not cholesterol. Lovastatin 4-14 CF transmembrane conductance regulator Homo sapiens 35-39 7559642-7 1995 Lovastatin reduced total cellular CFTR as assessed by immunoprecipitation. Lovastatin 0-10 CF transmembrane conductance regulator Homo sapiens 34-38 7559642-8 1995 Mevalonate or isoprenyl lipids protected CFTR levels from the actions of lovastatin. Lovastatin 73-83 CF transmembrane conductance regulator Homo sapiens 41-45 7588795-4 1995 HMGR1cd activity was completely blocked by the HMGR inhibitor mevinolin (IC50 = 12.5 nM). Lovastatin 62-71 hydroxy methylglutaryl CoA reductase 1 Arabidopsis thaliana 0-5 7588795-4 1995 HMGR1cd activity was completely blocked by the HMGR inhibitor mevinolin (IC50 = 12.5 nM). Lovastatin 62-71 hydroxy methylglutaryl CoA reductase 1 Arabidopsis thaliana 0-4 8573550-3 1995 This study analyzes the effects of the commonly used lipid-lowering drugs pravastatin (PRAV), lovastatin (LOV), and cholestyramine (CHOL) on serum Lp(a) and other serum lipid levels in a parallel study design. Lovastatin 94-104 lipoprotein(a) Homo sapiens 147-152 8573550-3 1995 This study analyzes the effects of the commonly used lipid-lowering drugs pravastatin (PRAV), lovastatin (LOV), and cholestyramine (CHOL) on serum Lp(a) and other serum lipid levels in a parallel study design. Lovastatin 106-109 lipoprotein(a) Homo sapiens 147-152 7585443-0 1995 Structural alterations of human immortal astrocytes after inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase by lovastatin. Lovastatin 133-143 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 72-129 7585443-2 1995 In our previous investigations, it has been demonstrated that lovastatin, which is a specific competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, effectively inhibited cholesterol synthesis in human primary and immortal astrocytes in serum and lipid-free media, and we also showed that the effects on both astrocytes of primary cultures and immortal astrocytes (ASCh-7) were very similar. Lovastatin 62-72 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 119-176 8595642-6 1995 Lovastatin significantly decreased levels of total cholesterol, calculated LDL, directly measured LDL, IDL, total triglycerides, VLDL, and the ratios of LDL:HDL, total cholesterol:HDL, and directly measured LDL:HDL and significantly increased total HDL and HDL3 levels. Lovastatin 0-10 HDL3 Homo sapiens 257-261 8595642-7 1995 Gemfibrozil was significantly more effective than lovastatin in raising total HDL and HDL3 levels and in lowering the IDL plus VLDL:HDL ratio. Lovastatin 50-60 HDL3 Homo sapiens 86-90 7564103-0 1995 Human mesangial cell production of monocyte chemoattractant protein-1: modulation by lovastatin. Lovastatin 85-95 C-C motif chemokine ligand 2 Homo sapiens 35-69 7564103-4 1995 Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase by lovastatin resulted in a reduction of the mesangial cell-derived chemotactic activity as well as MCP-1 mRNA expression. Lovastatin 75-85 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-71 7564103-4 1995 Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase by lovastatin resulted in a reduction of the mesangial cell-derived chemotactic activity as well as MCP-1 mRNA expression. Lovastatin 75-85 C-C motif chemokine ligand 2 Homo sapiens 172-177 7564103-5 1995 The inhibitory effects of lovastatin in the presence of exogenous cholesterol were reversed by mevalonate, suggesting a role for isoprenoid intermediates of the mevalonate pathway and/or isoprenylated proteins in mesangial cell MCP-1 regulation. Lovastatin 26-36 C-C motif chemokine ligand 2 Homo sapiens 228-233 7611249-0 1995 Reduction of lipoprotein(a) following treatment with lovastatin in patients with unremitting nephrotic syndrome. Lovastatin 53-63 lipoprotein(a) Homo sapiens 13-27 7611249-3 1995 We administered lovastatin (40 to 80 mg/day) to 20 adult patients with unremitting nephrotic syndrome for 8 weeks to assess its effect on plasma Lp(a) and other plasma lipid concentrations. Lovastatin 16-26 lipoprotein(a) Homo sapiens 145-150 7611249-11 1995 Treatment with lovastatin results in a favorable response in terms of total and low-density lipoprotein cholesterol lowering in patients with the nephrotic syndrome; however, plasma Lp(a) levels are uniformly and significantly reduced only in nephrotic patients with elevated baseline plasma Lp(a) concentrations. Lovastatin 15-25 lipoprotein(a) Homo sapiens 182-187 7611249-11 1995 Treatment with lovastatin results in a favorable response in terms of total and low-density lipoprotein cholesterol lowering in patients with the nephrotic syndrome; however, plasma Lp(a) levels are uniformly and significantly reduced only in nephrotic patients with elevated baseline plasma Lp(a) concentrations. Lovastatin 15-25 lipoprotein(a) Homo sapiens 292-297 7666000-8 1995 Treatment of homozygotes with lovastatin doubled both plasma cholesterol concentration and body cholesterol transport indicating the importance of apoE-dependent cell cholesterol transfer in synthetic down-regulation with this agent. Lovastatin 30-40 apolipoprotein E Mus musculus 147-151 7641024-2 1995 Interference with the cholesterol biosynthetic pathway with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (e.g., lovastatin) may preferentially slow malignant cell growth and offer a new approach to cancer chemotherapy. Lovastatin 127-137 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 62-109 7654731-10 1995 Apo AI levels increased with lovastatin. Lovastatin 29-39 apolipoprotein A1 Homo sapiens 0-6 7702060-3 1995 We assessed the efficacy and safety of the lipid-lowering drugs, nicotinic acid (short acting) and lovastatin, the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Lovastatin 99-109 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 115-162 7592544-4 1995 Feeding 5% cholestyramine plus 0.1% lovastatin (CL-diet) for 7 days led to approximately 4.0-fold induction of the isomerase activity. Lovastatin 36-46 EBP, cholestenol delta-isomerase Rattus norvegicus 115-124 7698979-4 1995 Both the formation of PrPSc and the initial degradation of PrPC were diminished by lovastatin-mediated depletion of cellular cholesterol but were insensitive to NH4Cl. Lovastatin 83-93 prion protein Mus musculus 22-27 7698979-4 1995 Both the formation of PrPSc and the initial degradation of PrPC were diminished by lovastatin-mediated depletion of cellular cholesterol but were insensitive to NH4Cl. Lovastatin 83-93 prion protein Mus musculus 59-63 8522067-8 1995 Additionally, trophic hormone treatment increased steroid production in Ki-GLOM cells and this increase was partially reversed by lovastatin, a pharmacological inhibitor of ras p21 function. Lovastatin 130-140 KRAS proto-oncogene, GTPase Rattus norvegicus 177-180 8534916-0 1995 Redistribution of the CDK inhibitor p27 between different cyclin.CDK complexes in the mouse fibroblast cell cycle and in cells arrested with lovastatin or ultraviolet irradiation. Lovastatin 141-151 cyclin-dependent kinase inhibitor 1B Mus musculus 36-39 8534916-8 1995 In cells arrested in G1 with lovastatin, cyclin D1 was degraded and p27 was redistributed to cyclin A.Cdk2. Lovastatin 29-39 cyclin D1 Mus musculus 41-50 8534916-8 1995 In cells arrested in G1 with lovastatin, cyclin D1 was degraded and p27 was redistributed to cyclin A.Cdk2. Lovastatin 29-39 cyclin-dependent kinase inhibitor 1B Mus musculus 68-71 8534916-8 1995 In cells arrested in G1 with lovastatin, cyclin D1 was degraded and p27 was redistributed to cyclin A.Cdk2. Lovastatin 29-39 cyclin A2 Mus musculus 93-101 8534916-8 1995 In cells arrested in G1 with lovastatin, cyclin D1 was degraded and p27 was redistributed to cyclin A.Cdk2. Lovastatin 29-39 cyclin-dependent kinase 2 Mus musculus 102-106 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin D1 Mus musculus 24-33 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin-dependent kinase 4 Mus musculus 34-38 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin-dependent kinase inhibitor 1B Mus musculus 63-66 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin-dependent kinase inhibitor 1B Mus musculus 72-75 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin D1 Mus musculus 98-107 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin-dependent kinase 4 Mus musculus 108-112 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin A2 Mus musculus 116-124 8534916-10 1995 These data suggest that cyclin D1.Cdk4 acts as a reservoir for p27, and p27 is redistributed from cyclin D1.Cdk4 to cyclin A.Cdk2 complexes during S phase, or when cells are arrested by growth factor deprivation, lovastatin treatment, or UV irradiation. Lovastatin 213-223 cyclin-dependent kinase 2 Mus musculus 125-129 7475995-1 1995 Pravastatin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, exhibits liver-selectivity in inhibiting sterol synthesis, when administered as a single oral dose to mice or rats, whereas lovastatin and simvastatin do not. Lovastatin 205-215 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 29-79 7660676-8 1995 Lovastatin inhibited PDGF (10 ng/ml in mesangial cell, 25 ng/ml in smooth muscle cell)-, ET (10(-7)M)- and Ang II (10(-7)M)-induced [3H] thymidine uptake significantly in a dose-dependent manner in both cells. Lovastatin 0-10 angiotensinogen Rattus norvegicus 107-113 7878672-1 1995 Pravastatin, lovastatin, and simvastatin, drugs which lower cholesterol by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, have been linked to skeletal myopathies in humans and rats. Lovastatin 13-23 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 86-143 7814446-1 1995 Lovastatin (LOV), a hydroxy-methylglutaryl-coenzyme A (HMGCoA) reductase competitive inhibitor, blocks epidermal growth factor (EGF)- or prostaglandin F2 alpha (PGF2 alpha)-induced mitogenesis in confluent resting Swiss 3T3 cells. Lovastatin 0-10 epidermal growth factor Mus musculus 128-131 7830728-2 1995 We hypothesized that cholesterol-lowering therapy with the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin could improve endothelium-mediated responses in patients with coronary atherosclerosis. Lovastatin 117-127 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-106 7862668-7 1995 Depletion of sterols by treatment with a bile acid-binding resin (colestipol) and a cholesterol synthesis inhibitor (mevinolin) led to a marked increase in the nuclear form of SREBP-2 and a reciprocal decline in the nuclear form of SREBP-1. Lovastatin 117-126 sterol regulatory element binding transcription factor 2 Homo sapiens 176-183 7862668-7 1995 Depletion of sterols by treatment with a bile acid-binding resin (colestipol) and a cholesterol synthesis inhibitor (mevinolin) led to a marked increase in the nuclear form of SREBP-2 and a reciprocal decline in the nuclear form of SREBP-1. Lovastatin 117-126 sterol regulatory element binding transcription factor 1 Homo sapiens 232-239 7836430-2 1995 Lovastatin blocked an ability of insulin to activate p21ras and mitogen-activated protein kinase. Lovastatin 0-10 insulin Homo sapiens 33-40 7836430-2 1995 Lovastatin blocked an ability of insulin to activate p21ras and mitogen-activated protein kinase. Lovastatin 0-10 HRas proto-oncogene, GTPase Homo sapiens 53-59 7836430-3 1995 Lovastatin also significantly (p < 0.01) reduced insulin effects on thymidine incorporation and glucose incorporation into glycogen. Lovastatin 0-10 insulin Homo sapiens 52-59 7829224-0 1995 Tumor resistance to oxidative stress: association with ras oncogene expression and reversal by lovastatin, an inhibitor of p21ras isoprenylation. Lovastatin 95-105 HRas proto-oncogene, GTPase Homo sapiens 123-129 7829224-7 1995 Lovastatin, an inhibitor of protein isoprenylation critical for p21ras membrane association and function, restored the sensitivity of ras-transformed cells to doxorubicin and hydrogen peroxide. Lovastatin 0-10 HRas proto-oncogene, GTPase Homo sapiens 64-70 7822276-7 1995 Treatment of cells with lovastatin to induce LDL receptors increased cellular binding, internalization, and degradation of RAP by 2.3-, 1.7-, and 2.6-fold, respectively. Lovastatin 24-34 LDL receptor related protein associated protein 1 Homo sapiens 123-126 7811739-4 1995 In order to show that the feedback regulation mechanism for 3-hydroxy-3-methylglutaryl-coenzyme A reductase was involved in this phenomena mRNA levels were measured in human vascular endothelial cells after incubation with the vastatins for 3.5 h and for 20 h. Indeed, lovastatin and simvastatin gave rise to higher levels of HMG-CoA reductase mRNA after 20 h than after 3.5 h of incubation. Lovastatin 269-279 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 60-107 7662319-3 1995 The purpose of the present study was to examine the possible role of cholesterol in regulating apoB secretion by the intestine by testing if the suppression of cholesterol synthesis by the reductase inhibitor lovastatin affected the secretion of apoB by CaCo-2 human intestinal cells. Lovastatin 209-219 apolipoprotein B Homo sapiens 95-99 7662319-3 1995 The purpose of the present study was to examine the possible role of cholesterol in regulating apoB secretion by the intestine by testing if the suppression of cholesterol synthesis by the reductase inhibitor lovastatin affected the secretion of apoB by CaCo-2 human intestinal cells. Lovastatin 209-219 apolipoprotein B Homo sapiens 246-250 7814446-1 1995 Lovastatin (LOV), a hydroxy-methylglutaryl-coenzyme A (HMGCoA) reductase competitive inhibitor, blocks epidermal growth factor (EGF)- or prostaglandin F2 alpha (PGF2 alpha)-induced mitogenesis in confluent resting Swiss 3T3 cells. Lovastatin 12-15 epidermal growth factor Mus musculus 128-131 7706943-11 1995 Lovastatin (20 mg/day) significantly decreased cholesterol (27.6 +/- 6%), LDL-cholesterol (27.6 +/- 9%) and plasma apoB (17.9 +/- 2.9%) (P < 0.01 for all). Lovastatin 0-10 apolipoprotein B Homo sapiens 115-119 7706943-13 1995 Lovastatin significantly decreased LDL-apoB production rate in all cases (34.1 +/- 14%, P = 0.03). Lovastatin 0-10 apolipoprotein B Homo sapiens 39-43 7706943-15 1995 Thus, lovastatin decreased LDL-cholesterol in nephrotic subjects mainly by inhibiting LDL-apoB production from VLDL. Lovastatin 6-16 apolipoprotein B Homo sapiens 90-94 7811252-1 1994 The competitive HMG-CoA reductase inhibitor lovastatin has been shown to suppress growth and induce morphological changes in a variety of non-glioma tumor cell lines. Lovastatin 44-54 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 16-33 7617079-6 1995 Our data suggest that lovastatin may synergistically potentiate the antitumor activity of TNF-alpha. Lovastatin 22-32 tumor necrosis factor Mus musculus 90-99 7811252-5 1994 Our data suggest that HMG-CoA reductase inhibitors such as lovastatin merit further investigation as potential therapeutic agents for the treatment of malignant gliomas. Lovastatin 59-69 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 22-39 7981178-0 1994 Effects of lovastatin on ApoA- and ApoB-containing lipoproteins. Lovastatin 11-21 apolipoprotein B Homo sapiens 35-39 7981178-2 1994 To establish whether lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, exhibits a specific effect on apolipoprotein (apo) A- and apoB-containing lipoproteins, 63 subjects, a subset of the 270 Monitored Atherosclerosis Regression Study (MARS) patients with hypercholesterolemia (190 to 295 mg/dL) and documented coronary artery disease, were randomized into either lovastatin 40 mg twice daily or matching placebo tablets twice daily. Lovastatin 21-31 apolipoprotein B Homo sapiens 166-170 7988444-8 1994 Pretreatment of neurons with lovastatin (2 micrograms/ml), an inhibitor of ras isoprenylation, completely blocked the activation of p21ras by insulin and IGF-I. Lovastatin 29-39 HRas proto-oncogene, GTPase Gallus gallus 132-138 19489169-2 1994 It is structurally distinct from the other currently available HMGCoA reductase inhibitors (lovastatin, simvastatin, and pravastatin), leading to unique biopharmaceutical properties relative to the other agents of this class. Lovastatin 92-102 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-79 7728297-7 1994 In contrast, lovastatin, at concentrations of 0.25 mumol/l, increased the LDL receptor activity in both control lymphocytes and lymphocytes from patients with familial hypercholesterolemia by 121% and 148%, respectively. Lovastatin 13-23 low density lipoprotein receptor Homo sapiens 74-86 7988444-8 1994 Pretreatment of neurons with lovastatin (2 micrograms/ml), an inhibitor of ras isoprenylation, completely blocked the activation of p21ras by insulin and IGF-I. Lovastatin 29-39 insulin Gallus gallus 142-149 7988444-8 1994 Pretreatment of neurons with lovastatin (2 micrograms/ml), an inhibitor of ras isoprenylation, completely blocked the activation of p21ras by insulin and IGF-I. Lovastatin 29-39 IGF-I Gallus gallus 154-159 7968602-0 1994 Regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in the rat ileum: effects of bile acids and lovastatin. Lovastatin 115-125 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 14-61 7954816-2 1994 We now show that treatment of cells with lovastatin, which inhibits modification of small GTP-binding proteins, reduced PIP2 levels and decreased calcium mobilization in response to PDGF and thrombin. Lovastatin 41-51 coagulation factor II, thrombin Homo sapiens 191-199 7955120-3 1994 We here report that exposure of HT-29 SF human colonic adenocarcinoma cells to DHEAS inhibited the incorporation of [3H]mevalonate into cellular proteins in a dose-dependent manner when endogenous mevalonate synthesis was blocked by lovastatin. Lovastatin 233-243 sulfotransferase family 2A member 1 Homo sapiens 79-84 7968602-4 1994 Feeding lovastatin (inhibitor of HMG-CoA reductase) stimulated total ileal HMG-CoA reductase activity threefold in washed microsomes, which were dissociated from the inhibitor. Lovastatin 8-18 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 33-50 7968602-4 1994 Feeding lovastatin (inhibitor of HMG-CoA reductase) stimulated total ileal HMG-CoA reductase activity threefold in washed microsomes, which were dissociated from the inhibitor. Lovastatin 8-18 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 75-92 7968602-10 1994 Furthermore, the stimulation of total ileal HMG-CoA reductase activity by lovastatin treatment was observed without a decrease in mucosal cholesterol. Lovastatin 74-84 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 44-61 7858293-5 1994 The increased sensitivity to lovastatin of the P-gp 170-expressing MDR cells 8226/Dox40 might be part of a more general phenomenon that merits further investigation. Lovastatin 29-39 phosphoglycolate phosphatase Homo sapiens 47-51 7888300-2 1994 Preincubation of the cells with lovastatin for 11-24 h reduced the Ca(2+)-influx induced by PAF of FMLP. Lovastatin 32-42 formyl peptide receptor 1 Homo sapiens 99-103 7888300-6 1994 Addition of mevalonate to lovastatin-treated cells completely reversed the inhibition of PAF- and FMLP-stimulated Ca(2+)-mobilization. Lovastatin 26-36 PCNA clamp associated factor Homo sapiens 89-93 7888300-6 1994 Addition of mevalonate to lovastatin-treated cells completely reversed the inhibition of PAF- and FMLP-stimulated Ca(2+)-mobilization. Lovastatin 26-36 formyl peptide receptor 1 Homo sapiens 98-102 7809022-6 1994 Lovastatin inhibited cell growth by 99% (MIA), 97% (H2T), 78% (CAV), 41% (CAPAN2), and 23% (PANC1), respectively, when cells were treated with 2.5 micrograms/ml lovastatin for 6 days. Lovastatin 0-10 caveolin 2 Homo sapiens 63-66 8068726-1 1994 Normolipidemic rats were treated with HMG-CoA reductase inhibitors (lovastatin or pravastatin) for periods of 1-3 days. Lovastatin 68-78 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 38-55 8068726-8 1994 The increase in PAP activity upon treatment with lovastatin or pravastatin was gradual and occurred simultaneously with the apparent increase in HMG-CoA reductase activity. Lovastatin 49-59 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 145-162 8068731-6 1994 Mevinolin treatment greatly increased peroxisomal and cytosolic farnesyl pyrophosphate synthase activities, but not the mitochondrial activity, and the cis-prenyltransferase activities were elevated in peroxisomes, but not in microsomes. Lovastatin 0-9 farnesyl diphosphate synthase Rattus norvegicus 64-95 8208513-0 1994 Inhibition of the membrane localization of p21 ras proteins by lovastatin in tumor cells possessing a mutated N-ras gene. Lovastatin 63-73 HRas proto-oncogene, GTPase Homo sapiens 43-50 8208513-4 1994 The membrane localization of p21 ras has been reduced by 30-36% after the tumor cells have grown in the presence of 10 microM lovastatin for 7 days. Lovastatin 126-136 HRas proto-oncogene, GTPase Homo sapiens 29-36 8077853-0 1994 Altered apolipoprotein B metabolism in very low density lipoprotein from lovastatin-treated guinea pigs. Lovastatin 73-83 apolipoprotein B-100 Cavia porcellus 8-24 8077853-7 1994 The fractions of control and lovastatin VLDL apoB converted to LDL averaged 0.15 +/- 0.15 and 0.02 +/- 0.02, respectively (P < 0.05, paired t test). Lovastatin 29-39 apolipoprotein B-100 Cavia porcellus 45-49 8077853-10 1994 Thus, the metabolic behavior of VLDL apoB is affected by lovastatin. Lovastatin 57-67 apolipoprotein B-100 Cavia porcellus 37-41 7842472-12 1994 PC-12 cells grown in the absence of NGF are highly sensitive to lovastatin (25 microM) and more than 70% of the cells die after 48 hr. Lovastatin 64-74 nerve growth factor Rattus norvegicus 36-39 7842472-13 1994 NGF confers lovastatin resistance on cells grown in the presence or in the absence of serum (only 30-40% cell death after 48 hr with lovastatin). Lovastatin 12-22 nerve growth factor Rattus norvegicus 0-3 7842472-13 1994 NGF confers lovastatin resistance on cells grown in the presence or in the absence of serum (only 30-40% cell death after 48 hr with lovastatin). Lovastatin 133-143 nerve