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Study utilized humanized mouse model expressing WT (control), G143E and catalytically dead S221A variants of human CES1 in the liver in the absence of endogenous expression of the mouse orthologous gene shows that compared to wild-type CES1, expression of the CES1G143E confers resistance to development of high-fat diet induced hepatic steatosis and leads to improved metabolic profile.
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Which selectively amplified CES1A1 and, if present, also CES1A2.
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These results are consistent with a model in which abrogation of CES1 function attenuates the CYP27A1-LXRalpha-ABCA1 signaling axis by depleting endogenous ligands for the nuclear receptors PPARgamma, RAR, and/or RXR that regulate cholesterol homeostasis.
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Anordrin is predominantly catalyzed by CES1 and CES2 to generate the main active metabolite, anordiol.
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genetic association and pharmacogenomic studies in population in Finland: Data suggest that 2 SNPs in CES1 (rs12443580, rs8192935) are associated with variations in expression of CES1 (in whole blood samples but not in liver); these CES1 SNPs do not affect pharmacokinetics or pharmacodynamics of clopidogrel, an inhibitor of platelet aggregation. A missense mutation in CES1 (rs71647871) impairs hydrolysis of clopidogrel.
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The frequencies of SNVs with a potential functional impact were below 0.02 suggesting limited pharmacogenetic potential for CES1 genotyping.
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none of the selected variations of CES1 had a clinically relevant impact on the metabolism of enalapril
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Study revealed that several nsSNPs significantly impaired CES1 activity on the metabolism of the CES1 substrates enalapril, clopidogrel, and sacubitril.
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Suggest a primary metabolic role for CES1 in the capacity of skin/keratinocytes to mediated biotransformation of penta-ethyl ester prodrug of DTPA.
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These data suggest that infants younger than 3 weeks of age would exhibit significantly lower CES1- and CES2-dependent metabolic clearance compared with older individuals.
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The intestinal transport of oseltamivir, a hCE1 substrate, could be evaluated in subclone #78 cell monolayers.
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An association was identified with a genetic variation in CES1 and early-onset capecitabine-related toxicity.
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Reduced CES1 expression/activity could promote development of METH-PAH.
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These data suggest that CES1 genetic variants and gender are important contributing factors to variability in dabigatran etexilate activation in humans.
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some functional CES1 genetic variants (for example, G143E) may impair ACE inhibitor activation, and consequently affect therapeutic outcomes of ACEI prodrugs.
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HNF4alpha regulated CES1 expression by directly binding to the proximal promoter of CES1.
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We conclude that the -816A>C variant is not associated with interindividual variability in CES1 expression and activity or therapeutic response to ACEI prodrugs
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Our study identified CYP2C19*3 and CES1 rs8192950 as genetic polymorphisms related to recurrent ischemic events in patients with extracranial or intracranial occlusive disease, demonstrating the important roles of CYP2C19 and CES1 in patients treated with clopidogrel
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Data suggest oseltamivir activation is associated with an SNP in CES1 (rs71647871, G143E); in liver from donors with genotype 143G/E activation is 40% of that from donors with genotype 143G/G. Hepatic CES1 expression in females is 17.3% higher than in males; oseltamivir activation rate in females is 27.8% higher than in males. (Liver tissues used were obtained from tissue banks located in the United States.)
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Study confirms previous reports of the CES1P1-CES1 translocation generating the CES1VAR allele with 11 SNPs in the 5'UTR, exon 1, and intron 1 derived from the CES1P1 sequence with decreased CES1 mRNA expression in the human liver by approximately 30% but normal protein expression.
