PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23166513-6 2012 Furthermore, inter-individual variation in statin-induced RHOA mRNA expression measured in vitro in CAP LCLs was correlated with the changes in plasma total cholesterol, LDL-cholesterol, and APOB induced by simvastatin treatment (40 mg/d for 6 wk) of the individuals from whom these cell lines were derived. Cholesterol 157-168 ras homolog family member A Homo sapiens 58-62 23166513-6 2012 Furthermore, inter-individual variation in statin-induced RHOA mRNA expression measured in vitro in CAP LCLs was correlated with the changes in plasma total cholesterol, LDL-cholesterol, and APOB induced by simvastatin treatment (40 mg/d for 6 wk) of the individuals from whom these cell lines were derived. Cholesterol 174-185 ras homolog family member A Homo sapiens 58-62 23166513-7 2012 Moreover, the minor allele of rs11716445, a SNP located in a novel cryptic RHOA exon, dramatically increased inclusion of the exon in RHOA transcripts during splicing and was associated with a smaller LDL-cholesterol reduction in response to statin treatment in 1,886 participants from the CAP and Pravastatin Inflamation and CRP Evaluation (PRINCE; pravastatin 40 mg/d) statin clinical trials. Cholesterol 205-216 ras homolog family member A Homo sapiens 75-79 23166513-7 2012 Moreover, the minor allele of rs11716445, a SNP located in a novel cryptic RHOA exon, dramatically increased inclusion of the exon in RHOA transcripts during splicing and was associated with a smaller LDL-cholesterol reduction in response to statin treatment in 1,886 participants from the CAP and Pravastatin Inflamation and CRP Evaluation (PRINCE; pravastatin 40 mg/d) statin clinical trials. Cholesterol 205-216 ras homolog family member A Homo sapiens 134-138 23166513-8 2012 Thus, an unbiased filter approach based on transcriptome-wide profiling identified RHOA as a gene contributing to variation in LDL-cholesterol response to statin, illustrating the power of this approach for identifying candidate genes involved in drug response phenotypes. Cholesterol 131-142 ras homolog family member A Homo sapiens 83-87 17495238-0 2007 Elevated cholesterol levels in the plasma membranes of macrophages inhibit migration by disrupting RhoA regulation. Cholesterol 9-20 ras homolog family member A Homo sapiens 99-103 23166513-0 2012 RHOA is a modulator of the cholesterol-lowering effects of statin. Cholesterol 27-38 ras homolog family member A Homo sapiens 0-4 20348106-0 2010 Binding of PDZ-RhoGEF to ATP-binding cassette transporter A1 (ABCA1) induces cholesterol efflux through RhoA activation and prevention of transporter degradation. Cholesterol 77-88 ras homolog family member A Homo sapiens 104-108 20348106-8 2010 Finally, depletion of RhoA or RhoGEFs/RhoA reduces the cholesterol efflux when transcriptional regulation via PPARgamma is eliminated. Cholesterol 55-66 ras homolog family member A Homo sapiens 22-26 20348106-8 2010 Finally, depletion of RhoA or RhoGEFs/RhoA reduces the cholesterol efflux when transcriptional regulation via PPARgamma is eliminated. Cholesterol 55-66 ras homolog family member A Homo sapiens 38-42 20348106-9 2010 Taken together, our results have identified a novel physical and functional interaction between ABCA1 and PDZ-RhoGEF/LARG, which activates RhoA, resulting in ABCA1 stabilization and cholesterol efflux activity. Cholesterol 182-193 ras homolog family member A Homo sapiens 139-143 19546217-7 2009 Thus, a functional N-cadherin-catenin complex occurs in cholesterol-rich membrane microdomains which allows the recruitment of RhoA and the regulation of its activity during myogenesis induction. Cholesterol 56-67 ras homolog family member A Homo sapiens 127-131 17495238-7 2007 Cholesterol loading decreased both the cellular levels of GTP-bound active RhoA and the phosphorylation of myosin light chain. Cholesterol 0-11 ras homolog family member A Homo sapiens 75-79 17495238-8 2007 Expression of constitutively active RhoA largely prevented the inhibition of cell migration by cholesterol loading. Cholesterol 95-106 ras homolog family member A Homo sapiens 36-40 17495238-9 2007 CONCLUSIONS: These results suggest that increases in plasma membrane cholesterol content alter RhoA activation, resulting in inhibition of cell migration. Cholesterol 69-80 ras homolog family member A Homo sapiens 95-99 17237547-6 2006 Geranylgeranyl-pyrophosphate (GGPP), a product of the cholesterol metabolic pathway that serves as a substrate for