growth factor Rattus norvegicus 0-3 7842472-15 1994 NGF-induced resistance on lovastatin develops with time and is apparent only in the well-differentiated PC-12 cells whether or not the cells express a high reductase activity. Lovastatin 26-36 nerve growth factor Rattus norvegicus 0-3 8133281-7 1994 Furthermore, a high lovastatin concentration in the brainstem slice incubation mixture altered the appearance of newly synthesized nonprenylated myelin proteins, including proteolipid protein and the 17-kDa subspecies of myelin basic protein. Lovastatin 20-30 myelin basic protein Rattus norvegicus 221-241 8018562-2 1994 When treated with lovastatin, the cells were blocked in G1 and appeared to express increased levels of wild-type p53 when examined by immunostaining. Lovastatin 18-28 tumor protein p53 Homo sapiens 113-116 8109970-4 1994 When rats were fed diets containing Lovastatin, a potent HMG-CoA reductase inhibitor which blocks synthesis of both nonsterols and sterols, similar 15- to 20-fold increases were observed for both HMG-CoA reductase mRNA and activity. Lovastatin 36-46 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 57-74 8109970-4 1994 When rats were fed diets containing Lovastatin, a potent HMG-CoA reductase inhibitor which blocks synthesis of both nonsterols and sterols, similar 15- to 20-fold increases were observed for both HMG-CoA reductase mRNA and activity. Lovastatin 36-46 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 196-213 8305412-10 1994 In a double-blind, placebo-controlled trial among the familial hypercholesterolemia patients, lovastatin alone or in combination with fish oil concentrate lowered plasma TFPI in parallel with LDL cholesterol. Lovastatin 94-104 tissue factor pathway inhibitor Homo sapiens 170-174 8010162-1 1994 Treatment with mevinolin, a competitive inhibitor of HMGCoAR, the key enzyme of isoprenoid metabolism, causes the arrest of proliferation and the differentiation of a neuroblastoma cell line (N18TG2). Lovastatin 15-24 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 53-60 8010162-3 1994 Cholesterol synthesis in the presence of mevinolin remains active, because in these cells the key enzyme HMG-CoA reductase is not completely inhibited by this drug. Lovastatin 41-50 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 105-122 7727042-0 1995 Inhibition of ras p21 membrane localization and modulation of protein kinase C isozyme expression during regression of chemical carcinogen-induced murine skin tumors by lovastatin. Lovastatin 169-179 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 18-21 7727042-4 1995 However, when ras p21 membrane localization was blocked in vivo in growing tumors by lovastatin, opposite results were evident. Lovastatin 85-95 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 18-21 7727042-5 1995 Compared with saline-treated animals, in which tumor growth continued, lovastatin-treated animals had significantly inhibited tumor growth, which led to tumor regression with concomitant inhibition of Ha-ras p21 membrane localization. Lovastatin 71-81 Harvey rat sarcoma virus oncogene Mus musculus 201-207 7727042-5 1995 Compared with saline-treated animals, in which tumor growth continued, lovastatin-treated animals had significantly inhibited tumor growth, which led to tumor regression with concomitant inhibition of Ha-ras p21 membrane localization. Lovastatin 71-81 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 208-211 7727042-6 1995 These regressing tumors from lovastatin-treated animals also showed a decrease in the expression and membrane translocation of PKC zeta and beta II but increased expression of PKC alpha. Lovastatin 29-39 protein kinase C, alpha Mus musculus 176-185 7802717-5 1994 Although only a decade has passed since the first HMG CoA reductase inhibitor, lovastatin, entered clinical trials this group of compounds are not only the most widely used lipid lowering agents, but more than six such agents have been or are currently being developed. Lovastatin 79-89 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 50-67 8039707-12 1994 We also found that lovastatin-induced cell cycle arrest resulted in increased RHOA RNA expression in breast cancer cell lines. Lovastatin 19-29 ras homolog family member A Homo sapiens 78-82 8169651-4 1994 Mevinolin, a competitive inhibitor of 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase activity, depletes cells of the intermediate products of the pathway that are required for the posttranslational modification of proteins, a process giving the proteins lipophilic anchors that bind to membranes. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-96 8147861-3 1994 In this study we show that HL-60 cells treated with lovastatin, an inhibitor of mevalonate synthesis, exhibit alterations in growth and morphology, as well as changes in the subcellular distribution of isoprenylated proteins like nuclear lamin A and p21Ras. Lovastatin 52-62 HRas proto-oncogene, GTPase Homo sapiens 250-256 8119922-6 1994 FPP synthase activities at different locations responded distinctly when rats were treated with a diet enriched in cholesterol or containing mevinolin or cholestyramine. Lovastatin 141-150 farnesyl diphosphate synthase Rattus norvegicus 0-12 8119922-8 1994 Both mevinolin and cholestyramine treatment resulted in 3-fold increases in cytosolic FPP synthase activities, without altering the mitochondrial activity. Lovastatin 5-14 farnesyl diphosphate synthase Rattus norvegicus 86-98 8295321-15 1994 Thus, a low dose of lovastatin appears highly effective for treatment of moderate hypercholesterolemia in most postmenopausal women, presumably because it reverses the reduction in LDL receptor activity associated with menopause. Lovastatin 20-30 low density lipoprotein receptor Homo sapiens 181-193 7809022-9 1994 Lovastatin inhibited the growth of CAV cells even though this cell line did not have ras mutation, suggesting that lovastatin inhibition of pancreatic cancer cell growth is not directly dependent on the presence of ras mutation. Lovastatin 0-10 caveolin 2 Homo sapiens 35-38 7487365-1 1994 We assessed the antiproliferative effect of tumor necrosis factor alpha (TNF-alpha) and lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, alone and in combination, on two murine tumor cell lines. Lovastatin 88-98 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 116-173 7487365-4 1994 In combination with tumor necrosis factor alpha lovastatin inhibited synergistically growth of both cell lines as assessed by isobologram analysis. Lovastatin 48-58 tumor necrosis factor Mus musculus 20-47 7487365-5 1994 Our data show that lovastatin, a cholesterol synthesis inhibitor, introduced to the clinic to treat hypercholesterolemia, used either as a single or in combination with TNF-alpha inhibits growth of MmB16 melanoma and L1210 leukemia cells. Lovastatin 19-29 tumor necrosis factor Mus musculus 169-178 8141838-0 1993 Effect of lovastatin on the secretion of very low density lipoprotein lipids and apolipoprotein B in the hypertriglyceridemic Zucker obese rat. Lovastatin 10-20 apolipoprotein B Rattus norvegicus 81-97 8294001-6 1993 In HepG2 cells, both mRNAs are induced 2-4-fold by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin. Lovastatin 114-124 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 55-102 8260364-4 1993 T24-ras transfectants with moderate or high p21ras expression showed reduced apoptosis, and this was reversed by pharmacological inhibition of membrane localisation of p21ras by mevinolin. Lovastatin 178-187 HRas proto-oncogene, GTPase Homo sapiens 168-174 8252688-8 1993 In five hypercholesterolemic subjects, treated with lovastatin to normalize serum cholesterol concentrations, maximal responsiveness to bradykinin decreased from 103 +/- 52% to 80 +/- 28%. Lovastatin 52-62 kininogen 1 Homo sapiens 136-146 8214993-9 1993 RESULTS: Lovastatin lowered total cholesterol level by 32%, low-density lipoprotein cholesterol by 38%, and the apolipoprotein B by 26% and raised the high-density lipoprotein cholesterol by 8.5% (P < 0.001). Lovastatin 9-19 apolipoprotein B Homo sapiens 112-128 8301234-4 1993 The polar sterol, 25-hydroxycholesterol, the squalene epoxide inhibitor, U18666A, and the inhibitor of HMG-CoA reductase, lovastatin, all significantly inhibited the synthesis of cholesterol without altering either SPT activity or long-chain base synthesis. Lovastatin 122-132 alanine--glyoxylate and serine--pyruvate aminotransferase Homo sapiens 215-218 8246233-3 1993 3,5-Dihydroxy-7-(N-imidazolyl)heptanoates 4 and the corresponding heptenoates 5 were synthesized as novel classes of potent HMG-CoA reductase (HMGR) inhibitors in which members of the latter series possess enzyme inhibitory activity greater than that of lovastatin 1 and pravastatin 2. Lovastatin 254-264 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 143-147 8270199-0 1993 Pleurotus fungi produce mevinolin, an inhibitor of HMG CoA reductase. Lovastatin 24-33 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 51-68 8270199-1 1993 Fungi of the genus Pleurotus were shown to produce the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor mevinolin. Lovastatin 106-115 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 55-95 8225233-4 1993 These gene products were well maintained for many days and were induced by treatment of the cultures with dexamethasone, phenobarbital, macrolide antibiotics, the HMG CoA reductase inhibitor lovastatin or an antifungal agent, clotrimazole. Lovastatin 191-201 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 163-180 7902394-8 1993 Treatment of cells with lovastatin, an inhibitor of ras-encoded p21ras post-translational processing via the mevalonate pathway, markedly decreased the yield of micronuclei formation in cells transfected with ras; the drug had no effect on radiation-induced micronuclei formation in parental cells. Lovastatin 24-34 HRas proto-oncogene, GTPase Homo sapiens 64-70 7905377-5 1993 Biotransformation of lovastatin occurred by three distinct routes, namely hydrolysis of the lactone ring to yield the pharmacologically active dihydroxy acid, cytochrome P-450-mediated oxidation of the fused-ring system, and beta-oxidation of the dihydroxy acid side chain. Lovastatin 21-31 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 159-175 7905377-11 1993 From these studies, cytochrome P-450 oxidation is the primary route of phase I metabolism for lovastatin in human and dog, but beta-oxidation plays a major metabolic role in rodents. Lovastatin 94-104 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 20-36 8263421-9 1993 This study also provides direct proof that lovastatin, a drug that enhances LDL receptor activity in the liver, also increases the hepatic uptake of LDL in humans. Lovastatin 43-53 low density lipoprotein receptor Homo sapiens 76-88 8288727-1 1993 Suppression of cholesterol synthesis by 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, such as lovastatin, has been shown to inhibit mitogen stimulated proliferation of natural killer (NK) cells and other lymphocytes in vitro. Lovastatin 118-128 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 40-97 8359807-10 1993 Continuous infusion of mevinolin completely prevented increases in cholesterol 7 alpha-hydroxylase specific activity and bile acid biosynthesis at both time intervals. Lovastatin 23-32 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 67-98 7693661-7 1993 However, upon exposure of cells to 10 microns lovastatin for 40 h, the level of autophosphorylated PDGFR associating with PI-3-kinase after PDGF stimulation decreases significantly (75% reduction). Lovastatin 46-56 platelet derived growth factor receptor, beta polypeptide Mus musculus 99-104 7693661-9 1993 These results demonstrate that lovastatin disrupts a major growth factor signaling pathway and that inhibition of PDGF-induced association of PI-3-kinase with PDGFR and subsequent inhibition of PI-3-kinase activity is one potential mechanism by which lovastatin inhibits cell growth. Lovastatin 251-261 platelet derived growth factor receptor, beta polypeptide Mus musculus 159-164 7504129-0 1993 Long-term treatment (2 years) with the HMG CoA reductase inhibitors lovastatin or pravastatin in combination with cholestyramine in patients with severe primary hypercholesterolemia. Lovastatin 68-78 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-56 8333817-12 1993 In addition, the use of lovastatin was high across all algorithms at all initial LDL-C levels modeled. Lovastatin 24-34 component of oligomeric golgi complex 2 Homo sapiens 81-86 8333817-19 1993 At moderate and severe initial LDL-C levels (4.91 and 5.69 mmol/L [190 and 220 mg/dL]), the lovastatin-first regimen may be advantageous. Lovastatin 92-102 component of oligomeric golgi complex 2 Homo sapiens 31-36 21573374-3 1993 Addition of mevinolin (an HMG CoA reductase inhibitor) depressed this increase in HMG CoA reductase activity with similar kinetics as it did in the transformed cells as well as in serum-stimulated normal cells. Lovastatin 12-21 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 26-43 21573374-3 1993 Addition of mevinolin (an HMG CoA reductase inhibitor) depressed this increase in HMG CoA reductase activity with similar kinetics as it did in the transformed cells as well as in serum-stimulated normal cells. Lovastatin 12-21 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 82-99 8345219-2 1993 Moreover, blockade of synthesis of these lipids with inhibitors of two of the rate-limiting enzymes, HMGCoA reductase (lovastatin, fluvastatin) and serine palmitoyl transferase (beta-chloroalanine), alters the kinetics of barrier repair. Lovastatin 119-129 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 101-117 8325896-4 1993 Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in isoprenoid and sterol biosynthesis, by the cholesterol-lowering drug, lovastatin, blocks Fc epsilon RI-dependent [3H] serotonin ([3H]5HT) release from the mast cell line, RBL-2H3. Lovastatin 171-181 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 14-71 8345800-0 1993 The response to lovastatin treatment in patients with heterozygous familial hypercholesterolemia is modulated by apolipoprotein E polymorphism. Lovastatin 16-26 low density lipoprotein receptor Homo sapiens 67-96 8345800-0 1993 The response to lovastatin treatment in patients with heterozygous familial hypercholesterolemia is modulated by apolipoprotein E polymorphism. Lovastatin 16-26 apolipoprotein E Homo sapiens 113-129 8345800-6 1993 Hence, apo E polymorphism influenced LDL-C (and HDL-C) response to lovastatin in men, but not in women, revealing the existence of a gene-by-gender interaction. Lovastatin 67-77 apolipoprotein E Homo sapiens 7-12 7685352-13 1993 A 2.7- and 4.0-fold increase of HSS mRNA was observed when HepG2 cells were grown in the presence of 5 micrograms/ml lovastatin in lipid-depleted or full serum, respectively. Lovastatin 117-127 growth factor, augmenter of liver regeneration Homo sapiens 32-35 7684605-8 1993 Administration of 10 mg/day lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, markedly attenuated both the reduced basal NO production and the increased adhesiveness of the endothelium. Lovastatin 28-38 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 42-89 8213497-5 1993 Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which include lovastatin, simvastatin, and pravastatin, are the most effective of the currently available drugs and show dose-dependent effects on the concentrations of LDL cholesterol, which decrease by 20-45% in response to these drugs when used over the full dosage range. Lovastatin 87-97 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-71 8517861-3 1993 As a consequence of this inhibition, the HMG-CoA reductase mRNA levels and squalene synthase activity, both negatively-regulated by sterols, were increased equally by simvastatin and lovastatin, whereas the induction by pravastatin was much less. Lovastatin 183-193 farnesyl-diphosphate farnesyltransferase 1 Homo sapiens 75-92 1488408-0 1992 Influence of age and gender on the plasma profiles of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitory activity following multiple doses of lovastatin and simvastatin. Lovastatin 160-170 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 54-111 8511800-0 1993 Regulation of phenobarbital-inducible cytochrome P450 2B1/2 mRNA by lovastatin and oxysterols in primary cultures of adult rat hepatocytes. Lovastatin 68-78 UDP glucuronosyltransferase family 2 member B17 Rattus norvegicus 54-59 8511800-5 1993 In contrast to the potentiation of 2B1/2 mRNA induction produced by treatments with LOVA in combination with PB or CTZ, cotreatment of hepatocytes with PB and CTZ did not result in increased induction relative to that seen in cells treated with either agent alone. Lovastatin 84-88 UDP glucuronosyltransferase family 2 member B17 Rattus norvegicus 35-40 8511800-7 1993 Taken together, our results demonstrate that LOVA is a unique inducer of P450 mRNA in cultured rat hepatocytes and implicate oxysterols as potential intracellular modulators of 2B1/2 induction. Lovastatin 45-49 UDP glucuronosyltransferase family 2 member B17 Rattus norvegicus 177-182 8482726-1 1993 Blockade of mevalonate synthesis by the 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitor mevinolin (lovastatin) causes FRTL-5 thyroid cells to undergo significant morphological changes; these include a transition from a flat, polygonal to a round shape, the development of cytoplasmic arborizations, and the loss of contact between neighboring cells. Lovastatin 98-107 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 40-87 8482726-1 1993 Blockade of mevalonate synthesis by the 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitor mevinolin (lovastatin) causes FRTL-5 thyroid cells to undergo significant morphological changes; these include a transition from a flat, polygonal to a round shape, the development of cytoplasmic arborizations, and the loss of contact between neighboring cells. Lovastatin 109-119 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 40-87 8474436-8 1993 Inhibition of sterol synthesis in S. cerevisiae and S. pombe cells or in cultured human fibroblasts by treatment with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor lovastatin resulted in elevated levels of squalene synthetase mRNA in all three cell types. Lovastatin 180-190 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 122-169 8474436-8 1993 Inhibition of sterol synthesis in S. cerevisiae and S. pombe cells or in cultured human fibroblasts by treatment with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor lovastatin resulted in elevated levels of squalene synthetase mRNA in all three cell types. Lovastatin 180-190 farnesyl-diphosphate farnesyltransferase 1 Homo sapiens 222-241 8330475-2 1993 In 18 patients with coronary artery disease and hypercholesterolemia resistant to low-lipid diet a 12 week treatment with lovastatin (HMG-CoA reductase inhibitor) leads to the reduction of total cholesterol, LDL-cholesterol and triglycerides but also to a marked increase of platelet activity. Lovastatin 122-132 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 134-151 8516264-1 1993 The aim of the present study was to investigate the effect of the hydroxymethylglutaryl (HMG)-CoA reductase inhibitor lovastatin on some aspects of cholesterol metabolism in cholesterol-fed rabbits. Lovastatin 118-128 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 66-107 8434806-1 1993 The effects of lovastatin treatment on high-density lipoprotein subfractions (HDL2 and HLD3) were investigated in 34 patients with severe peripheral vascular disease and type IIa or type IIb hyperlipoproteinemia by use of a density gradient ultracentrifugation method. Lovastatin 15-25 junctophilin 3 Homo sapiens 78-82 8434806-1 1993 The effects of lovastatin treatment on high-density lipoprotein subfractions (HDL2 and HLD3) were investigated in 34 patients with severe peripheral vascular disease and type IIa or type IIb hyperlipoproteinemia by use of a density gradient ultracentrifugation method. Lovastatin 15-25 aminoacyl tRNA synthetase complex interacting multifunctional protein 1 Homo sapiens 87-91 8434806-2 1993 Lovastatin therapy caused greater percentage changes in HDL2 than in HDL3. Lovastatin 0-10 junctophilin 3 Homo sapiens 56-60 8434806-2 1993 Lovastatin therapy caused greater percentage changes in HDL2 than in HDL3. Lovastatin 0-10 HDL3 Homo sapiens 69-73 8485218-8 1993 Lovastatin, an inhibitor of 3-hydroxymethyl-3-glutaryl coenzyme A (HMG-CoA) reductase, stimulated cholesterol absorption in a dose-dependent manner. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 28-85 8430072-3 1993 Cellular internalization of chol-modified oligonucleotide occurred at least partially through the LDL receptor; it was increased in mouse spleen cells by cell culture in lipoprotein-deficient medium and/or lovastatin, and it was decreased by culture in high serum medium. Lovastatin 206-216 low density lipoprotein receptor Mus musculus 98-110 8442035-0 1993 HMGCoA reductase inhibitors lovastatin and simvastatin in the treatment of hypercholesterolemia after renal transplantation. Lovastatin 28-38 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-16 8425769-0 1993 Increased radioresistance of EJras-transformed human osteosarcoma cells and its modulation by lovastatin, an inhibitor of p21ras isoprenylation. Lovastatin 94-104 HRas proto-oncogene, GTPase Homo sapiens 122-128 8425769-4 1993 Interestingly, treatment of the ras-transformed cells with lovastatin, an inhibitor of p21ras post-translational processing via the mevalonate pathway, markedly decreased their radioresistance. Lovastatin 59-69 HRas proto-oncogene, GTPase Homo sapiens 87-93 8425769-5 1993 Under the experimental conditions used, lovastatin prevented the membrane association, but not the biosynthesis, of p21. Lovastatin 40-50 H3 histone pseudogene 16 Homo sapiens 116-119 8424783-0 1993 Blockade of mevalonate production by lovastatin attenuates bombesin and vasopressin potentiation of nutrient-induced insulin secretion in HIT-T15 cells. Lovastatin 37-47 insulin Mesocricetus auratus 117-124 8424783-3 1993 We have examined protein isoprenylation, subcellular distribution of SMGs, cytosolic Ca2+ changes and insulin secretion in HIT-T15 cells after treatment with lovastatin, which inhibits the production of isoprenoids by blocking mevalonate production by 3-hydroxy-3-methylglutaryl-CoA reductase. Lovastatin 158-168 insulin Mesocricetus auratus 102-109 8424783-3 1993 We have examined protein isoprenylation, subcellular distribution of SMGs, cytosolic Ca2+ changes and insulin secretion in HIT-T15 cells after treatment with lovastatin, which inhibits the production of isoprenoids by blocking mevalonate production by 3-hydroxy-3-methylglutaryl-CoA reductase. Lovastatin 158-168 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 252-292 8424783-7 1993 Lovastatin selectively attenuated the potentiating action of bombesin and vasopressin, which activate phospholipase C in these cells, on insulin secretion stimulated by nutrients (glucose + leucine + glutamine). Lovastatin 0-10 insulin Mesocricetus auratus 137-144 8424783-13 1993 In conclusion, lovastatin selectively attenuated the potentiation of nutrient-induced insulin secretion by bombesin and vasopressin without affecting their activation of phospholipase C. The concomitant changes in SMG isoprenylation and their subcellular distribution after lovastatin treatment suggest that SMGs could play an important role in the bombesin and vasopressin action on insulin secretion. Lovastatin 15-25 insulin Mesocricetus auratus 86-93 8424783-13 1993 In conclusion, lovastatin selectively attenuated the potentiation of nutrient-induced insulin secretion by bombesin and vasopressin without affecting their activation of phospholipase C. The concomitant changes in SMG isoprenylation and their subcellular distribution after lovastatin treatment suggest that SMGs could play an important role in the bombesin and vasopressin action on insulin secretion. Lovastatin 15-25 insulin Mesocricetus auratus 384-391 7992552-3 1993 In the same cell model, lovastatin, an inhibitor of beta hydroxy-beta methyl-glutaryl-CoA-reductase and, hence, of farnesylation of p21ras, partially protects aspartate transport from the inhibition observed upon steroid treatment. Lovastatin 24-34 Harvey rat sarcoma virus oncogene Mus musculus 132-138 8487493-0 1993 The effect of lovastatin on very low-density lipoprotein apolipoprotein B production by the liver in familial combined hyperlipidaemia. Lovastatin 14-24 apolipoprotein B Homo sapiens 57-73 8487493-3 1993 Following 4-6 months of therapy with lovastatin, very low-density lipoprotein apolipoprotein B production in all four subjects had returned to the normal range. Lovastatin 37-47 apolipoprotein B Homo sapiens 78-94 8487493-4 1993 This demonstrates that lovastatin, an inhibitor of cholesterol biosynthesis, acts also to reduce the apparent production rate of apolipoprotein B by the liver. Lovastatin 23-33 apolipoprotein B Homo sapiens 129-145 8435109-2 1993 Farnesyl synthesis and p21 ras farnesylation are inhibited by hydroxymethylglutaryl-CoA reductase inhibitors such as lovastatin. Lovastatin 117-127 KRAS proto-oncogene, GTPase Rattus norvegicus 23-26 8435109-5 1993 Membrane association of p21 ras in these cells was inhibited after in vitro treatment with lovastatin (0.1-0.5 microM) for 48 h. Concomitantly, the cells displayed a more normal morphology, decreased growth in soft agar, and enhanced GJIC. Lovastatin 91-101 KRAS proto-oncogene, GTPase Rattus norvegicus 24-27 8435109-10 1993 These results suggest that lovastatin reversed the transformed phenotype of WB-ras cells by inhibiting p21 ras plasma membrane association. Lovastatin 27-37 KRAS proto-oncogene, GTPase Rattus norvegicus 103-106 8289991-1 1993 A few cases of severe rhabdomyolysis have been reported in heart transplant recipients treated simultaneously with ciclosporin (CS) and the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin. Lovastatin 208-218 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 140-197 8429920-6 1993 Methylation and membrane association of the small GTP-binding proteins were blocked by lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, which also enhanced their labeling by 3H-MVA-metabolites. Lovastatin 87-97 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 115-165 8399631-3 1993 After 8 weeks of lovastatin treatment, total cholesterol was significantly reduced by 28.6% (6.68 +/- 0.26 mmol/L, mean +/- SEM, to 4.77 +/- 0.12, p < 0.01); low-density lipoprotein cholesterol by 40.5% (4.57 +/- 0.27 mmol/L to 2.72 +/- 0.09, p < 0.01); apolipoprotein B by 32.4% (115.9 +/- 6.99 mg/dL to 78.3 +/- 2.9 mg/dL, p < 0.01); and triglyceride by 17.8% (1.92 +/- 0.38 mmol/L to 1.58 +/- 0.32, p < 0.05). Lovastatin 17-27 apolipoprotein B Homo sapiens 260-276 1487489-5 1992 They also responded to mevinolin (an HMG CoA reductase inhibitor) by a similar G1-block, indicating that a mevalonate-derived product is involved in the G1-located cell cycle control of HDF. Lovastatin 23-32 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 37-54 16653244-2 1992 Various studies have shown that mevalonic acid-derived compounds are required for growth of plant and animal cells, a conclusion supported by the observation that cells treated with lovastatin (a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase) cease growth. Lovastatin 182-192 3-hydroxy-3-methylglutaryl-coenzyme A reductase Nicotiana tabacum 216-263 8354954-6 1993 Three hours after lovastatin administration, cholesterol 7 alpha-hydroxylase specific activity, enzyme mass, mRNA, and gene transcriptional activity were decreased by 35%, 32%, 56%, and 34%, respectively, in rats with chronic bile fistula. Lovastatin 18-28 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 45-76 8354954-7 1993 In rats with intact enterohepatic circulation, lovastatin administration resulted in a similar decrease (34%) of cholesterol 7 alpha-hydroxylase specific activity. Lovastatin 47-57 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 113-144 8390855-7 1993 Because Ha-Ras requires isoprenylation for membrane binding, we examined the effect of the isoprenylation inhibitors lovastatin and perillic acid on PMA-induced c-Jun phosphorylation. Lovastatin 117-127 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-166 8385478-4 1993 All VLDL subspecies bound to the LDL receptor of cultured human fibroblasts with similar, high affinities on both placebo and lovastatin, but VLDL Sf 100-400 and VLDL Sf 60-100 caused less suppression of 3-hydroxy-3-methyl glutaryl coenzyme A reductase activity after lovastatin therapy, indicating reduced LDL receptor-mediated cholesterol delivery. Lovastatin 126-136 low density lipoprotein receptor Homo sapiens 33-45 8440094-2 1993 This report describes the design and methodological features of a double-masked, randomized, placebo-controlled trial to determine whether administration of the HMG CoA reductase inhibitor lovastatin retards the progression or facilitates the regression of coronary atherosclerosis. Lovastatin 189-199 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 161-178 21573552-1 1993 Treatment with mevinolin (an HMG CoA reductase inhibitor) blocks proliferation and causes characteristic morphological changes in human breast cancer cells (MDA231). Lovastatin 15-24 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 29-46 8419360-11 1993 When rats were fed mevinolin (lovastatin), FPP and all-trans-GGPP synthase activities were affected differently in certain tissues. Lovastatin 19-28 geranylgeranyl diphosphate synthase 1 Rattus norvegicus 61-74 8419360-11 1993 When rats were fed mevinolin (lovastatin), FPP and all-trans-GGPP synthase activities were affected differently in certain tissues. Lovastatin 30-40 geranylgeranyl diphosphate synthase 1 Rattus norvegicus 61-74 8419360-12 1993 Mevinolin treatment resulted in an increase in FPP but a decrease in all-trans-GGPP synthase activity in rat liver and kidney. Lovastatin 0-9 geranylgeranyl diphosphate synthase 1 Rattus norvegicus 79-92 8419360-13 1993 In spleen mevinolin treatment caused a greater than 70% decrease in all-trans-GGPP synthase activity, while FPP synthase was almost unaffected. Lovastatin 10-19 geranylgeranyl diphosphate synthase 1 Rattus norvegicus 78-91 7860224-1 1993 Lovastatin (LST) is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a rate-limiting enzyme that regulates the biosynthesis of cholesterol. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 36-93 7860224-1 1993 Lovastatin (LST) is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a rate-limiting enzyme that regulates the biosynthesis of cholesterol. Lovastatin 12-15 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 36-93 8429920-10 1993 The efficacy of lovastatin blockage of protein methylation and enhancement of 3H-MVA-metabolites incorporation into GTP-binding proteins was lower in NGF-induced cells than in controls. Lovastatin 16-26 nerve growth factor Rattus norvegicus 150-153 1289236-5 1992 Mevinolin which inhibits cholesterol synthesis significantly reduced the secretion of apoB. Lovastatin 0-9 apolipoprotein B Rattus norvegicus 86-90 1420339-12 1992 The results indicate that mevinolin affects not only HMG-CoA reductase but, to some extent, also affects certain of the peripheral enzymes, resulting in considerable effects on the various mevalonate pathway lipids. Lovastatin 26-35 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 53-70 1493355-4 1992 The HMG-CoA reductase inhibitors lovastatin, simvastatin and pravastatin are potent well tolerated hypolipidaemic therapies in young subjects. Lovastatin 33-43 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-21 1517204-14 1992 Lovastatin treatment also caused the accumulation of the noncomplexed form of CDC42 but not of rho proteins. Lovastatin 0-10 cell division cycle 42 Homo sapiens 78-83 1503903-2 1992 The effect of ONC alone and in combination with lovastatin (LVT), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, a rate-limiting enzyme of mevalonate (MVA) and cholesterol synthesis pathway, in three human tumour cell lines ASPC-1 pancreatic, A-549 lung, and HT-520 lung carcinomas, has been presently studied. Lovastatin 48-58 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 82-139 1499946-3 1992 In the present study, the effect of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, the rate-limiting enzyme of cholesterol synthesis, on the growth of five pancreatic cancer cell lines (human-CAV, MIA Paca2, CAPAN2 and PANC1, and hamster-H2T) in vitro and of two cell lines (CAV and H2T) in vivo was examined. Lovastatin 36-46 caveolin 2 Homo sapiens 212-215 1499946-3 1992 In the present study, the effect of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, the rate-limiting enzyme of cholesterol synthesis, on the growth of five pancreatic cancer cell lines (human-CAV, MIA Paca2, CAPAN2 and PANC1, and hamster-H2T) in vitro and of two cell lines (CAV and H2T) in vivo was examined. Lovastatin 36-46 caveolin 1, caveolae protein Mus musculus 295-298 1499946-4 1992 Inhibition of cell growth was observed with lovastatin doses at or above 2.5 micrograms/mL for H2T, CAV, MIA Paca2, and CAPAN2 or 10 micrograms/mL in PANC1. Lovastatin 44-54 caveolin 2 Homo sapiens 95-103 1499946-10 1992 Growth of pancreatic carcinoma xenografts (CAV and H2T) in nude mice was inhibited by a subcutaneous infusion of lovastatin (50 micrograms/h). Lovastatin 113-123 caveolin 1, caveolae protein Mus musculus 43-46 1324944-7 1992 Further analysis demonstrated that Cx26 is a cell-cycle regulated gene expressed at a moderate level during G1 and S, and strongly up-regulated in late S and G2, as shown with lovastatin-synchronized NMECs. Lovastatin 176-186 gap junction protein beta 2 Homo sapiens 35-39 1637788-2 1992 In the present study, the effect of Maxepa plus lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on apo B metabolism was assessed. Lovastatin 48-58 3-hydroxy-3-methylglutaryl-CoA reductase Sus scrofa 62-109 1637288-7 1992 Finally, cultivation of lymphocytes with conditioned medium from macrophages increased Dil-HDL binding/uptake, while it was decreased by mevinolin-induced inhibition of hydroxymethylglutaryl-coA reductase. Lovastatin 137-146 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 169-204 1392453-3 1992 The median Lp(a) level was insignificantly reduced by 10.3% during the first 20 weeks when the subjects were on a standardized medication of increasing doses of lovastatin and cholestyramine. Lovastatin 161-171 lipoprotein(a) Homo sapiens 11-16 1392453-6 1992 Thus, it appears that the reduction in Lp(a) level could be ascribed to lovastatin alone. Lovastatin 72-82 lipoprotein(a) Homo sapiens 39-44 1613316-3 1992 Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions. Lovastatin 16-26 junctophilin 3 Homo sapiens 85-89 1613316-3 1992 Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions. Lovastatin 16-26 HDL3 Homo sapiens 94-98 1613316-6 1992 Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01). Lovastatin 103-113 junctophilin 3 Homo sapiens 146-150 1431581-8 1992 Lovastatin therapy in CESD appears to be clinically beneficial and has complex effects on lipid metabolism that may include a dominant inhibitory effect on hepatic lipoprotein production, posttranscriptionally mediated induction of the LDL receptor, and alterations of LDL particles that interfere with their clearance by the LDL receptor in vivo. Lovastatin 0-10 low density lipoprotein receptor Homo sapiens 236-248 1613316-6 1992 Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01). Lovastatin 103-113 HDL3 Homo sapiens 174-178 1431581-8 1992 Lovastatin therapy in CESD appears to be clinically beneficial and has complex effects on lipid metabolism that may include a dominant inhibitory effect on hepatic lipoprotein production, posttranscriptionally mediated induction of the LDL receptor, and alterations of LDL particles that interfere with their clearance by the LDL receptor in vivo. Lovastatin 0-10 low density lipoprotein receptor Homo sapiens 326-338 1619360-4 1992 Inhibition of cholesterol synthesis with a bolus dose of mevinolin (lovastatin) a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, profoundly decreases the specific activity of cholesterol 7 alpha-hydroxylase and rate of bile acid synthesis in rats with complete biliary diversion. Lovastatin 57-66 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 107-164 1480917-10 1992 The current data suggest that Lovastatin (an inhibitor of HMG-Coa reductase) may provide one important means for lipid-lowering therapy in patients with primary hypercholesterolemia. Lovastatin 30-40 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 58-75 1634641-5 1992 The possible relevance of Lp(a) levels for the hemorheologic effects of lovastatin remains to be elucidated. Lovastatin 72-82 lipoprotein(a) Homo sapiens 26-31 10146977-6 1992 Studies to date therefore suggest that therapy with HMG-CoA reductase inhibitors (i.e. lovastatin and simvastatin) is substantially more cost-effective than treatment with bile-acid sequestrants. Lovastatin 87-97 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 52-69 1619360-4 1992 Inhibition of cholesterol synthesis with a bolus dose of mevinolin (lovastatin) a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, profoundly decreases the specific activity of cholesterol 7 alpha-hydroxylase and rate of bile acid synthesis in rats with complete biliary diversion. Lovastatin 57-66 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 212-243 1619360-4 1992 Inhibition of cholesterol synthesis with a bolus dose of mevinolin (lovastatin) a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, profoundly decreases the specific activity of cholesterol 7 alpha-hydroxylase and rate of bile acid synthesis in rats with complete biliary diversion. Lovastatin 68-78 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 107-164 1619360-4 1992 Inhibition of cholesterol synthesis with a bolus dose of mevinolin (lovastatin) a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, profoundly decreases the specific activity of cholesterol 7 alpha-hydroxylase and rate of bile acid synthesis in rats with complete biliary diversion. Lovastatin 68-78 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 212-243 1311272-2 1992 Mevinolin is known to inhibit 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase (EC 1.1.1.34), the rate-limiting step in cholesterol biosynthesis. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 30-80 1581407-11 1992 Long-term treatment with lovastatin was associated with a significant reduction of fibrinogen levels and platelet aggregation induced by ADP in type-IIa hypercholesterolemic patients. Lovastatin 25-35 fibrinogen beta chain Homo sapiens 83-93 1412144-1 1992 HMG-CoA reductase inhibitors: lovastatin and simvastatin]. Lovastatin 30-40 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-17 1412144-2 1992 Lovastatin and simvastatin are the first licensed compounds of a potent new class of lipid lowering drugs whose mechanism of action is to inhibit HMG-CoA reductase, a rate-limiting enzyme in the cholesterol biosynthetic pathway in the liver. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 146-163 1730692-5 1992 Moreover, a serine substitution for Cys558 resulted in a single RK species whose migration on sodium dodecyl sulfate-polyacrylamide gels was identical to that of RK from cells treated with mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and, thus, of isoprenoid biosynthesis. Lovastatin 189-198 G protein-coupled receptor kinase 1 Bos taurus 64-66 1730692-5 1992 Moreover, a serine substitution for Cys558 resulted in a single RK species whose migration on sodium dodecyl sulfate-polyacrylamide gels was identical to that of RK from cells treated with mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and, thus, of isoprenoid biosynthesis. Lovastatin 189-198 G protein-coupled receptor kinase 1 Bos taurus 162-164 1311272-0 1992 Transcriptional derepression of the murine Cyp1a-1 gene by mevinolin. Lovastatin 59-68 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 43-50 1729592-0 1992 Lipopolysaccharide-induced NF-kappa B activation in mouse 70Z/3 pre-B lymphocytes is inhibited by mevinolin and 5"-methylthioadenosine: roles of protein isoprenylation and carboxyl methylation reactions. Lovastatin 98-107 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 27-37 1729592-3 1992 We also find that NF-kappa B and kappa gene activation in LPS-treated 70Z/3 cells is blocked by mevinolin, an inhibitor that prevents protein isoprenylation. Lovastatin 96-105 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 18-28 1314986-4 1992 Lovastatin was effective in reducing serum cholesterol, LDL-C and apolipoprotein B in the remaining 12 patients. Lovastatin 0-10 component of oligomeric golgi complex 2 Homo sapiens 56-82 1302351-6 1992 Significant relationship between apolipoprotein B concentration and dosage of lovastatin was found. Lovastatin 78-88 apolipoprotein B Homo sapiens 33-49 1546367-0 1992 Regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase synthesis in Syrian hamster C100 cells by mevinolin, 25-hydroxycholesterol, and mevalonate: the role of posttranscriptional control. Lovastatin 104-113 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 14-61 1546367-2 1992 In this study the effects of the oxysterol 25-hydroxycholesterol and mevalonate on the mRNA level and rate of synthesis for HMG-CoA reductase were evaluated in C100 cells treated with mevinolin, a competitive inhibitor of HMG-CoA reductase. Lovastatin 184-193 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 124-141 1546367-2 1992 In this study the effects of the oxysterol 25-hydroxycholesterol and mevalonate on the mRNA level and rate of synthesis for HMG-CoA reductase were evaluated in C100 cells treated with mevinolin, a competitive inhibitor of HMG-CoA reductase. Lovastatin 184-193 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 222-239 1546367-6 1992 Degradation of HMG-CoA reductase was rapid in the presence (t1/2 = 1.34 h) or absence (t1/2 = 1.17 h) of mevinolin and was not changed significantly by adding either 25-hydroxycholesterol, alone (t1/2 = 1.30 h) or both 25-hydroxycholesterol and mevalonate (t1/2 = 1.30 h) to mevinolin-treated cells. Lovastatin 105-114 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 15-32 1546367-6 1992 Degradation of HMG-CoA reductase was rapid in the presence (t1/2 = 1.34 h) or absence (t1/2 = 1.17 h) of mevinolin and was not changed significantly by adding either 25-hydroxycholesterol, alone (t1/2 = 1.30 h) or both 25-hydroxycholesterol and mevalonate (t1/2 = 1.30 h) to mevinolin-treated cells. Lovastatin 275-284 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 15-32 1546367-7 1992 This study demonstrates that mevalonate and 25-hydroxycholesterol act synergistically in the presence of mevinolin to achieve a greater degree of suppression in the rate of HMG-CoA reductase synthesis than can be accounted for by their individual effects on HMG-CoA reductase mRNA. Lovastatin 105-114 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 173-190 1546367-7 1992 This study demonstrates that mevalonate and 25-hydroxycholesterol act synergistically in the presence of mevinolin to achieve a greater degree of suppression in the rate of HMG-CoA reductase synthesis than can be accounted for by their individual effects on HMG-CoA reductase mRNA. Lovastatin 105-114 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 258-275 1395911-5 1992 The results were as follows: Lovastatin reduced significantly the mean serum level of total cholesterol (TC) by 31.5% (P