the posttranslational lipidation of RhoA, was required for membrane localization, but not farnesylpyrophosphate (FPP), the substrate for the lipidation of Ras. Cholesterol 54-65 ras homolog family member A Homo sapiens 151-155 17121865-8 2007 Restoration of caveolae by coincubation of cyclodextrin with cholesterol rescued both RhoA activation and RhoA/cav-1 association in response to strain. Cholesterol 61-72 ras homolog family member A Homo sapiens 86-90 17121865-8 2007 Restoration of caveolae by coincubation of cyclodextrin with cholesterol rescued both RhoA activation and RhoA/cav-1 association in response to strain. Cholesterol 61-72 ras homolog family member A Homo sapiens 106-110 16982613-6 2006 Depletion of cholesterol from rafts with methyl-beta-cyclodextrin caused a redistribution of TNFR1 to nonraft plasma membrane and prevented ligand-induced RhoA activation. Cholesterol 13-24 ras homolog family member A Homo sapiens 155-159 16207810-7 2005 Furthermore, cholesterol was required for dampening Gi-dependent negative feedback on the RhoA signaling pathway, thus enabling RhoA activation and uropod function. Cholesterol 13-24 ras homolog family member A Homo sapiens 128-132 15817453-7 2005 A role for RhoA was established, because two inhibitors of Rho protein activity, a geranylgeranyl transferase inhibitor and C3 exoenzyme, increased cholesterol efflux to apoAI (20-35%, p < 0.05), and macrophage expression of dominant-negative RhoA enhanced cholesterol efflux to apoAI (20%, p < 0.05). Cholesterol 148-159 ras homolog family member A Homo sapiens 11-15 16207810-7 2005 Furthermore, cholesterol was required for dampening Gi-dependent negative feedback on the RhoA signaling pathway, thus enabling RhoA activation and uropod function. Cholesterol 13-24 ras homolog family member A Homo sapiens 90-94 15817453-0 2005 Regulation of macrophage cholesterol efflux through hydroxymethylglutaryl-CoA reductase inhibition: a role for RhoA in ABCA1-mediated cholesterol efflux. Cholesterol 134-145 ras homolog family member A Homo sapiens 111-115 15817453-7 2005 A role for RhoA was established, because two inhibitors of Rho protein activity, a geranylgeranyl transferase inhibitor and C3 exoenzyme, increased cholesterol efflux to apoAI (20-35%, p < 0.05), and macrophage expression of dominant-negative RhoA enhanced cholesterol efflux to apoAI (20%, p < 0.05). Cholesterol 260-271 ras homolog family member A Homo sapiens 11-15 15817453-9 2005 Atorvastatin treatment activated peroxisome proliferator activated receptor gamma and increased LXR-mediated gene expression suggesting that atorvastatin induces cholesterol efflux through a molecular cascade involving inhibition of RhoA signaling, leading to increased peroxisome proliferator activated receptor gamma activity, enhanced LXR activation, increased ABCA1 expression, and cholesterol efflux. Cholesterol 162-173 ras homolog family member A Homo sapiens 233-237 33597925-4 2020 The inhibitory effect of simvastatin on TGF-beta-induced RhoA, ROCK1, and alpha-SMA expression could be reversed by geranylgeranyl pyrophosphate, an intermediate in the biosynthesis of cholesterol. Cholesterol 185-196 ras homolog family member A Homo sapiens 57-61 34147675-11 2022 Knocking down Prkaca, inhibiting RhoA activity can all reverse cholesterol-induced elevation of BNP and inflammatory factors. Cholesterol 63-74 ras homolog family member A Homo sapiens 33-37 34147675-12 2022 CONCLUSION: ASTER B-mediated intracellular accumulation of cholesterol in cardiac muscle cells may cause cardiomyocyte damage and inflammatory factor infiltration through PKA-Ca2+-RhoA pathways. Cholesterol 59-70 ras homolog family member A Homo sapiens 180-184 32259482-4 2020 ASTER-B/C-mediated internalization of plasma membrane cholesterol activates soluble adenylyl cyclase (sAC; ADCY10), triggering a calcium-RhoA-mediated pathway that suppresses beta-TrCP/proteasome-mediated TAZ degradation. Cholesterol 54-65 ras homolog family member A Homo sapiens 137-141 32259482-6 2020 The cholesterol-TAZ pathway is present in primary human hepatocytes, and associations among liver cholesterol, TAZ, and RhoA in human NASH liver are consistent with the pathway. Cholesterol 4-15 ras homolog family member A Homo sapiens 120-124 25243430-5 2014 Lipopolysaccharide induced RhoA membrane translocation that was attenuated by methyl-beta-cyclodextrin (cholesterol sequester) or targeted mutation of caveolin-1. Cholesterol 104-115 ras homolog family member A Homo sapiens 27-31