less than 0.001), LDL-C by 39.8% (P less than 0.001), Apo-B by 27.3% (P less than 0.002), and the ratio TC/HDL-C by 35.9% (P less than 0.01). Lovastatin 29-39 apolipoprotein B Homo sapiens 175-180 1395911-11 1992 We are, therefore, of the opinion that Lovastatin is an effective agent for lowering the serum level of TC, LDL-C and Apo-B. Lovastatin 39-49 apolipoprotein B Homo sapiens 118-123 1961130-1 1991 Vigorous physical activity and lovastatin (Mevacor) a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, have both been independently associated with elevated creatine kinase (CK) levels. Lovastatin 31-41 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 54-111 1961130-1 1991 Vigorous physical activity and lovastatin (Mevacor) a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, have both been independently associated with elevated creatine kinase (CK) levels. Lovastatin 43-50 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 54-111 1953779-1 1991 Human fibroblasts treated with the antihypercholesterolaemic drug, lovastatin, displayed a diminished signaling response to epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Lovastatin 67-77 epidermal growth factor Homo sapiens 124-147 1953779-1 1991 Human fibroblasts treated with the antihypercholesterolaemic drug, lovastatin, displayed a diminished signaling response to epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Lovastatin 67-77 epidermal growth factor Homo sapiens 149-152 1953779-1 1991 Human fibroblasts treated with the antihypercholesterolaemic drug, lovastatin, displayed a diminished signaling response to epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Lovastatin 67-77 insulin Homo sapiens 155-162 1953779-1 1991 Human fibroblasts treated with the antihypercholesterolaemic drug, lovastatin, displayed a diminished signaling response to epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Lovastatin 67-77 insulin like growth factor 1 Homo sapiens 167-195 1953779-1 1991 Human fibroblasts treated with the antihypercholesterolaemic drug, lovastatin, displayed a diminished signaling response to epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Lovastatin 67-77 insulin like growth factor 1 Homo sapiens 197-202 1940775-0 1991 Effect of apolipoprotein E polymorphism and XbaI polymorphism of apolipoprotein B on response to lovastatin treatment in familial and non-familial hypercholesterolaemia. Lovastatin 97-107 apolipoprotein B Homo sapiens 65-81 1666129-4 1991 Inhibition of isoprenoid synthesis by Lovastatin blocks the binding of newly synthesized CNP to cell membranes; binding is restored upon addition of mevalonate to the culture medium. Lovastatin 38-48 2',3'-cyclic nucleotide 3' phosphodiesterase Homo sapiens 89-92 1740442-8 1992 When cellular isoprenoid synthesis is blocked by treatment of cells with lovastatin, rab proteins that are normally localized in membranes of the endoplasmic reticulum, Golgi apparatus, and endosomes accumulate in the cytosol. Lovastatin 73-83 ArfGAP with FG repeats 1 Homo sapiens 85-88 1311272-3 1992 We show here that in the absence of TCDD, mevinolin markedly increases Cyp1a-1 transcription, CYP1A1 mRNA and protein levels and enzyme activity, and NMO1 mRNA concentrations. Lovastatin 42-51 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 71-78 1311272-3 1992 We show here that in the absence of TCDD, mevinolin markedly increases Cyp1a-1 transcription, CYP1A1 mRNA and protein levels and enzyme activity, and NMO1 mRNA concentrations. Lovastatin 42-51 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 94-100 1311272-3 1992 We show here that in the absence of TCDD, mevinolin markedly increases Cyp1a-1 transcription, CYP1A1 mRNA and protein levels and enzyme activity, and NMO1 mRNA concentrations. Lovastatin 42-51 NAD(P)H dehydrogenase, quinone 1 Mus musculus 150-154 1311272-6 1992 Mevinolin-induced Cyp1a-1 gene activation: (1) occurs independently of the lipid content of the growth medium, (2) is not suppressed by adding 25-hydroxycholesterol, which blocks MHG-CoA reductase activity, and (3) requires a functional Ah receptor and unimpaired nuclear translocation of the receptor. Lovastatin 0-9 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 18-25 1311272-6 1992 Mevinolin-induced Cyp1a-1 gene activation: (1) occurs independently of the lipid content of the growth medium, (2) is not suppressed by adding 25-hydroxycholesterol, which blocks MHG-CoA reductase activity, and (3) requires a functional Ah receptor and unimpaired nuclear translocation of the receptor. Lovastatin 0-9 aryl-hydrocarbon receptor Mus musculus 237-248 1311272-7 1992 It is possible that an unknown metabolite (or metabolites) of mevinolin activates Cyp1a-1 expression and that high concentrations of mevalonate act via the same mechanism. Lovastatin 62-71 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 82-89 1311272-8 1992 Using chimaeric plasmids that contain different lengths of Cyp1a-1 5" flanking regions fused to the bacterial neomycin (neo) gene, we find that the mevinolin effect on Cyp1a-1 induction requires the 5" flanking sequences between -1647 and -824, which are also needed for TCDD induction. Lovastatin 148-157 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 59-66 1311272-8 1992 Using chimaeric plasmids that contain different lengths of Cyp1a-1 5" flanking regions fused to the bacterial neomycin (neo) gene, we find that the mevinolin effect on Cyp1a-1 induction requires the 5" flanking sequences between -1647 and -824, which are also needed for TCDD induction. Lovastatin 148-157 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 168-175 1311272-10 1992 Gel mobility shift assays revealed that Cyp1a-1 activation caused by mevinolin does not involve the ligand-dependent formation of a functional Ah receptor-dependent DNA-binding complex, but instead appears to be correlated with release of a putative repressor from its cognate DNA site. Lovastatin 69-78 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 40-47 1311272-12 1992 We propose that Cyp1a-1 transcriptional activation can result not only from induction by polycyclic aromatic compounds but also from derepression by mevinolin, independent of HMG-CoA reductase inhibition. Lovastatin 149-158 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 16-23 1919427-6 1991 These results strongly suggest that an increase in LDL-receptor activity is the major mechanism whereby LDL levels are lowered during lovastatin therapy. Lovastatin 134-144 low density lipoprotein receptor Homo sapiens 51-63 1911702-1 1991 Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and a potent hypocholesterolemic agent, induces a hyperplastic thickening of the rat forestomach mucosa after oral administration of its active form, a hydroxyacid. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 28-85 1800703-0 1991 Relative lipophilicities, solubilities, and structure-pharmacological considerations of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors pravastatin, lovastatin, mevastatin, and simvastatin. Lovastatin 170-180 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 88-145 1648647-1 1991 We examined the effect of a 16 week therapy with the HMG CoA reductase inhibitor lovastatin in 29 patients (mean age 43 years) with primary hypercholesterolemia. Lovastatin 81-91 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 53-70 1712015-5 1991 The importance of HMG-CoA reductase induction and mevalonate production in cell cycle progression was demonstrated by the observation that either 25-hydroxycholesterol, which inhibits this induction, or lovastatin, a competitive inhibitor of HMG-CoA reductase, inhibited anti-CD3-induced T cell mitogenesis in a dose-dependent manner. Lovastatin 203-213 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 18-35 1712015-5 1991 The importance of HMG-CoA reductase induction and mevalonate production in cell cycle progression was demonstrated by the observation that either 25-hydroxycholesterol, which inhibits this induction, or lovastatin, a competitive inhibitor of HMG-CoA reductase, inhibited anti-CD3-induced T cell mitogenesis in a dose-dependent manner. Lovastatin 203-213 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 242-259 2066708-0 1991 Lovastatin therapy in heterozygous familial hypercholesterolaemic patients: effect on blood rheology and fibrinogen levels. Lovastatin 0-10 fibrinogen beta chain Homo sapiens 105-115 1832610-6 1991 The first includes inactive lactone prodrugs, as Lovastatin and Simvastatin, that are enzymatically hydrolyzed to the corresponding ring-opened active forms in the liver, where the HMGCoA reductase inhibitors must chiefly reduce cholesterol synthesis. Lovastatin 49-59 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 181-197 1907839-0 1991 Pharmacokinetic interaction between propranolol and the HMG-CoA reductase inhibitors pravastatin and lovastatin. Lovastatin 101-111 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 56-73 1880215-0 1991 Lovastatin therapy in hypercholesterolemia: effect on fibrinogen, hemorrheologic parameters, platelet activity, and red blood cell morphology. Lovastatin 0-10 fibrinogen beta chain Homo sapiens 54-64 1827487-2 1991 We report here that 20 h incubation of RBL-2H3 cells with 10 microM lovastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMG CoA reductase), inhibits both the secretory and morphologic responses to IgE receptor cross-linking. Lovastatin 68-78 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 146-163 1827487-5 1991 Receptor-mediated Ca2+ mobilization, secretion, and ruffling are all restored by 0.5- to 4-h incubation of lovastatin-treated cells with mevalonic acid, the product of HMG CoA reductase and the first committed intermediate of the isoprenoid biosynthetic pathway. Lovastatin 107-117 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 168-185 2043425-0 1991 Lovastatin, a cholesterol biosynthesis inhibitor, inhibits the growth of human H-ras oncogene transformed cells in nude mice. Lovastatin 0-10 HRas proto-oncogene, GTPase Homo sapiens 79-84 2043425-4 1991 Immunoprecipitation studies with transformed EJ cells showed that lovastatin (1-100 microM) inhibited p21ras membrane association in a concentration-dependent manner and that a 10 microM concentration reduced the amount of p21ras bound to the membrane by 50%. Lovastatin 66-76 Harvey rat sarcoma virus oncogene Mus musculus 102-108 2043425-4 1991 Immunoprecipitation studies with transformed EJ cells showed that lovastatin (1-100 microM) inhibited p21ras membrane association in a concentration-dependent manner and that a 10 microM concentration reduced the amount of p21ras bound to the membrane by 50%. Lovastatin 66-76 Harvey rat sarcoma virus oncogene Mus musculus 223-229 2043425-5 1991 Lovastatin also inhibited EJ cell growth in a concentration range that closely paralleled that required for inhibition of p21ras membrane association. Lovastatin 0-10 Harvey rat sarcoma virus oncogene Mus musculus 122-128 2043425-7 1991 Western blotting studies showed that lovastatin (50 mg/kg) was also able to inhibit p21ras membrane association in EJ tumors implanted s.c. in nude mice. Lovastatin 37-47 Harvey rat sarcoma virus oncogene Mus musculus 84-90 2043425-8 1991 These results demonstrate that lovastatin, an inhibitor of cholesterol biosynthesis, inhibited in vivo tumor growth of H-ras oncogene transformed cells. Lovastatin 31-41 Harvey rat sarcoma virus oncogene Mus musculus 119-124 2043425-9 1991 The results also suggest that inhibition of p21ras membrane association, an essential step in ras oncogene neoplastic transformation, is one mechanism by which lovastatin may express its antitumor activity. Lovastatin 160-170 Harvey rat sarcoma virus oncogene Mus musculus 44-50 2018137-1 1991 Lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, is effective in the treatment of hypercholesterolemic patients and is currently being evaluated as a potential agent for dissolving gallstones. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-96 2051734-4 1991 Lovastatin (1st month 20 mg; 2nd and 3rd months 40 mg day-1) and simvastatin (1st month 10 mg, 2nd month 20 mg and 3rd month 40 mg day-1) reduced total serum cholesterol from 280.3 +/- 9.4 to 213.0 +/- 6.7 (-24%) and 295.0 +/- 12.2 to 202.3 +/- 8.9 mg/dl (-31.4%), LDL cholesterol from 161.9 +/- 10.7 to 112.1 +/- 7.9 (-30.8%) and 181.8 +/- 14.7 to 107.4 +/- 8.1 mg/dl (-40.9%), as well as apolipoprotein B (apo B) from 116.0 +/- 6.6 to 83.3 +/- 3.7 (-28.2%) and 134.4 +/- 8.2 to 84.1 +/- 5.3 mg/dl (-37.4%), respectively. Lovastatin 0-10 apolipoprotein B Homo sapiens 390-406 2246324-0 1990 Reversal of lovastatin-mediated inhibition of natural killer cell cytotoxicity by interleukin 2. Lovastatin 12-22 interleukin 2 Homo sapiens 82-95 1899896-1 1991 To determine the cost-effectiveness of HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors (such as lovastatin) for the primary and secondary prevention of coronary heart disease, we used the Coronary Heart Disease Policy Model, a computer-stimulated model that estimates the risk factor-specific annual incidence of coronary heart disease and the risk of recurrent coronary events in persons with prevalent coronary heart disease. Lovastatin 117-127 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 48-96 2062789-6 1991 From these data we conclude that in bypassed rabbits lovastatin lowers total and LDL cholesterol mainly by reducing apolipoprotein B production rate. Lovastatin 53-63 apolipoprotein B Oryctolagus cuniculus 116-132 16296004-7 1991 Deprivation of isoprenyl precursors by the addition of lovastatin, a drug that blocks the synthesis of mevalonate, also abolished the ability of activated K-ras(B) to induce meiosis, although this inhibition could be overcome by the addition of exogenous mevalonate. Lovastatin 55-65 kirsten rat sarcoma viral oncogene homolog L homeolog Xenopus laevis 155-163 2044637-1 1991 Lovastatin and simvastatin are potent competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 64-111 1986017-7 1991 When the twins were treated with lovastatin, however, FCRs for LDL increased significantly, suggesting enhancement of LDL receptor activity. Lovastatin 33-43 low density lipoprotein receptor Homo sapiens 118-130 2176219-3 1990 Mevinolin, a 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitor, was then added at a concentration (37 microM) which inhibited cholesterol biosynthesis by greater than 85% and decreased total cell cholesterol from 36.1 to 27.4 micrograms/ml of cell protein. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 13-63 2176219-4 1990 Mevinolin treatment caused a 4.9 +/- 0.8-fold increase in the amount of H-TGL activity secreted into the medium, a 1.8 +/- 0.4-fold rise in H-TGL-specific mRNA, and a concurrent 14-fold increase in HMG-CoA reductase mRNA. Lovastatin 0-9 lipase C, hepatic type Homo sapiens 72-77 2176219-4 1990 Mevinolin treatment caused a 4.9 +/- 0.8-fold increase in the amount of H-TGL activity secreted into the medium, a 1.8 +/- 0.4-fold rise in H-TGL-specific mRNA, and a concurrent 14-fold increase in HMG-CoA reductase mRNA. Lovastatin 0-9 lipase C, hepatic type Homo sapiens 140-145 2176219-5 1990 Addition of 1 mM mevalonic acid to normal or mevinolin-treated cells raised the cellular cholesterol content and decreased the amount of secreted H-TGL activity to levels below control values. Lovastatin 45-54 lipase C, hepatic type Homo sapiens 146-151 2176219-6 1990 Mevalonic acid also prevented mevinolin-induction of H-TGL and HMG-CoA reductase mRNA, suggesting a common regulatory step for H-TGL and HMG-CoA reductase. Lovastatin 30-39 lipase C, hepatic type Homo sapiens 53-58 2176219-6 1990 Mevalonic acid also prevented mevinolin-induction of H-TGL and HMG-CoA reductase mRNA, suggesting a common regulatory step for H-TGL and HMG-CoA reductase. Lovastatin 30-39 lipase C, hepatic type Homo sapiens 127-132 2176219-7 1990 Exposure of cells to mevinolin and 25-hydroxycholesterol together resulted in a marked repression of HMG-CoA reductase mRNA levels, whereas these conditions further enhanced the secretion of H-TGL activity and the expression of H-TGL mRNA. Lovastatin 21-30 lipase C, hepatic type Homo sapiens 191-196 2176219-7 1990 Exposure of cells to mevinolin and 25-hydroxycholesterol together resulted in a marked repression of HMG-CoA reductase mRNA levels, whereas these conditions further enhanced the secretion of H-TGL activity and the expression of H-TGL mRNA. Lovastatin 21-30 lipase C, hepatic type Homo sapiens 228-233 2268271-0 1990 Effect of lovastatin on acyl-CoA: cholesterol O-acyltransferase (ACAT) activity and the basolateral-membrane secretion of newly synthesized lipids by CaCo-2 cells. Lovastatin 10-20 sterol O-acyltransferase 1 Homo sapiens 65-69 2253372-2 1990 Lovastatin, a hypocholesterolemic agent, decreases endogenous cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.88). Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 98-145 2124543-4 1990 The membrane association of p21rho and its biological activity were inhibited by lovastatin, an inhibitor of the 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 81-91 3-hydroxy-3-methylglutaryl-CoA reductase L homeolog Xenopus laevis 113-160 2176080-9 1990 A similar induction of HMG-CoA reductase and LDL receptor was also found after preincubations of cells with 0.3 microM-mevinolin, suggesting that the underlying mechanism for this induction is identical for both drugs. Lovastatin 119-128 low density lipoprotein receptor Homo sapiens 45-57 2246270-8 1990 Our results indicate that the degree of inhibition of p21ras and prelamin A maturation by lovastatin is identical. Lovastatin 90-100 HRas proto-oncogene, GTPase Homo sapiens 54-60 2241455-4 1990 Therefore, prothrombin time should be monitored diligently when warfarin is prescribed to patients receiving lovastatin. Lovastatin 109-119 coagulation factor II, thrombin Homo sapiens 11-22 2246324-2 1990 Earlier, we reported that treatment of NK cells with an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase such as compactin or lovastatin significantly abrogates the in vitro killing of a susceptible human erythroleukemic cell line and that this inhibition can be completely reversed by 2 hr of exposure to mevalonate (J. Lovastatin 148-158 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 69-126 2246324-5 1990 We report here that 24 hr of treatment with IL-2 also reverses lovastatin inhibition of NK cell function. Lovastatin 63-73 interleukin 2 Homo sapiens 44-48 2246324-6 1990 In addition to natural cytotoxicity, IL-2 also restores chemotactic and antibody dependent cellular cytotoxicity functions to lovastatin-treated cells. Lovastatin 126-136 interleukin 2 Homo sapiens 37-41 2246324-8 1990 Although IL-2 was able to reverse the lovastatin-mediated inhibition of every cell function we examined, it had no effect on the inhibition of cholesterol biosynthesis as measured by [3H]acetate incorporation into non-saponifiable lipids, nor did it stimulate HMG CoA reductase activity. Lovastatin 38-48 interleukin 2 Homo sapiens 9-13 2086705-5 1990 It was unlikely that the increase in LDL receptor mRNA levels observed in mitogen-stimulated cells related merely to sterol deprivation since suppression of endogenous cholesterol synthesis with lovastatin increased LDL receptor mRNA only modestly. Lovastatin 195-205 low density lipoprotein receptor Homo sapiens 216-228 2243142-4 1990 Here we show that topical lovastatin, a competitive inhibitor of HMG CoA reductase, inhibits cholesterol synthesis. Lovastatin 26-36 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 65-82 2243142-6 1990 When lovastatin animals are simultaneously treated topically with either mevalonate, the immediate product of HMG CoA reductase, or cholesterol, the final end product of the pathway, the recovery of the barrier is normalized. Lovastatin 5-15 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 110-127 2086706-3 1990 Three percent cholestyramine feeding increased the hepatic squalene epoxidase activity by 2.5-fold, and the administration of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, increased its activity by 2.1-fold. Lovastatin 126-136 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 154-211 2247468-2 1990 The mechanism of action of lovastatin is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. Lovastatin 27-37 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 55-102 2211719-6 1990 These results contrast with those observed when sterol biosynthesis was blocked with lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 85-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 113-160 2278880-3 1990 Lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, may prevent the farnesylation of de novo synthesized ras p21. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 145-148 2225707-4 1990 Lovastatin levels for a 4-hour period (measured as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitory activity) were similar to those measured previously in nondiabetic patients. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 51-98 2079605-3 1990 Lovastatin caused reduction of the apparent number of 125I-labeled HDL3 binding sites without affecting the binding affinity. Lovastatin 0-10 HDL3 Homo sapiens 67-71 2079605-5 1990 Mevalonic acid reversed the effect of lovastatin on 125I-labeled HDL3 binding. Lovastatin 38-48 HDL3 Homo sapiens 65-69 2079605-6 1990 Lovastatin blocked up-regulation of the HDL receptor in response to loading of cells with nonlipoprotein cholesterol and modified cholesterol-induced changes of 125I-labeled HDL3 degradation. Lovastatin 0-10 HDL3 Homo sapiens 174-178 2248616-8 1990 Despite unremitting hyperglycemia, treatment with lovastatin resulted in pronounced decreases in plasma cholesterol, HDL1 and apoE to concentrations below those observed in nondiabetic animals. Lovastatin 50-60 apolipoprotein E Canis lupus familiaris 126-130 2206030-1 1990 This study reports the results of a 6-month, open-label multicenter study of the efficacy and tolerability of lovastatin, a 3-hydroxy-3-methylglutaryl co-enzyme A (HMG CoA) reductase inhibitor, in the management of nonfamilial primary hypercholesterolemia. Lovastatin 110-120 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 124-182 2206035-4 1990 These drugs, including lovastatin and simvastatin, competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme of intracellular cholesterol synthesis. Lovastatin 23-33 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 73-120 2279522-1 1990 We examined the effects of a prolonged treatment with lovastatin, a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on the morphology and function of rat Leydig cells. Lovastatin 54-64 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 100-157 2394831-9 1990 Thus, hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibition by lovastatin at the therapeutic dose used here did not change the steady-state rate of whole-body cholesterol synthesis. Lovastatin 73-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 6-58 2394831-12 1990 In the new steady state that exists during long-term lovastatin therapy, along with increased expression of the genes for HMG-CoA reductase and the LDL receptor, the body compensates for the effects of the drug so that cholesterol production rate and tissue pool sizes are not changed from pretreatment values. Lovastatin 53-63 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 122-139 2394831-12 1990 In the new steady state that exists during long-term lovastatin therapy, along with increased expression of the genes for HMG-CoA reductase and the LDL receptor, the body compensates for the effects of the drug so that cholesterol production rate and tissue pool sizes are not changed from pretreatment values. Lovastatin 53-63 low density lipoprotein receptor Homo sapiens 148-160 2390136-3 1990 Three months of treatment with lovastatin resulted in a marked decrease in red cell aggregation and plasma viscosity, parallel to a fall in cholesterol (the following pretreatment values were monitored after a standard lipid-lowering diet; RCA-S: 7.59 +/- 1 vs. 6.65 +/- 0.9, RCA-L: 9.34 +/- 1 vs. 8.15 +/- 1 arbitrary units; PV: 1.74 vs. 1.65 mPa/s; Chol: 309.8 +/- 41 vs. 217.1 +/- 30 mg/dl; all P less than 0.01); fibrinogen however, remained unchanged throughout the treatment period (346.4 +/- 73.3 vs. 330.5 +/- 70.2 mg/dl, n.s.). Lovastatin 31-41 fibrinogen beta chain Homo sapiens 417-427 2225417-2 1990 Lovastatin, which inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase, in doses of 40-80 mg/day effectively lowers cholesterol in the general cardiac population but has been associated with rhabdomyolysis in cardiac transplant recipients. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 27-74 2115642-4 1990 Our results show that pretreatment of quiescent human fibroblasts with mevinolin, an HMG CoA reductase inhibitor, partially suppresses fos and myc mRNA accumulation in response to serum stimulation. Lovastatin 71-80 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-138 2115642-4 1990 Our results show that pretreatment of quiescent human fibroblasts with mevinolin, an HMG CoA reductase inhibitor, partially suppresses fos and myc mRNA accumulation in response to serum stimulation. Lovastatin 71-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 143-146 2360916-0 1990 Effects of lovastatin therapy on LDL receptor activity in circulating monocytes and on structure and composition of plasma lipoproteins. Lovastatin 11-21 low density lipoprotein receptor Homo sapiens 33-45 2360916-1 1990 The effect of lovastatin therapy on LDL-receptor activity in fresh monocytes and on the structure and composition of lipoproteins was determined in 9 patients with familial hypercholesterolemia (FH) and 8 patients with non-familial hypercholesterolemia (NFH). Lovastatin 14-24 low density lipoprotein receptor Homo sapiens 36-48 2360916-7 1990 The investigations thus demonstrated that lovastatin therapy is associated with a measurable and significant increase of LDL-receptor activity in circulating monocytes that may contribute to the lipid lowering action of the drug. Lovastatin 42-52 low density lipoprotein receptor Homo sapiens 121-133 2361135-1 1990 The mechanism of slow binding inhibition of 3-hydroxy-3-methylglutaryl- coenzyme A reductase by lovastatin, fluindostatin, and related compounds was studied. Lovastatin 96-106 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 44-92 2335559-4 1990 Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by mevinolin (lovastatin) specifically depletes endogenous isoprenoid pools and inhibits the conversion of prelamin A to lamin A. Prelamin A processing is also blocked by mevalonate starvation of Mev-1, a CHO cell line auxotrophic for mevalonate. Lovastatin 65-74 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-61 2335559-4 1990 Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by mevinolin (lovastatin) specifically depletes endogenous isoprenoid pools and inhibits the conversion of prelamin A to lamin A. Prelamin A processing is also blocked by mevalonate starvation of Mev-1, a CHO cell line auxotrophic for mevalonate. Lovastatin 76-86 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 14-61 2325654-2 1990 In testis, an FPP synthetase-related RNA was detected that was larger than the liver FPP synthetase mRNA and was present at very high levels comparable with liver FPP synthetase RNA levels obtained from rats fed diets supplemented with cholestyramine and mevinolin. Lovastatin 255-264 farnesyl diphosphate synthase Rattus norvegicus 14-28 2153681-6 1990 The levels of mevalonate kinase protein and enzyme activity were determined in the livers of rats treated with either cholesterol-lowering agents (cholestyramine, pravastatin, and lovastatin) or with dietary modifications. Lovastatin 180-190 mevalonate kinase Rattus norvegicus 14-31 1971574-8 1990 The major metabolites excreted in bile of rats treated with the hydroxy acid form of the drug were identified as the 3"-hydroxy analog and a taurine conjugate of a beta-oxidation product of lovastatin. Lovastatin 190-200 amyloid beta precursor protein Rattus norvegicus 162-168 1971576-2 1990 In vitro metabolism by rat and mouse liver microsomes and involvement of cytochrome P-450 in dehydrogenation of lovastatin. Lovastatin 112-122 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 73-89 1971576-9 1990 The conversion of lovastatin to the novel 6"-exomethylene metabolite was catalyzed by cytochrome P-450 since it required microsomes and NADPH and was inhibited by SKF-525A, metyrapone, and 2,4,-dichloro-6-phenylphenoxyethylamine (DPEA). Lovastatin 18-28 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 86-102 2187311-8 1990 A reduction of the cholesterol synthesis by the HMG CoA reductase inhibitor Lovastatin leads to a disturbed permeability barrier and epidermal hyperplasia. Lovastatin 76-86 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 48-65 2310768-4 1990 PHA enhanced 125I-labelled LDL receptor-mediated binding by lymphocytes cultured in lipoprotein-deficient medium over a 4 day period and mevinolin augmented the effect. Lovastatin 137-146 low density lipoprotein receptor Homo sapiens 27-39 2153681-7 1990 Diets containing cholestyramine alone or cholestyramine and either pravastatin or lovastatin increased mevalonate kinase activity 3-6-fold. Lovastatin 82-92 mevalonate kinase Rattus norvegicus 103-120 17016224-3 2006 Lovastatin enhances BMP2 gene expression in rodents, reverses the effects of glucocorticoids on bone, and prevents glucocorticoid-induced osteonecrosis in chickens and humans. Lovastatin 0-10 bone morphogenetic protein 2 Gallus gallus 20-24 2299987-0 1990 The influence of apolipoprotein E phenotype on the response to lovastatin therapy in patients with heterozygous familial hypercholesterolemia. Lovastatin 63-73 apolipoprotein E Homo sapiens 17-33 2299987-0 1990 The influence of apolipoprotein E phenotype on the response to lovastatin therapy in patients with heterozygous familial hypercholesterolemia. Lovastatin 63-73 low density lipoprotein receptor Homo sapiens 112-141 2111917-0 1990 HMG CoA reductase inhibitors as lipid-lowering agents: five years experience with lovastatin and an appraisal of simvastatin and pravastatin. Lovastatin 82-92 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-17 2294737-5 1990 Lovastatin reduced total cholesterol by 27% from 8.6 +/- 0.6 mmol/L (331 +/- 24 mg/dL) to 6.3 +/- 0.4 mmol/L (242 +/- 17 mg/dL) (P less than 0.01), low-density lipoprotein cholesterol by 27%, from 5.8 +/- 0.5 mmol/L (223 +/- 20 mg/dL) to 4.2 +/- 0.6 mmol/L (163 +/- 22 mg/dL) (P less than 0.01), and apolipoprotein B by 29%, from 153 +/- 12 mg/dL to 109 +/- 8 mg/dL to 109 +/- 8 mg/dL P less than 0.01). Lovastatin 0-10 apolipoprotein B Homo sapiens 300-316 2073669-8 1990 Thus, the lowering of cholesterol by lovastatin, but not by bezafibrate, can be attributed to inhibition of HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase. Lovastatin 37-47 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 117-165 2289408-6 1990 Hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors (such as lovastatin) and cation-exchange resins (e.g. cholestyramine) reduce LDL levels by stimulating the hepatic synthesis of apolipoprotein (apo) B,E receptors. Lovastatin 73-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-52 25395200-2 2015 We assessed the effect of tamoxifen, raloxifene and toremifene and their combinations with lovastatin on LDL receptor activity in lymphocytes from normolipidaemic and familial hypercholesterolaemic (FH) subjects, and human HepG2 hepatocytes and MOLT-4 lymphoblasts. Lovastatin 91-101 low density lipoprotein receptor Homo sapiens 105-117 25395200-11 2015 There is a mild enhancement between SERMs and lovastatin of lymphocyte LDLR activity, the potentiation being greater in HepG2 and MOLT-4 cells. Lovastatin 46-56 low density lipoprotein receptor Homo sapiens 71-75 19615773-7 2009 RESULTS: Lovastatin attenuated IR-induced activation of NF-kappaB, mRNA expression of cell adhesion molecules and mRNA expression of pro-inflammatory and pro-fibrotic marker genes (i.e. TNFalpha, IL-6, TGFbeta, CTGF, and type I and type III collagen) in a tissue- and time-dependent manner. Lovastatin 9-19 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 56-65 19615773-7 2009 RESULTS: Lovastatin attenuated IR-induced activation of NF-kappaB, mRNA expression of cell adhesion molecules and mRNA expression of pro-inflammatory and pro-fibrotic marker genes (i.e. TNFalpha, IL-6, TGFbeta, CTGF, and type I and type III collagen) in a tissue- and time-dependent manner. Lovastatin 9-19 tumor necrosis factor Mus musculus 186-194 19615773-7 2009 RESULTS: Lovastatin attenuated IR-induced activation of NF-kappaB, mRNA expression of cell adhesion molecules and mRNA expression of pro-inflammatory and pro-fibrotic marker genes (i.e. TNFalpha, IL-6, TGFbeta, CTGF, and type I and type III collagen) in a tissue- and time-dependent manner. Lovastatin 9-19 interleukin 6 Mus musculus 196-200 19615773-7 2009 RESULTS: Lovastatin attenuated IR-induced activation of NF-kappaB, mRNA expression of cell adhesion molecules and mRNA expression of pro-inflammatory and pro-fibrotic marker genes (i.e. TNFalpha, IL-6, TGFbeta, CTGF, and type I and type III collagen) in a tissue- and time-dependent manner. Lovastatin 9-19 cellular communication network factor 2 Mus musculus 211-215 2351867-0 1990 Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production. Lovastatin 0-10 apolipoprotein B Homo sapiens 51-55 2351867-0 1990 Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production. Lovastatin 0-10 apolipoprotein B Homo sapiens 134-138 2351867-0 1990 Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production. Lovastatin 0-10 apolipoprotein B Homo sapiens 134-138 2351867-2 1990 Lovastatin therapy significantly reduced plasma levels of LDL cholesterol (142 vs 93 mg/dl, P less than 0.0005) and apoB (1328 vs 797 micrograms/ml, P less than 0.001). Lovastatin 0-10 apolipoprotein B Homo sapiens 116-120 2351867-5 1990 Compared to baseline, treatment with lovastatin was associated with a significant reduction in the total rate of entry of apoB-containing lipoproteins into plasma in all seven CHL subjects (40.7 vs. 25.7 mg/kg.day, P less than 0.003). Lovastatin 37-47 apolipoprotein B Homo sapiens 122-126 2351867-9 1990 In three patients with familial hypercholesterolemia who were studied for comparison, lovastatin treatment increased LDL apoB FCR but did not consistently alter LDL apoB PR. Lovastatin 86-96 apolipoprotein B Homo sapiens 121-125 2351867-10 1990 We conclude that lovastatin lowers LDL cholesterol and apoB concentrations in CHL patients by reducing the rate of entry of apoB-containing lipoproteins into plasma, either as VLDL or as directly secreted LDL. Lovastatin 17-27 apolipoprotein B Homo sapiens 55-59 2351867-10 1990 We conclude that lovastatin lowers LDL cholesterol and apoB concentrations in CHL patients by reducing the rate of entry of apoB-containing lipoproteins into plasma, either as VLDL or as directly secreted LDL. Lovastatin 17-27 apolipoprotein B Homo sapiens 124-128 33820798-5 2021 The SHP2 agonist lovastatin was able to enhance SHP2 activity and promote STING pathway activation. Lovastatin 17-27 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 4-8 33820798-5 2021 The SHP2 agonist lovastatin was able to enhance SHP2 activity and promote STING pathway activation. Lovastatin 17-27 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 48-52 33820798-7 2021 These findings suggest that SHP2 exacerbates STING pathway activation by restricting PARP1-mediated DNA repair in tumor cells, providing a basis for the combined use of lovastatin and chemotherapy in the treatment of colon cancer. Lovastatin 169-179 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 28-32 33820798-7 2021 These findings suggest that SHP2 exacerbates STING pathway activation by restricting PARP1-mediated DNA repair in tumor cells, providing a basis for the combined use of lovastatin and chemotherapy in the treatment of colon cancer. Lovastatin 169-179 poly(ADP-ribose) polymerase 1 Homo sapiens 85-90 34911669-7 2022 Importantly, domain I of nsp4 inhibited Sendai virus-induced interferon beta production, and this inhibitory effect was eliminated by Lovastatin, an HMGCR inhibitor, indicating that the upregulation of cellular cholesterol by nsp4 is a strategy used by PRRSV to suppress the antiviral innate immunity of its host. Lovastatin 134-144 interferon beta 1 Homo sapiens 61-76 34911669-7 2022 Importantly, domain I of nsp4 inhibited Sendai virus-induced interferon beta production, and this inhibitory effect was eliminated by Lovastatin, an HMGCR inhibitor, indicating that the upregulation of cellular cholesterol by nsp4 is a strategy used by PRRSV to suppress the antiviral innate immunity of its host. Lovastatin 134-144 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 149-154 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 3-hydroxy-3-methylglutaryl-CoA reductase a Danio rerio 187-193 34896780-0 2022 Lovastatin enhances chemosensitivity of paclitaxel-resistant prostate cancer cells through inhibition of CYP2C8. Lovastatin 0-10 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 105-111 34896780-4 2022 Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 101-118 34896780-4 2022 Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 120-125 34896780-4 2022 Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment. Lovastatin 12-14 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 101-118 34896780-4 2022 Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment. Lovastatin 12-14 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 120-125 34896780-11 2022 Quantitative RT-PCR showed that the combination of paclitaxel and LV could significantly reduce the expression of CYP2C8, an important drug-metabolizing enzyme. Lovastatin 66-68 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 114-120 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 lanosterol synthase (2,3-oxidosqualene-lanosterol cyclase) Danio rerio 202-205 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 cytochrome P450, family 2, subfamily R, polypeptide 1 Danio rerio 207-213 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 phosphoinositide-3-kinase, regulatory subunit 3a (gamma) Danio rerio 215-222 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 glycerophosphodiester phosphodiesterase domain containing 1 Danio rerio 224-229 34782205-8 2022 While, lovastatin treatment effectively ameliorated PPVII-induced zebrafish liver injury by improving the liver tissue structure and regulate the expression of associated genes including HMGCRA, SREBP, LSS, CYP2R1, PIK3R3A, GDPD1 and PFKFB-2. Lovastatin 7-17 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2a Danio rerio 234-241 34873318-0 2021 Author Correction: Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin. Lovastatin 162-172 KRAS proto-oncogene, GTPase Homo sapiens 71-75 34987392-5 2021 The miR-638 expression profiles were detected in PAH patients, XZK-treated subjects and lovastatin treated pulmonary arterial smooth muscle cells (PA-SMCs). Lovastatin 88-98 microRNA 638 Homo sapiens 4-11 34987392-10 2021 A significantly reduction in miR-638 expression were found in PDGF-BB-treated hPA-SMCs compared to the control cells, and the pre-treatment of the cells with lovastatin significantly re-gain the expression levels in miR-638. Lovastatin 158-168 microRNA 638 Homo sapiens 29-36 34987392-10 2021 A significantly reduction in miR-638 expression were found in PDGF-BB-treated hPA-SMCs compared to the control cells, and the pre-treatment of the cells with lovastatin significantly re-gain the expression levels in miR-638. Lovastatin 158-168 microRNA 638 Homo sapiens 216-223 34969327-7 2021 Our study suggests that targeting cholesterol-using lovastatin could be a therapeutic strategy to enhance responses to R-CHOP in DLBCL patients. Lovastatin 52-62 DNA damage inducible transcript 3 Homo sapiens 121-125 34572136-4 2021 Four statins, namely simvastatin, atorvastatin, lovastatin, and fluvastatin, decreased PD-L1 expression in melanoma and lung cancer cells. Lovastatin 48-58 CD274 molecule Homo sapiens 87-92 34607230-8 2021 Besides, in patients, receiving lovastatin the CRP, IL-6, IL-8 levels were significantly decreased from T1 to T3 than to the control group. Lovastatin 32-42 C-reactive protein Homo sapiens 47-50 34607230-8 2021 Besides, in patients, receiving lovastatin the CRP, IL-6, IL-8 levels were significantly decreased from T1 to T3 than to the control group. Lovastatin 32-42 interleukin 6 Homo sapiens 52-56 34607230-8 2021 Besides, in patients, receiving lovastatin the CRP, IL-6, IL-8 levels were significantly decreased from T1 to T3 than to the control group. Lovastatin 32-42 C-X-C motif chemokine ligand 8 Homo sapiens 58-62 34438015-3 2021 Lovastatin inhibits the binding of the substrate to HMG-CoA reductase, and strongly competes with HMG-CoA reductase (HMGR), thereby exerting a hypolipidemic effect. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 52-69 34438015-3 2021 Lovastatin inhibits the binding of the substrate to HMG-CoA reductase, and strongly competes with HMG-CoA reductase (HMGR), thereby exerting a hypolipidemic effect. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 98-115 34438015-3 2021 Lovastatin inhibits the binding of the substrate to HMG-CoA reductase, and strongly competes with HMG-CoA reductase (HMGR), thereby exerting a hypolipidemic effect. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 117-121 34600840-2 2021 She had been on lovastatin for eight years without any adverse effects. Lovastatin 16-26 Src homology 2 domain containing E Homo sapiens 0-3 34769187-6 2021 Lovastatin"s effect on RhoKinase was investigated through pharmacological testing and in vitro analysis of increased MLC and MYPT1 phosphorylation within primary isolated LMCs. Lovastatin 0-10 protein phosphatase 1, regulatory subunit 12A Rattus norvegicus 125-130 34150623-6 2021 Lovastatin inhibited EMT as demonstrated by down-regulation of the protein levels of Vimentin and Twist in MDA-MB-231 CSCs in vitro and vivo and by reversal of TGF-beta1-induced morphological change in MCF10A cells. Lovastatin 0-10 vimentin Homo sapiens 85-93 34107900-10 2021 The cholesterol inhibitor lovastatin diminished ERK/MAPK activation by A1542, thereby reducing leukemic cell death induced by this ERK1/2 agonist. Lovastatin 26-36 mitogen-activated protein kinase 1 Mus musculus 48-51 34107900-10 2021 The cholesterol inhibitor lovastatin diminished ERK/MAPK activation by A1542, thereby reducing leukemic cell death induced by this ERK1/2 agonist. Lovastatin 26-36 mitogen-activated protein kinase 3 Mus musculus 131-137 34150623-6 2021 Lovastatin inhibited EMT as demonstrated by down-regulation of the protein levels of Vimentin and Twist in MDA-MB-231 CSCs in vitro and vivo and by reversal of TGF-beta1-induced morphological change in MCF10A cells. Lovastatin 0-10 transforming growth factor beta 1 Homo sapiens 160-169 34122084-4 2021 Our data show that the open probability of ENaC in principal cells of split-open cortical collecting ducts was significantly increased after treatment of rats with CsA; the increase was attenuated by lovastatin. Lovastatin 200-210 sodium channel epithelial 1 subunit gamma Rattus norvegicus 43-47 34122084-6 2021 Lovastatin also abolished CsA-induced elevation of alpha-, ss-, and gamma-ENaC expressions. Lovastatin 0-10 sodium channel epithelial 1 subunit gamma Rattus norvegicus 68-78 35461954-8 2022 Exposure to AOH, LOVA and MbetaCD-CHOL coherently modulated membrane cholesterol, expression of PIEZO1 and caveolin-1 as well as the formation of actin stress fibers. Lovastatin 17-21 piezo type mechanosensitive ion channel component 1 Homo sapiens 96-102 35461954-8 2022 Exposure to AOH, LOVA and MbetaCD-CHOL coherently modulated membrane cholesterol, expression of PIEZO1 and caveolin-1 as well as the formation of actin stress fibers. Lovastatin 17-21 caveolin 1 Homo sapiens 107-117 34381332-0 2021 Lovastatin Alleviates alpha-Synuclein Aggregation and Phosphorylation in Cellular Models of Synucleinopathy. Lovastatin 0-10 synuclein alpha Homo sapiens 22-37 34381332-4 2021 In this study, we investigated the effects of lovastatin on the aggregation and phosphorylation of alpha-syn in vitro. Lovastatin 46-56 synuclein alpha Homo sapiens 99-108 34381332-7 2021 Collectively, lovastatin alleviates alpha-syn aggregation and phosphorylation in cellular models of synucleinopathy, indicating its potential value of being adopted in the management of PD. Lovastatin 14-24 synuclein alpha Homo sapiens 36-45 34150623-6 2021 Lovastatin inhibited EMT as demonstrated by down-regulation of the protein levels of Vimentin and Twist in MDA-MB-231 CSCs in vitro and vivo and by reversal of TGF-beta1-induced morphological change in MCF10A cells. Lovastatin 0-10 twist family bHLH transcription factor 1 Homo sapiens 98-103 35459869-0 2022 AGR2-induced cholesterol synthesis drives lovastatin resistance that is overcome by combination therapy with allicin. Lovastatin 42-52 anterior gradient 2 Mus musculus 0-4 35459869-6 2022 Moreover, elevated AGR2 led to a significant decrease in the lipid-lowering efficacy of lovastatin (10 mg kg-1 d-1, ip, for 2 weeks) in mice with hypercholesterolemia (hyperCho), which was validated by results obtained from clinical samples in statin-treated patients. Lovastatin 88-98 anterior gradient 2 Mus musculus 19-23 35459869-9 2022 Importantly, the AGR2-reduced lipid-lowering efficacy of lovastatin was attenuated, at least partially, by co-administration of a sulfhydryl-reactive compound allicin (20 mg kg-1 d-1, ip, for 2 weeks). Lovastatin 57-67 anterior gradient 2 Mus musculus 17-21 35571660-0 2022 Inhibitory effect of lovastatin on human lung cancer cell proliferation by regulating the ERK1/2 and COX-2 pathways. Lovastatin 21-31 mitogen-activated protein kinase 3 Homo sapiens 90-96 35455976-5 2022 We found that exposure of zebrafish larvae to lovastatin caused skeletal muscle disruption observed as a reduction of birefringence, changes in muscle ultrastructure, and an increase in atrogin-1. Lovastatin 46-56 F-box protein 32 Danio rerio 186-195 35571660-0 2022 Inhibitory effect of lovastatin on human lung cancer cell proliferation by regulating the ERK1/2 and COX-2 pathways. Lovastatin 21-31 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 35571660-11 2022 The principal finding of this research was that lovastatin still suppressed A549 cell growth after LPS+ATP stimulation via modulation of ERK1/2, c-JUN, COX-2, BCL-2, and BAX protein levels (P<0.05). Lovastatin 48-58 mitogen-activated protein kinase 3 Homo sapiens 137-143 35571660-11 2022 The principal finding of this research was that lovastatin still suppressed A549 cell growth after LPS+ATP stimulation via modulation of ERK1/2, c-JUN, COX-2, BCL-2, and BAX protein levels (P<0.05). Lovastatin 48-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-150 35571660-11 2022 The principal finding of this research was that lovastatin still suppressed A549 cell growth after LPS+ATP stimulation via modulation of ERK1/2, c-JUN, COX-2, BCL-2, and BAX protein levels (P<0.05). Lovastatin 48-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 152-157 35571660-11 2022 The principal finding of this research was that lovastatin still suppressed A549 cell growth after LPS+ATP stimulation via modulation of ERK1/2, c-JUN, COX-2, BCL-2, and BAX protein levels (P<0.05). Lovastatin 48-58 BCL2 apoptosis regulator Homo sapiens 159-164 35571660-11 2022 The principal finding of this research was that lovastatin still suppressed A549 cell growth after LPS+ATP stimulation via modulation of ERK1/2, c-JUN, COX-2, BCL-2, and BAX protein levels (P<0.05). Lovastatin 48-58 BCL2 associated X, apoptosis regulator Homo sapiens 170-173 35571660-12 2022 Conclusions: Collectively, the findings presented in this study confirmed that lovastatin can inhibit A549 cell proliferation by regulating the ERK1/2 and COX-2 pathways. Lovastatin 79-89 mitogen-activated protein kinase 3 Homo sapiens 144-150 35571660-12 2022 Conclusions: Collectively, the findings presented in this study confirmed that lovastatin can inhibit A549 cell proliferation by regulating the ERK1/2 and COX-2 pathways. Lovastatin 79-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 155-160 35168393-0 2022 Lovastatin Inhibits RhoA to Suppress Canonical Wnt/beta-Catenin Signaling and Alternative Wnt-YAP/TAZ Signaling in Colon Cancer. Lovastatin 0-10 ras homolog family member A Homo sapiens 20-24 34994373-0 2022 A study of lovastatin and L-arginine co-loaded PLGA nanomedicine for enhancing nitric oxide production and eNOS expression. Lovastatin 11-21 nitric oxide synthase 3 Homo sapiens 107-111 35087119-4 2022 Accordingly, we have previously developed the combination of docetaxel and the cholesterol-lowering drug, lovastatin, as a powerful trigger of HGT-1 human GC cells" apoptosis using 2D cultures. Lovastatin 106-116 solute carrier family 25 member 16 Homo sapiens 143-148 35168393-0 2022 Lovastatin Inhibits RhoA to Suppress Canonical Wnt/beta-Catenin Signaling and Alternative Wnt-YAP/TAZ Signaling in Colon Cancer. Lovastatin 0-10 catenin beta 1 Homo sapiens 51-63 35168393-0 2022 Lovastatin Inhibits RhoA to Suppress Canonical Wnt/beta-Catenin Signaling and Alternative Wnt-YAP/TAZ Signaling in Colon Cancer. Lovastatin 0-10 Yes1 associated transcriptional regulator Homo sapiens 94-97 35168393-0 2022 Lovastatin Inhibits RhoA to Suppress Canonical Wnt/beta-Catenin Signaling and Alternative Wnt-YAP/TAZ Signaling in Colon Cancer. Lovastatin 0-10 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 98-101 35168393-3 2022 Furthermore, reverse transcription polymerase chain reaction (RT-PCR) analysis of colonic mass tissues showed a potent inhibitory effect in both Wnt/beta-catenin signaling and YAP/TAZ signaling in the lovastatin treatment group. Lovastatin 201-211 catenin (cadherin associated protein), beta 1 Mus musculus 149-161 35168393-3 2022 Furthermore, reverse transcription polymerase chain reaction (RT-PCR) analysis of colonic mass tissues showed a potent inhibitory effect in both Wnt/beta-catenin signaling and YAP/TAZ signaling in the lovastatin treatment group. Lovastatin 201-211 yes-associated protein 1 Mus musculus 176-179 35168393-3 2022 Furthermore, reverse transcription polymerase chain reaction (RT-PCR) analysis of colonic mass tissues showed a potent inhibitory effect in both Wnt/beta-catenin signaling and YAP/TAZ signaling in the lovastatin treatment group. Lovastatin 201-211 tafazzin, phospholipid-lysophospholipid transacylase Mus musculus 180-183 35168393-5 2022 Moreover, lovastatin suppressed important genes and proteins related to the canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ signaling pathways in RKO and SW480 cells, and these effects were rescued by mevalonic acid (MVA), as confirmed through a series of Western blotting, RT-PCR, and reporter assays. Lovastatin 10-20 catenin beta 1 Homo sapiens 90-102 35168393-5 2022 Moreover, lovastatin suppressed important genes and proteins related to the canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ signaling pathways in RKO and SW480 cells, and these effects were rescued by mevalonic acid (MVA), as confirmed through a series of Western blotting, RT-PCR, and reporter assays. Lovastatin 10-20 Yes1 associated transcriptional regulator Homo sapiens 123-126 35168393-5 2022 Moreover, lovastatin suppressed important genes and proteins related to the canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ signaling pathways in RKO and SW480 cells, and these effects were rescued by mevalonic acid (MVA), as confirmed through a series of Western blotting, RT-PCR, and reporter assays. Lovastatin 10-20 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 127-130 35168393-6 2022 Given that statins suppress oncogenic processes primarily through the inhibition of Rho GTPase in the mevalonate pathway, we speculate that lovastatin can inhibit certain Rho GTPases to suppress both canonical Wnt/beta-catenin signaling and alternative Wnt-YAP/TAZ signaling. Lovastatin 140-150 catenin beta 1 Homo sapiens 214-226 35168393-6 2022 Given that statins suppress oncogenic processes primarily through the inhibition of Rho GTPase in the mevalonate pathway, we speculate that lovastatin can inhibit certain Rho GTPases to suppress both canonical Wnt/beta-catenin signaling and alternative Wnt-YAP/TAZ signaling. Lovastatin 140-150 Yes1 associated transcriptional regulator Homo sapiens 257-260 35168393-6 2022 Given that statins suppress oncogenic processes primarily through the inhibition of Rho GTPase in the mevalonate pathway, we speculate that lovastatin can inhibit certain Rho GTPases to suppress both canonical Wnt/beta-catenin signaling and alternative Wnt-YAP/TAZ signaling. Lovastatin 140-150 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 261-264 35168393-7 2022 In RKO cells, lovastatin showed similar inhibitory properties as the RhoA inhibitor CCG1423, being able to inhibit beta-catenin, TAZ, and p-LATS1 protein activity. Lovastatin 14-24 catenin beta 1 Homo sapiens 115-127 35168393-7 2022 In RKO cells, lovastatin showed similar inhibitory properties as the RhoA inhibitor CCG1423, being able to inhibit beta-catenin, TAZ, and p-LATS1 protein activity. Lovastatin 14-24 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 129-132 35168393-7 2022 In RKO cells, lovastatin showed similar inhibitory properties as the RhoA inhibitor CCG1423, being able to inhibit beta-catenin, TAZ, and p-LATS1 protein activity. Lovastatin 14-24 large tumor suppressor kinase 1 Homo sapiens 140-145 35168393-8 2022 Our results revealed that lovastatin inhibited RhoA activity, thereby suppressing the downstream canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ pathways in colon cancer cells. Lovastatin 26-36 ras homolog family member A Homo sapiens 47-51 35168393-8 2022 Our results revealed that lovastatin inhibited RhoA activity, thereby suppressing the downstream canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ pathways in colon cancer cells. Lovastatin 26-36 catenin beta 1 Homo sapiens 111-123 35168393-8 2022 Our results revealed that lovastatin inhibited RhoA activity, thereby suppressing the downstream canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ pathways in colon cancer cells. Lovastatin 26-36 Yes1 associated transcriptional regulator Homo sapiens 144-147 35168393-8 2022 Our results revealed that lovastatin inhibited RhoA activity, thereby suppressing the downstream canonical Wnt/beta-catenin and alternative Wnt-YAP/TAZ pathways in colon cancer cells. Lovastatin 26-36 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 148-151 2810673-4 1989 Lovastatin reduced total and low-density lipoprotein cholesterol and apolipoprotein B levels by 28%, 34%, and 24%, respectively. Lovastatin 0-10 apolipoprotein B Homo sapiens 69-85 2590222-2 1989 Induction of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity was observed in mevinolin treated cultures. Lovastatin 86-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 13-60 2568358-2 1989 Addition of either delipidized serum and mevinolin or low density lipoprotein, 25-hydroxycholesterol, or mevalonic acid to HepG2 cells resulted in rapid changes both in the levels of the mRNAs and in the rates of synthesis of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase, HMG-CoA reductase, and farnesyl pyrophosphate synthetase (prenyltranferase). Lovastatin 41-50 3-hydroxy-3-methylglutaryl-CoA synthase 2 Homo sapiens 226-282 2568358-2 1989 Addition of either delipidized serum and mevinolin or low density lipoprotein, 25-hydroxycholesterol, or mevalonic acid to HepG2 cells resulted in rapid changes both in the levels of the mRNAs and in the rates of synthesis of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase, HMG-CoA reductase, and farnesyl pyrophosphate synthetase (prenyltranferase). Lovastatin 41-50 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 284-301 2741883-9 1989 The advent of lovastatin and other HMG COA reductase inhibitors is likely to decrease the use of partial ileal bypass to treat familial hypercholesterolemia. Lovastatin 14-24 low density lipoprotein receptor Homo sapiens 127-156 2722887-4 1989 However, incubation of cells with lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, for as little as 1 h prior to addition of cycloheximide rendered the isoprenylation step insensitive to cycloheximide. Lovastatin 34-44 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 73-130 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 59-65 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 101-158 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 59-65 liver carboxylesterase 1 Oryctolagus cuniculus 193-237 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 59-65 sterol O-acyltransferase 1 Oryctolagus cuniculus 239-243 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 67-77 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 101-158 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 67-77 liver carboxylesterase 1 Oryctolagus cuniculus 193-237 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 67-77 sterol O-acyltransferase 1 Oryctolagus cuniculus 239-243 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 79-88 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 101-158 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 79-88 liver carboxylesterase 1 Oryctolagus cuniculus 193-237 2776246-1 1989 Relatively high concentrations of MK-733 (simvastatin) and MK-803 (lovastatin, mevinolin), which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were found to inhibit acyl coenzyme A: cholesterol acyltransferase (ACAT) of rabbit intestinal microsomes with IC50"s of 2.0 x 10(-5) and 3.6 x 10(-5) M, respectively. Lovastatin 79-88 sterol O-acyltransferase 1 Oryctolagus cuniculus 239-243 2725293-6 1989 Similar decreases in urinary mevalonate excretions were observed when patients with FH were treated directly with 40 mg (20 mg twice daily) or 80 mg (40 mg twice daily) mg of lovastatin daily. Lovastatin 175-185 low density lipoprotein receptor Homo sapiens 84-86 2621421-7 1989 Both the 20-mg bid dose and the 40-mg bid dose of lovastatin administered for a 4-week period decreased serum cholesterol by 25-34%. Lovastatin 50-60 BH3 interacting domain death agonist Homo sapiens 38-41 2621421-8 1989 Lovastatin at 20 mg bid decreased ML sterol synthesis by 23 +/- 6% (P less than 0.02) and increased ML HMG-CoA reductase 3.8 times (P less than 0.001) the baseline values. Lovastatin 0-10 BH3 interacting domain death agonist Homo sapiens 20-23 2621421-10 1989 The higher dose of lovastatin (40 mg bid) decreased ML sterol synthesis by 16 +/- 3% (P less than 0.05) and induced HMG-CoA reductase to 53.7 times (P less than 0.01) the baseline value at 4 weeks. Lovastatin 19-29 BH3 interacting domain death agonist Homo sapiens 37-40 2690933-9 1989 Lovastatin increases mRNA levels for farnesyl pyrophosphate synthetase 2.5-fold while mevalonic acid, low-density lipoprotein, and 25-hydroxycholesterol decrease mRNA levels to 40-50% of control values. Lovastatin 0-10 farnesyl diphosphate synthase Rattus norvegicus 37-70 2614261-1 1989 Lovastatin therapy is known to induce hepatic low density lipoprotein (LDL) receptor mRNA and LDL receptor activity. Lovastatin 0-10 low-density lipoprotein receptor Cavia porcellus 46-84 2614261-1 1989 Lovastatin therapy is known to induce hepatic low density lipoprotein (LDL) receptor mRNA and LDL receptor activity. Lovastatin 0-10 low-density lipoprotein receptor Cavia porcellus 94-106 2614261-6 1989 Several independent lines of investigation documented that a substantial increase in hepatic LDL receptor activity occurred in response to the lovastatin treatment. Lovastatin 143-153 low-density lipoprotein receptor Cavia porcellus 93-105 2552800-9 1989 These results provide direct evidence that therapy with lovastatin and a bile acid-binding resin can lead to increased expression of functional LDL receptors by lymphocytes in the majority (eight of 12) of patients with heterozygous FH. Lovastatin 56-66 low density lipoprotein receptor Homo sapiens 233-235 2918466-1 1989 Lovastatin, a specific inhibitor of the rate-limiting enzyme in cholesterol biosynthesis, HMG-CoA reductase, has been shown to be highly effective in lowering serum cholesterol in animals and humans and thus represents a promising approach to the treatment and prevention of cardiovascular disease. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 90-107 2917701-6 1989 Addition of lovastatin to gemfibrozil effectively reduced total cholesterol (25%), LDL-chol (30%), and LDL-apoB (19%). Lovastatin 12-22 apolipoprotein B Homo sapiens 107-111 2918466-6 1989 All histopathological and serum biochemical changes induced by lovastatin were completely prevented by coadministration of mevalonate, the product of the inhibited HMG-CoA reductase enzyme. Lovastatin 63-73 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 164-181 2912427-2 1989 This investigation was carried out in 10 male patients with heterozygous familial hypercholesterolemia to determine the effects of combined drug therapy with lovastatin and colestipol on the kinetics of apolipoprotein B (apo B) in low density lipoproteins (LDL) and very low density lipoproteins (VLDL). Lovastatin 158-168 apolipoprotein B Homo sapiens 203-219 2912432-8 1989 Patients with heterozygous FH respond to therapy with mevinolin and a bile-acid-binding resin by lowering plasma cholesterol levels. Lovastatin 54-63 low density lipoprotein receptor Homo sapiens 27-29 2515162-0 1989 Suppression of lymphoid cell function in vitro by inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by lovastatin. Lovastatin 115-125 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 64-111 2515162-5 1989 At higher concentrations (10 microM) for shorter periods of time (48 h), lovastatin inhibited phytohemagglutin and Concanavalin A-stimulated proliferation by 83% and 38% respectively, natural killer cell cytotoxicity by 93%, and interferon gamma production by 98%. Lovastatin 73-83 interferon gamma Homo sapiens 229-245 2904178-4 1988 In this report, we demonstrate that this mutant is defective in regulation of the mRNA levels for HMG-CoA reductase and HMG-CoA synthase by 25-hydroxycholesterol and mevinolin. Lovastatin 166-175 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 98-115 3055923-7 1988 Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Lovastatin 27-37 apolipoprotein B Homo sapiens 238-254 3254824-1 1988 Simvastatin (MK733), derived from lovastatin by substituting CH3 for H at the 2" position, is a potent hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitor. Lovastatin 34-44 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 103-155 3056429-1 1988 We have studied the effect of lovastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase), alone and in combination with the bile acid sequestrant cholestyramine on lipid parameters in 30 heterozygous patients with familial hypercholesterolemia (FH) during a 20-week open trial. Lovastatin 30-40 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 112-159 3056429-2 1988 Lovastatin 40 mg bid (twice daily) decreased significantly total serum cholesterol, low density lipoprotein (LDL)-cholesterol, triglycerides and apolipoprotein B by 36%, 45%, 29% and 11%, respectively, while high density lipoprotein (HDL)-cholesterol and apolipoprotein A-I were increased significantly by 16% and 37%, respectively. Lovastatin 0-10 BH3 interacting domain death agonist Homo sapiens 17-20 3056429-2 1988 Lovastatin 40 mg bid (twice daily) decreased significantly total serum cholesterol, low density lipoprotein (LDL)-cholesterol, triglycerides and apolipoprotein B by 36%, 45%, 29% and 11%, respectively, while high density lipoprotein (HDL)-cholesterol and apolipoprotein A-I were increased significantly by 16% and 37%, respectively. Lovastatin 0-10 apolipoprotein B Homo sapiens 145-161 3056429-2 1988 Lovastatin 40 mg bid (twice daily) decreased significantly total serum cholesterol, low density lipoprotein (LDL)-cholesterol, triglycerides and apolipoprotein B by 36%, 45%, 29% and 11%, respectively, while high density lipoprotein (HDL)-cholesterol and apolipoprotein A-I were increased significantly by 16% and 37%, respectively. Lovastatin 0-10 apolipoprotein A1 Homo sapiens 255-273 3170653-1 1988 In order to investigate a requirement for isoprenoid compounds in the cell cycle, DNA synthesis was examined in cultured Chinese hamster ovary cells in which mevalonate biosynthesis was blocked with mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Lovastatin 199-208 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 237-294 3414776-1 1988 The cholesterol lowering compound lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.34 HMG CoA reductase), was given in nine separate experiments to normocholesterolemic dogs at rates up to 180 times the maximum therapeutic dose in man (1 mg/kg/day). Lovastatin 34-44 3-hydroxy-3-methylglutaryl-CoA reductase Canis lupus familiaris 73-120 2902179-0 1988 Localization of 3-hydroxy-3-methylglutaryl CoA reductase and 3-hydroxy-3-methylglutaryl CoA synthase in the rat liver and intestine is affected by cholestyramine and mevinolin. Lovastatin 166-175 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 16-56 2902179-3 1988 Addition of cholestyramine and mevinolin to the diet resulted in all liver cells showing strong positive staining for both HMG-CoA reductase and HMG-CoA synthase. Lovastatin 31-40 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 123-140 2902179-3 1988 Addition of cholestyramine and mevinolin to the diet resulted in all liver cells showing strong positive staining for both HMG-CoA reductase and HMG-CoA synthase. Lovastatin 31-40 3-hydroxy-3-methylglutaryl-CoA synthase 2 Rattus norvegicus 145-161 2902179-8 1988 Addition of cholestyramine and mevinolin to the diet led to a dramatic increase in the concentration of HMG-CoA reductase in the apical region of the villi of the ileum and jejunum and in the crypt cells of the duodenum. Lovastatin 31-40 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 104-121 2902179-10 1988 Cholestyramine and mevinolin feeding induced in the liver, but not intestine, whorls of smooth endoplasmic reticulum that were proximal to the nucleus and contained high concentrations of HMG-CoA reductase. Lovastatin 19-28 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 188-205 3053982-8 1988 Based on growth data, sterol analysis, and the lack of detection of HMGCoA reductase activity differences between strain MV71 and the wild-type, mevinolin resistance is concluded to result possibly from a mutation in HMG2, one of the two functional yeast HMGCoA reductase genes, which accounts for a minor (up to 17%) amount of total cellular reductase activity. Lovastatin 145-154 hydroxymethylglutaryl-CoA reductase (NADPH) HMG2 Saccharomyces cerevisiae S288C 217-221 3162680-0 1988 Lovastatin therapy in familial dysbetalipoproteinemia: effects on kinetics of apolipoprotein B. Lovastatin 0-10 apolipoprotein B Homo sapiens 78-94 3278736-17 1988 Adaptation to drugs such as compactin and mevinolin, which inhibit HMG-CoA reductase, have been used to produce mutants which overexpress enzymes in the pathway. Lovastatin 42-51 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 67-84 3422105-4 1988 As compared with the placebo, lovastatin reduced total cholesterol by 26 percent, low-density lipoprotein (LDL) cholesterol by 28 percent, and LDL apolipoprotein B by 26 percent. Lovastatin 30-40 apolipoprotein B Homo sapiens 147-163 3076120-3 1988 Treatment of these animals with the HMG CoA reductase inhibitor lovastatin from the time of weaning results in a significant degree of inhibition of lesion formation. Lovastatin 64-74 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 36-53 3076124-4 1988 The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate and inhibitors of hydroxymethylglutaryl coenzyme A (HMG CoA) reductase (e.g. lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolaemia; these agents reduce plasma concentrations of total and LDL-cholesterol by 15 to 45%. Lovastatin 165-175 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 106-158 3076125-2 1988 Lovastatin (MK-803, mevinolin) and simvastatin (MK-733, synvinolin), 2 highly potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, have been heralded as breakthrough therapy for the treatment of atherosclerotic disease. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 85-142 3076125-2 1988 Lovastatin (MK-803, mevinolin) and simvastatin (MK-733, synvinolin), 2 highly potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, have been heralded as breakthrough therapy for the treatment of atherosclerotic disease. Lovastatin 12-18 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 85-142 3076125-2 1988 Lovastatin (MK-803, mevinolin) and simvastatin (MK-733, synvinolin), 2 highly potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, have been heralded as breakthrough therapy for the treatment of atherosclerotic disease. Lovastatin 20-29 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 85-142 3076125-5 1988 Lovastatin and simvastatin are the first HMG CoA reductase inhibitors to receive regulatory agency approval for marketed use. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 41-58 2725293-0 1989 Reduction in plasma low-density lipoprotein cholesterol and urinary mevalonic acid by lovastatin in patients with heterozygous familial hypercholesterolemia. Lovastatin 86-96 low density lipoprotein receptor Homo sapiens 127-156 3216281-2 1988 The HMG-CoA reductase inhibition activities of mevinolin analogs and 6-substituted 4-hydroxypyran-2 ones have been mostly found to be significantly correlated with the molecular size of substituents. Lovastatin 47-56 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-21 3046888-1 1988 Lovastatin is the first 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor approved for the treatment of primary hypercholesterolemia. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 24-81 3278832-2 1988 Lovastatin is the first agent marketed in a new class of pharmacologic compounds called the 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 92-149 3680522-10 1987 Lovastatin reduced both the rate of cholesterol synthesis and the secretion of apoB-containing lipoproteins. Lovastatin 0-10 apolipoprotein B Homo sapiens 79-83 3076126-2 1988 Lovastatin and simvastatin are the 2 best-known members of the class of hypolipidaemic agents known as HMG CoA reductase inhibitors. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 103-120 3680522-0 1987 Suppression of apolipoprotein B production during treatment of cholesteryl ester storage disease with lovastatin. Lovastatin 102-112 apolipoprotein B Homo sapiens 15-31 2445765-0 1987 Differentiation of human keratinocytes: changes in lipid synthesis, plasma membrane lipid composition, and 125I-EGF binding upon administration of 25-hydroxycholesterol and mevinolin. Lovastatin 173-182 epidermal growth factor Homo sapiens 112-115 2445765-5 1987 The experimental modulation of plasma membrane composition by 25-hydroxycholesterol or mevinolin were accompanied by a decreased cornified envelope formation and by high expression of EGF binding sites. Lovastatin 87-96 epidermal growth factor Homo sapiens 184-187 3114306-5 1987 Lovastatin (mevinolin) is a new hypolipidemic agent which blocks cholesterol synthesis by competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 116-163 3113763-7 1987 At 40 mg bid, lovastatin produces the following approximate mean changes: total plasma cholesterol, -33%; low-density lipoprotein (LDL) cholesterol, -40%; very low-density lipoprotein cholesterol, -35%; plasma triglycerides, -25%; high-density lipoprotein cholesterol, +10%; apolipoprotein B, -20%. Lovastatin 14-24 BH3 interacting domain death agonist Homo sapiens 9-12 3113763-7 1987 At 40 mg bid, lovastatin produces the following approximate mean changes: total plasma cholesterol, -33%; low-density lipoprotein (LDL) cholesterol, -40%; very low-density lipoprotein cholesterol, -35%; plasma triglycerides, -25%; high-density lipoprotein cholesterol, +10%; apolipoprotein B, -20%. Lovastatin 14-24 apolipoprotein B Homo sapiens 275-291 3114306-5 1987 Lovastatin (mevinolin) is a new hypolipidemic agent which blocks cholesterol synthesis by competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 12-21 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 116-163 3040778-8 1987 By treating 3T3 cells stimulated to resume proliferation by addition of conditioned media with mevinolin (a competitive inhibitor of HMG CoA reductase) the activity of HMG CoA reductase as well as the DNA synthesis and cell division were efficiently inhibited. Lovastatin 95-104 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 133-150 3670308-2 1987 The level of CR39 mRNA was increased seven- to ninefold over normal levels by dietary cholestyramine and mevinolin and decreased about fourfold compared with normal levels by cholesterol feeding or administration of mevalonate. Lovastatin 105-114 farnesyl diphosphate synthase Rattus norvegicus 13-17 3650077-1 1987 When normal or hypophysectomized rats maintained on a diet containing mevinolin and colestipol were switched to a normal chow diet, HMG-CoA reductase mRNA fell rapidly with a half-life of 3 hrs. Lovastatin 70-79 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 132-149 3040778-8 1987 By treating 3T3 cells stimulated to resume proliferation by addition of conditioned media with mevinolin (a competitive inhibitor of HMG CoA reductase) the activity of HMG CoA reductase as well as the DNA synthesis and cell division were efficiently inhibited. Lovastatin 95-104 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 168-185 16665452-7 1987 Application of nanomolar amounts of mevinolin, a highly specific inhibitor of HMG-CoA reductase, to elicitor-treated tuber tissue produced a large decline in lubimin accumulation and did not markedly alter rishitin accumulation. Lovastatin 36-45 3-hydroxy-3-methylglutaryl-coenzyme A reductase 2 Solanum tuberosum 78-95 3648095-3 1987 Reversal of the resulting quiescent state by the return of the cultures to 10% serum caused after 24 h a marked increase in DNA synthesis, and this increase was prevented by the simultaneous addition of mevinolin, a specific inhibitor of the sterol biosynthetic pathway at the 3-hydroxy-3-methylglutaryl coenzyme A reductase step, at the time of serum repletion. Lovastatin 203-212 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 277-324 3033149-5 1987 Mevinolin (10 microM), a specific inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme of the sterol biosynthetic pathway, completely inhibited the induction of CNP by dBcAMP, while not affecting either the accumulation of cellular protein per flask or rate of protein synthesis. Lovastatin 0-9 2',3'-cyclic nucleotide 3' phosphodiesterase Rattus norvegicus 195-198 3033149-6 1987 Simultaneous addition of mevalonate (20 mM) prevented the inhibition of the induction of CNP by mevinolin. Lovastatin 96-105 2',3'-cyclic nucleotide 3' phosphodiesterase Rattus norvegicus 89-92 3448024-4 1987 This mitogen-induced increase in lymphocyte sterol synthesis can be observed within 4 h of stimulation and is prevented by suppressing the activity of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase with the specific inhibitors ML-236B or mevinolin. Lovastatin 250-259 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 151-209 3328165-1 1987 Lovastatin is a potent new drug for lowering serum cholesterol through inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme for cholesterol biosynthesis. Lovastatin 0-10 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 85-132 3646060-1 1987 Mevinolin is a potent competitive inhibitor of HMG-CoA reductase, the enzyme catalyzing the major rate-limiting step in cholesterol synthesis. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 47-64 3029155-9 1987 These results suggest that treatment of patients with defects in the LDL receptor pathway with mevinolin improves the plasma lipid profile and does not result in adrenal dysfunction or further exacerbation of the mild impairment of adrenal function during maximal ACTH stimulation. Lovastatin 95-104 low density lipoprotein receptor Homo sapiens 69-81 16665062-4 1986 When grown in 10 micromolar mevinolin, a competitive inhibitor of HMG-CoA reductase, O. malhamensis shows a 10- to 15-fold increase in HMG-CoA reductase activity (after washing) with little or no effect on cell growth rate. Lovastatin 28-37 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 66-83 2892309-2 1987 The effects of a 7-day infusion with mevinolin, a potent competitive inhibitor of hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase, on the adrenal zona fasciculata were examined in normal and dexamethasone/ACTH-treated rats. Lovastatin 37-46 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 82-135 2877984-8 1986 Approximately 9-fold increases in both HMG-CoA synthase mRNA mass and synthase mRNA activity were observed when control diets were supplemented with cholestyramine and mevinolin. Lovastatin 168-177 3-hydroxy-3-methylglutaryl-CoA synthase 2 Rattus norvegicus 39-55 16665062-4 1986 When grown in 10 micromolar mevinolin, a competitive inhibitor of HMG-CoA reductase, O. malhamensis shows a 10- to 15-fold increase in HMG-CoA reductase activity (after washing) with little or no effect on cell growth rate. Lovastatin 28-37 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 135-152 3464957-0 1986 Mevinolin, an inhibitor of cholesterol synthesis, induces mRNA for low density lipoprotein receptor in livers of hamsters and rabbits. Lovastatin 0-9 low-density lipoprotein receptor Oryctolagus cuniculus 67-99 3906004-0 1985 Mevinolin and cholestyramine inhibit the direct synthesis of low density lipoprotein apolipoprotein B in miniature pigs. Lovastatin 0-9 apolipoprotein B Sus scrofa 85-101 3464957-1 1986 Through the use of a quantitative solution hybridization assay with 32P-labeled cDNA probes, we found that mevinolin, an inhibitor of cholesterol synthesis, elevates the level of mRNA for the low density lipoprotein receptor in livers of hamsters and rabbits. Lovastatin 107-116 low-density lipoprotein receptor Oryctolagus cuniculus 192-224 3464957-5 1986 In normal rabbits, mevinolin produced a 90% reduction in plasma low density lipoprotein-cholesterol levels, which was associated with a 2.5-fold increase in low density lipoprotein receptor mRNA levels. Lovastatin 19-28 low-density lipoprotein receptor Oryctolagus cuniculus 157-189 3464957-7 1986 These data are consistent with the hypothesis that mevinolin and other inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase lower plasma cholesterol levels in part by stimulating production of mRNA for the low density lipoprotein receptor in liver. Lovastatin 51-60 low-density lipoprotein receptor Oryctolagus cuniculus 208-240 2874807-2 1986 Acetoacetyl CoA thiolase, HMG CoA synthase and HMG CoA reductase activities were elevated in the mevinolin resistant line, KH 2.0. Lovastatin 97-106 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 47-64 3636157-10 1986 The inhibitory effect of mevinolin on cholesterol 7 alpha-hydroxylase activity under experimental conditions where most of the effect of mevinolin on hydroxymethylglutaryl-CoA reductase was abolished by treatment with cholesterol suggest that the effect of mevinolin on the cholesterol 7 alpha-hydroxylase may be independent of its effect on cholesterol synthesis. Lovastatin 25-34 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 38-69 3636157-10 1986 The inhibitory effect of mevinolin on cholesterol 7 alpha-hydroxylase activity under experimental conditions where most of the effect of mevinolin on hydroxymethylglutaryl-CoA reductase was abolished by treatment with cholesterol suggest that the effect of mevinolin on the cholesterol 7 alpha-hydroxylase may be independent of its effect on cholesterol synthesis. Lovastatin 25-34 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 274-305 3636157-10 1986 The inhibitory effect of mevinolin on cholesterol 7 alpha-hydroxylase activity under experimental conditions where most of the effect of mevinolin on hydroxymethylglutaryl-CoA reductase was abolished by treatment with cholesterol suggest that the effect of mevinolin on the cholesterol 7 alpha-hydroxylase may be independent of its effect on cholesterol synthesis. Lovastatin 137-146 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 38-69 3636157-10 1986 The inhibitory effect of mevinolin on cholesterol 7 alpha-hydroxylase activity under experimental conditions where most of the effect of mevinolin on hydroxymethylglutaryl-CoA reductase was abolished by treatment with cholesterol suggest that the effect of mevinolin on the cholesterol 7 alpha-hydroxylase may be independent of its effect on cholesterol synthesis. Lovastatin 137-146 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 38-69 3515897-4 1986 Compared with placebo treatment, both apolipoprotein B and LDL cholesterol levels were reduced (p less than 0.01) in both FH and non-FH patients by 28 to 34% with mevinolin treatment. Lovastatin 163-172 apolipoprotein B Homo sapiens 38-54 3851809-5 1985 When mevinolin was removed from the culture medium, most of the cells retracted their neurites within 2 h, but ACE activity did not decline until DNA synthesis began to return to control levels after 10 h. Similarly, retraction of neurites in differentiated cells exposed to colchicine was not accompanied by a decrease in ACE activity. Lovastatin 5-14 acetylcholinesterase Mus musculus 323-326 3851809-12 1985 These studies suggest that the stimulation of neurite outgrowth and the increase in ACE activity induced by mevinolin are independent phenomena. Lovastatin 108-117 acetylcholinesterase Mus musculus 84-87 3853581-4 1985 Compared to placebo, a low dose of mevinolin (10 mg, twice daily (BID] caused reductions of plasma total cholesterol and LDL-cholesterol averaging 15% and 20%, respectively; corresponding reductions on high doses of mevinolin (20 mg BID) were 22% and 31%, respectively. Lovastatin 35-44 BH3 interacting domain death agonist Homo sapiens 66-69 3853581-4 1985 Compared to placebo, a low dose of mevinolin (10 mg, twice daily (BID] caused reductions of plasma total cholesterol and LDL-cholesterol averaging 15% and 20%, respectively; corresponding reductions on high doses of mevinolin (20 mg BID) were 22% and 31%, respectively. Lovastatin 35-44 BH3 interacting domain death agonist Homo sapiens 233-236 4055772-11 1985 We have concluded that mevalonate, fluoromevalonate, homomevalonate, and compactin (mevinolin) modulated HMG-CoA reductase activity because they altered isoprenoid carbon flow to a post-isopentenyl 1-pyrophosphate regulatory, signal molecule. Lovastatin 84-93 Pyrroline 5-carboyxlate reductase Drosophila melanogaster 113-122 3906004-2 1985 The possibility that cholestyramine alone (a bile acid sequestrant) or in combination with mevinolin (a cholesterol synthesis inhibitor) could regulate the direct LDL apoB synthetic pathway was investigated. Lovastatin 91-100 apolipoprotein B Sus scrofa 167-171 3906004-9 1985 The combination of mevinolin and cholestyramine resulted in an even more marked inhibition of the direct LDL apoB synthesis pathway (by 90%), and in two animals this pathway was completely abolished. Lovastatin 19-28 apolipoprotein B Sus scrofa 109-113 3906004-12 1985 These results are consistent with the idea that cholestyramine and mevinolin increase LDL catabolism by inducing hepatic apoB, E receptors. Lovastatin 67-76 apolipoprotein B Sus scrofa 121-125 6569064-0 1984 Hypocholesterolemic effects of mevinolin in patients with heterozygous familial hypercholesterolemia. Lovastatin 31-40 low density lipoprotein receptor Homo sapiens 71-100 3849281-2 1985 Two therapeutic measures that seem to increase the synthesis of LDL receptors are interruption of the enterohepatic circulation of bile acids with either bile-acid sequestrants or the ileal-exclusion operation, and competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase with mevinolin or compactin. Lovastatin 294-303 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 241-288 2994068-2 1985 Mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase [mevalonate:NAD+ oxidoreductase (CoA-acylating), EC 1.1.1.88] is an effective hypolipidemic agent in patients with heterozygous familial hypercholesterolemia. Lovastatin 0-9 thioredoxin reductase 1 Homo sapiens 85-99 3847351-1 1985 A somatic cell mutant has been isolated which is resistant to killing and growth inhibition by mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Lovastatin 95-104 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 133-190 2411835-1 1985 H4-II-E-C3 hepatoma cells in culture respond to lipid-depleted media and to mevinolin with increased sterol synthesis from [14C]acetate and rise of 3-hydroxy-3-methylglutaryl coenzyme A reductase levels. Lovastatin 76-85 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 148-195 3851809-1 1985 Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, stimulates neurite outgrowth and acetylcholinesterase (ACE) activity in C1300 (Neuro-2A) murine neuroblastoma cells. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 38-95 3851809-1 1985 Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, stimulates neurite outgrowth and acetylcholinesterase (ACE) activity in C1300 (Neuro-2A) murine neuroblastoma cells. Lovastatin 0-9 acetylcholinesterase Mus musculus 130-150 3851809-1 1985 Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, stimulates neurite outgrowth and acetylcholinesterase (ACE) activity in C1300 (Neuro-2A) murine neuroblastoma cells. Lovastatin 0-9 acetylcholinesterase Mus musculus 152-155 6569064-1 1984 We have evaluated the hypolipidemic effects of mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis in 13 patients with heterozygous familial hypercholesterolemia (FH). Lovastatin 47-56 low density lipoprotein receptor Homo sapiens 220-249 6569064-1 1984 We have evaluated the hypolipidemic effects of mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis in 13 patients with heterozygous familial hypercholesterolemia (FH). Lovastatin 47-56 low density lipoprotein receptor Homo sapiens 251-253 6569064-7 1984 These results indicate that mevinolin is an effective hypolipidemic agent in patients with heterozygous FH but that the optimal doses in these patients are greater than those previously reported in normal volunteers. Lovastatin 28-37 low density lipoprotein receptor Homo sapiens 104-106 6569064-8 1984 If long-term safety can be satisfactorily established, mevinolin offers considerable promise in the therapy of heterozygous FH. Lovastatin 55-64 low density lipoprotein receptor Homo sapiens 124-126 6087838-3 1984 Furthermore, this increased LDL receptor activity in cells incubated for 24 h with mevinolin and lipoprotein-depleted serum (LPDS) led to a nearly 3-fold increase in the formation of cholesteryl esters when these cells were then incubated with LDL for 24 h. Continuous exposure to mevinolin did not result in a constant increase in LDL receptor activity. Lovastatin 83-92 low density lipoprotein receptor Homo sapiens 28-40 6087838-3 1984 Furthermore, this increased LDL receptor activity in cells incubated for 24 h with mevinolin and lipoprotein-depleted serum (LPDS) led to a nearly 3-fold increase in the formation of cholesteryl esters when these cells were then incubated with LDL for 24 h. Continuous exposure to mevinolin did not result in a constant increase in LDL receptor activity. Lovastatin 83-92 low density lipoprotein receptor Homo sapiens 332-344 6087838-3 1984 Furthermore, this increased LDL receptor activity in cells incubated for 24 h with mevinolin and lipoprotein-depleted serum (LPDS) led to a nearly 3-fold increase in the formation of cholesteryl esters when these cells were then incubated with LDL for 24 h. Continuous exposure to mevinolin did not result in a constant increase in LDL receptor activity. Lovastatin 281-290 low density lipoprotein receptor Homo sapiens 28-40 6087838-4 1984 Cells exposed to mevinolin for 24 h on day 3 had increased LDL receptor activity, but continuous exposure to mevinolin with 5% human serum (HS) from day 3-9 resulted in degradation of [125I]LDL at the same rate as observed in cells incubated with 5% HS alone. Lovastatin 17-26 low density lipoprotein receptor Homo sapiens 59-71 6371816-2 1984 In these patients, mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase [mevalonate:NAD+ oxidoreductase (CoA-acylating), EC 1.1.1.88], increases receptors for LDL and decreases LDL concentrations. Lovastatin 19-28 thioredoxin reductase 1 Homo sapiens 104-118 6665743-1 1983 Mevinolin is a fungal metabolite, and in the hydroxyacid form, mevinolinic acid, it is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-Co A) reductase, an enzyme essential in cholesterol biosynthesis. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 103-161 6139093-4 1983 Mevinolin, a competitive inhibitor of HMG CoA reductase, has no effect on HMG CoA synthase activity measured in vitro. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 38-55 6317039-7 1983 To assess the functional role of the hepatic LDL receptor in response to mevinolin, the catabolism of 125I-labeled LDL by perfused rabbit livers was studied. Lovastatin 73-82 low-density lipoprotein receptor Oryctolagus cuniculus 45-57 6139093-5 1983 Incubation of CHO cells with sublethal concentrations of mevinolin produces an inhibition of the conversion of [14C]acetate to cholesterol and results in elevated levels of both HMG CoA synthase and HMG CoA reductase activities. Lovastatin 57-66 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 199-216 6554277-0 1983 Alterations in the rates of synthesis and degradation of rat liver 3-hydroxy-3-methylglutaryl coenzyme A reductase produced by cholestyramine and mevinolin. Lovastatin 146-155 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 67-114 6553055-0 1983 Inhibition of degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase by mevinolin. Lovastatin 80-89 3-hydroxy-3-methylglutaryl-coenzyme A reductase Cricetulus griseus 29-76 6863245-2 1983 Antibody raised to enzyme purified from rats fed a diet supplemented with cholestyramine and mevinolin inactivated HMG-CoA reductase. Lovastatin 93-102 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 115-132 6190175-1 1983 Addition of cholestyramine or cholestyramine plus mevinolin to the diet has been reported to increase the activity and mass of rat liver 3-hydroxy-3-methylglutaryl-CoA reductase. Lovastatin 50-59 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 137-177 6903572-1 1980 Compactin (ML-236B) and the related compound, mevinolin, are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase), the rate-controlling enzyme in cholesterol synthesis. Lovastatin 46-55 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 136-153 6400479-15 1983 In its hydroxyacid form (mevinolinic acid), mevinolin is a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase from liver. Lovastatin 25-34 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 91-138 6918402-0 1982 Cholesterol-lowering effect of mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme a reductase, in healthy volunteers. Lovastatin 31-40 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 58-105 6918402-1 1982 Mevinolin reduces cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Lovastatin 0-9 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 54-101 6903572-5 1980 Administration of mevinolin to mice on a control diet produced a 6- to 10-fold increase in the amount of HMG CoA reductase in liver microsomes. Lovastatin 18-27 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 105-122 6903572-7 1980 The administration of mevinolin to cholesterol-fed mice produced a three to eightfold increase in HMG CoA reductase. Lovastatin 22-31 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 98-115 6903572-8 1980 Despite the abundant amount of cholesterol that was already present in the livers of the mevinolin-treated, cholesterol-fed animals, their elevated HMG CoA reductase could be rapidly suppressed by the subcutaneous injection of small amounts of mevalonate, the product of HMG CoA reductase. Lovastatin 89-98 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 148-165 6903572-8 1980 Despite the abundant amount of cholesterol that was already present in the livers of the mevinolin-treated, cholesterol-fed animals, their elevated HMG CoA reductase could be rapidly suppressed by the subcutaneous injection of small amounts of mevalonate, the product of HMG CoA reductase. Lovastatin 89-98 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 271-288 6903572-11 1980 The ability to suppress the elevated HMG CoA reductase with mevalonate may prove useful in potentiating the effectiveness of mevinolin as a hypocholesterolemic agent. Lovastatin 125-134 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 37-54 7380744-0 1980 Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. Lovastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 72-119 33930349-5 2021 We found that various statins, including pitavastatin, atorvastatin, fluvastatin, and lovastatin, but not squalene synthase inhibitor, repressed IL-1beta release upon MWCNT stimulation. Lovastatin 86-96 interleukin 1 alpha Mus musculus 145-153 34048842-9 2021 In addition, Abeta plaque area and contents of soluble Abeta1-40 and Abeta1-42 in the hippocampal tissues were decreased upon lovastatin treatment. Lovastatin 126-136 amyloid beta (A4) precursor protein Mus musculus 13-18 34048842-10 2021 Furthermore, lovastatin reversed sevoflurane-induced Abeta accumulation via up-regulating IDE expression, and down-regulating amyloid precursor protein (APP)-related protein expression (beta-C-terminal fragment (CTF), BACE1 and gamma-secretase). Lovastatin 13-23 amyloid beta (A4) precursor protein Mus musculus 53-58 34048842-10 2021 Furthermore, lovastatin reversed sevoflurane-induced Abeta accumulation via up-regulating IDE expression, and down-regulating amyloid precursor protein (APP)-related protein expression (beta-C-terminal fragment (CTF), BACE1 and gamma-secretase). Lovastatin 13-23 insulin degrading enzyme Mus musculus 90-93 34048842-10 2021 Furthermore, lovastatin reversed sevoflurane-induced Abeta accumulation via up-regulating IDE expression, and down-regulating amyloid precursor protein (APP)-related protein expression (beta-C-terminal fragment (CTF), BACE1 and gamma-secretase). Lovastatin 13-23 beta-secretase 1 Rattus norvegicus 218-223 34048842-11 2021 In conclusion, lovastatin alleviates sevoflurane-induced cognitive deficient in aged rats via promoting Abeta degradation and reducing Abeta production. Lovastatin 15-25 amyloid beta precursor protein Rattus norvegicus 104-109 34048842-11 2021 In conclusion, lovastatin alleviates sevoflurane-induced cognitive deficient in aged rats via promoting Abeta degradation and reducing Abeta production. Lovastatin 15-25 amyloid beta precursor protein Rattus norvegicus 135-140 33987937-0 2021 Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21. Lovastatin 0-10 mitogen-activated protein kinase 3 Homo sapiens 56-62 33987937-0 2021 Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21. Lovastatin 0-10 tumor protein p53 Homo sapiens 125-128 33987937-0 2021 Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21. Lovastatin 0-10 H3 histone pseudogene 16 Homo sapiens 141-144 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 signal transducer and activator of transcription 3 Homo sapiens 52-57 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 mitogen-activated protein kinase 3 Homo sapiens 67-73 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 tumor protein p53 Homo sapiens 129-132 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 mitogen-activated protein kinase 3 Homo sapiens 162-168 33987937-4 2021 At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21. Lovastatin 20-30 H3 histone pseudogene 16 Homo sapiens 196-199 33987937-5 2021 However, p21 played a pro-survival role in this setting, as its inhibition by UC2288 further reduced cell survival in PEL cells undergoing Lovastatin treatment. Lovastatin 139-149 H3 histone pseudogene 16 Homo sapiens 9-12 33987937-6 2021 In conclusion, this study suggests that Lovastatin may represent a valid therapeutic alternative against PEL cells, especially if used in combination with p21 inhibitors. Lovastatin 40-50 H3 histone pseudogene 16 Homo sapiens 155-158 33608672-0 2021 Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin. Lovastatin 143-153 KRAS proto-oncogene, GTPase Homo sapiens 52-56 34048842-0 2021 Lovastatin attenuates sevoflurane-induced cognitive disorder in aged rats via reducing Abeta accumulation. Lovastatin 0-10 amyloid beta precursor protein Rattus norvegicus 87-92 34048842-6 2021 The results showed that lovastatin enhanced exosomal IDE secretion from sevoflurane-exposed BV-2 cells and promoted Abeta degradation. Lovastatin 24-34 insulin degrading enzyme Mus musculus 53-56 34048842-6 2021 The results showed that lovastatin enhanced exosomal IDE secretion from sevoflurane-exposed BV-2 cells and promoted Abeta degradation. Lovastatin 24-34 amyloid beta (A4) precursor protein Mus musculus 116-121 34048842-7 2021 Lovastatin treatment also inhibited the increased expressions of beta-secretase 1 (BACE1) and gamma-secretase in hippocampal neurons under sevoflurane exposure in vitro. Lovastatin 0-10 beta-secretase 1 Rattus norvegicus 65-81 34048842-7 2021 Lovastatin treatment also inhibited the increased expressions of beta-secretase 1 (BACE1) and gamma-secretase in hippocampal neurons under sevoflurane exposure in vitro. Lovastatin 0-10 beta-secretase 1 Rattus norvegicus 83-88 32892346-6 2021 Through fermentation, the production of lovastatin in fermentation broth could reach up to 32.97 +- 0.17 mug mL-1 and the total antioxidant capacity was improved by more than two times. Lovastatin 40-50 L1 cell adhesion molecule Mus musculus 109-113 33716161-5 2021 Inhibition of cholesterol metabolism with lovastatin diminishes neuronal ApoE4"s stimulatory effects. Lovastatin 42-52 apolipoprotein E Homo sapiens 73-78 33740503-6 2021 Conversely, ALDH2 mutant or ALDH2 deficiency in AKI or AKO mice stabilizes HMGCR, resulting in enhanced cholesterol synthesis, which can be reversed by Lovastatin. Lovastatin 152-162 aldehyde dehydrogenase 2, mitochondrial Mus musculus 12-17 33740503-6 2021 Conversely, ALDH2 mutant or ALDH2 deficiency in AKI or AKO mice stabilizes HMGCR, resulting in enhanced cholesterol synthesis, which can be reversed by Lovastatin. Lovastatin 152-162 aldehyde dehydrogenase 2, mitochondrial Mus musculus 28-33 33740503-6 2021 Conversely, ALDH2 mutant or ALDH2 deficiency in AKI or AKO mice stabilizes HMGCR, resulting in enhanced cholesterol synthesis, which can be reversed by Lovastatin. Lovastatin 152-162 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 75-80 33742146-10 2021 Treatment of cells with the specific BMP inhibitor Noggin as well as PTEN knockdown and transfection of cells with a constitutively active form of AKT abolishes the effect of Lovastatin on mTOR phosphorylation. Lovastatin 175-185 noggin Homo sapiens 51-57 33742146-10 2021 Treatment of cells with the specific BMP inhibitor Noggin as well as PTEN knockdown and transfection of cells with a constitutively active form of AKT abolishes the effect of Lovastatin on mTOR phosphorylation. Lovastatin 175-185 phosphatase and tensin homolog Homo sapiens 69-73 33742146-10 2021 Treatment of cells with the specific BMP inhibitor Noggin as well as PTEN knockdown and transfection of cells with a constitutively active form of AKT abolishes the effect of Lovastatin on mTOR phosphorylation. Lovastatin 175-185 AKT serine/threonine kinase 1 Homo sapiens 147-150 33742146-10 2021 Treatment of cells with the specific BMP inhibitor Noggin as well as PTEN knockdown and transfection of cells with a constitutively active form of AKT abolishes the effect of Lovastatin on mTOR phosphorylation. Lovastatin 175-185 mechanistic target of rapamycin kinase Homo sapiens 189-193 33608672-4 2021 In this study we investigated the effect of a combination of 2-deoxy-D-glucose with lovastatin (a known inhibitor of mevalonate pathway and oxidative phosphorylation) on growth of KRAS-mutant human colorectal cancer cell lines HCT116 and LoVo. Lovastatin 84-94 KRAS proto-oncogene, GTPase Homo sapiens 180-184 33237691-13 2000 One needs to be aware that certain drugs that are used to treat COVID-19 infections may interact with lipid lowering drugs. Remdesivir is metabolized by the Cyp3A4 pathway and statins that are also metabolized by this pathway should be avoided (atorvastatin, simvastatin, and lovastatin). Lovastatin 275-285 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 33445966-6 2021 In bioactivity, the lovastatin analogues 5, 6, 9 and 10 showed potential immunosuppressive activity against anti-CD3/anti-CD28 monoclonal antibodies (mAbs)-irritated murine splenocytes proliferation, with IC50 values ranging from (5.30 +- 0.51) muM to (16.51 +- 1.62) muM. Lovastatin 20-30 CD247 antigen Mus musculus 113-116 33445966-6 2021 In bioactivity, the lovastatin analogues 5, 6, 9 and 10 showed potential immunosuppressive activity against anti-CD3/anti-CD28 monoclonal antibodies (mAbs)-irritated murine splenocytes proliferation, with IC50 values ranging from (5.30 +- 0.51) muM to (16.51 +- 1.62) muM. Lovastatin 20-30 CD28 antigen Mus musculus 122-126 33459228-7 2021 The statins like Simvastatin, Lovastatin, and Atorvastatin are substrates of CYP3A4 enzyme and P-glycoprotein and their concomitant use with the drugs inhibiting or inducing them would result in changes in plasma concentrations and toxicity/efficacy. Lovastatin 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 33459228-7 2021 The statins like Simvastatin, Lovastatin, and Atorvastatin are substrates of CYP3A4 enzyme and P-glycoprotein and their concomitant use with the drugs inhibiting or inducing them would result in changes in plasma concentrations and toxicity/efficacy. Lovastatin 30-40 ATP binding cassette subfamily B member 1 Homo sapiens 95-109 33408297-0 2021 Effects of fenofibrate and its combination with lovastatin on the expression of genes involved in skeletal muscle atrophy, including FoxO1 and its targets. Lovastatin 48-58 forkhead box O1 Mus musculus 133-138 33408297-8 2021 When the effect of combination treatment with fenofibrate and lovastatin was investigated, a significant increase in FoxO1 protein levels was observed despite the lack of deterioration of muscle atrophy. Lovastatin 62-72 forkhead box O1 Mus musculus 117-122 33408297-9 2021 Collectively, our findings suggest that a high dose of fenofibrate over one week causes skeletal muscle atrophy via enhancement of FoxO1, and combination treatment with fenofibrate and lovastatin may further increase FoxO1 protein level. Lovastatin 185-195 forkhead box O1 Mus musculus 217-222 32998959-6 2020 Here, we determined the potential of lovastatin, simvastatin, and rosuvastatin in preclinically modulating epidermal growth factor receptor (EGFR) and prostate-specific membrane antigen (PSMA) receptor density at the tumor cell surface. Lovastatin 37-47 epidermal growth factor receptor Homo sapiens 107-139 32998959-6 2020 Here, we determined the potential of lovastatin, simvastatin, and rosuvastatin in preclinically modulating epidermal growth factor receptor (EGFR) and prostate-specific membrane antigen (PSMA) receptor density at the tumor cell surface. Lovastatin 37-47 epidermal growth factor receptor Homo sapiens 141-145 33514686-0 2021 SHP2-mediated mitophagy boosted by lovastatin in neuronal cells alleviates parkinsonism in mice. Lovastatin 35-45 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 0-4 33224343-5 2020 Among statins, rosuvastatin had the strongest interaction with CRP (pKi = 16.14), followed by fluvastatin (pKi = 15.58), pitavastatin (pKi = 15.26), atorvastatin (pKi = 14.68), pravastatin (pKi = 13.95), simvastatin (pKi = 7.98) and lovastatin (pKi = 7.10). Lovastatin 233-243 C-reactive protein Homo sapiens 63-66 33250768-5 2020 Furthermore, we found that the expression of PTTG1 was markedly suppressed by lipophilic statins, such as simvastatin, fluvastatin, mevastatin, and lovastatin, but not by hydrophilic pravastatin. Lovastatin 148-158 PTTG1 regulator of sister chromatid separation, securin Homo sapiens 45-50 32727917-0 2020 Clinical trial in a dish using iPSCs shows lovastatin improves endothelial dysfunction and cellular cross-talk in LMNA cardiomyopathy. Lovastatin 43-53 lamin A/C Homo sapiens 114-118 32782396-0 2020 Lovastatin improves endothelial cell function in LMNA-related DCM. Lovastatin 0-10 lamin A/C Homo sapiens 49-53 32729746-3 2020 Potent inhibitors of cytochrome P450 (CYP) 3A4 significantly increase plasma concentrations of the active forms of simvastatin, lovastatin, and atorvastatin. Lovastatin 128-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-46 32651266-2 2020 Recently, we compared the efficacy of lovastatin to the more potent and brain-penetrant drug simvastatin for correcting phenotypes in the Fmr1-/y mouse (Muscas et al., 2019). Lovastatin 38-48 fragile X messenger ribonucleoprotein 1 Mus musculus 138-142 32727917-7 2020 Gain-of-function studies showed that treatment of LMNA iPSC-ECs with KLF2 agonists, including lovastatin, rescued the EC dysfunction. Lovastatin 94-104 lamin A/C Homo sapiens 50-54 32727917-7 2020 Gain-of-function studies showed that treatment of LMNA iPSC-ECs with KLF2 agonists, including lovastatin, rescued the EC dysfunction. Lovastatin 94-104 Kruppel like factor 2 Homo sapiens 69-73 32727917-8 2020 Patients with LMNA-related DCM treated with lovastatin showed improvements in clinical endothelial dysfunction as indicated by increased reactive hyperemia index. Lovastatin 44-54 lamin A/C Homo sapiens 14-18 32305147-9 2020 Increased myocyte cross sectional area, cardiac interstitial fibrosis, immunoreactivity of cardiac collagen-I and III and cardiac TIMP-2 activation, were significantly reduced following G226 treatment. Lovastatin 186-190 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 130-136 32305147-10 2020 Although we did not observe improvement in GFR, G226 significantly reduced renal interstitial fibrosis, diminished renal collagen-I and -IV, kidney injury molecule-1 immunoreactivity as well as macrophage infiltration and SMAD2 phosphorylation. Lovastatin 48-52 SMAD family member 2 Rattus norvegicus 222-227 31628482-3 2020 The objectives of this study were to determine whether treatment of patients with RA with lovastatin decreased CRP or reduced disease activity. Lovastatin 90-100 C-reactive protein Homo sapiens 111-114 31628482-4 2020 METHODS: We conducted a randomized double-blind placebo-controlled 12 week trial of lovastatin vs placebo in 64 RA patients with mild clinical disease activity but an elevated CRP. Lovastatin 84-94 C-reactive protein Homo sapiens 176-179 31628482-12 2020 A post hoc analysis of subjects not using biologic therapy demonstrated a significantly greater proportion achieving >=20% reduction in CRP from baseline in the lovastatin group compared with placebo (P-value = 0.007). Lovastatin 161-171 C-reactive protein Homo sapiens 136-139 31628482-16 2020 Lovastatin had a modest effect on CRP in subjects not using biologics, suggesting statins may be anti-inflammatory in selected patients. Lovastatin 0-10 C-reactive protein Homo sapiens 34-37 32391276-9 2020 We already identified the first MACC1 transcriptional inhibitors, such as lovastatin, by high-throughput screening of clinically approved small molecule drugs. Lovastatin 74-84 MET transcriptional regulator MACC1 Homo sapiens 32-37 32421147-7 2020 Prior incubation with simvastatin, lovastatin, and atorvastatin inhibited TGF-beta2-mediated MMP-2 and MMP-9 expression and activities. Lovastatin 35-45 transforming growth factor beta 2 Homo sapiens 74-83 32421147-7 2020 Prior incubation with simvastatin, lovastatin, and atorvastatin inhibited TGF-beta2-mediated MMP-2 and MMP-9 expression and activities. Lovastatin 35-45 matrix metallopeptidase 2 Homo sapiens 93-98 32421147-7 2020 Prior incubation with simvastatin, lovastatin, and atorvastatin inhibited TGF-beta2-mediated MMP-2 and MMP-9 expression and activities. Lovastatin 35-45 matrix metallopeptidase 9 Homo sapiens 103-108 32399094-9 2020 Conclusions: These results indicate, based upon the binding energy of pitavastatin, rosuvastatin, lovastatin, and fluvastatin, that statins could be efficient SARS-CoV-2 Mpro inhibitors. Lovastatin 98-108 NEWENTRY Severe acute respiratory syndrome-related coronavirus 170-174 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Lovastatin 153-163 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 31628882-6 2020 The 16 cases of statin-clarithromycin adverse drug reactions (rhabdomyolysis (n = 14) or less severe clinical myopathy) involved a CYP3A4-metabolized statin (simvastatin, lovastatin or atorvastatin). Lovastatin 171-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Lovastatin 450-460 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Lovastatin 450-460 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Lovastatin 450-460 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142