2014
DOI: 10.1016/j.cca.2013.11.010
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ABCG5/ABCG8 in cholesterol excretion and atherosclerosis

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Cited by 153 publications
(100 citation statements)
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“…Consistent with these functions, ABCG5 and ABCG8 are expressed almost exclusively on the brush border membranes of enterocytes and in the canalicular membranes of hepatocytes (Yu et al, 2014). LXRα is regarded as the major regulator of ABCG5 and ABCG8 mRNA expression, and the LXR agonist T0901317 markedly upregulates ABCG5 and ABCG8 expression in the small intestine and liver of wild type but not LXRα knockout mice (GonzalezGranillo et al, 2012;van der Veen et al, 2007).…”
Section: Abcg5 and Abcg8mentioning
confidence: 99%
See 1 more Smart Citation
“…Consistent with these functions, ABCG5 and ABCG8 are expressed almost exclusively on the brush border membranes of enterocytes and in the canalicular membranes of hepatocytes (Yu et al, 2014). LXRα is regarded as the major regulator of ABCG5 and ABCG8 mRNA expression, and the LXR agonist T0901317 markedly upregulates ABCG5 and ABCG8 expression in the small intestine and liver of wild type but not LXRα knockout mice (GonzalezGranillo et al, 2012;van der Veen et al, 2007).…”
Section: Abcg5 and Abcg8mentioning
confidence: 99%
“…Two additional members of the ABC transporter family, ABCG5 and ABCG8, form the obligate heterodimer that limits intestinal absorption and facilitates the biliary secretion of cholesterol and phytosterols (Graf et al, 2002;Yu et al, 2014). Consistent with these functions, ABCG5 and ABCG8 are expressed almost exclusively on the brush border membranes of enterocytes and in the canalicular membranes of hepatocytes (Yu et al, 2014).…”
Section: Abcg5 and Abcg8mentioning
confidence: 99%
“…Specifically, mutations in ABCG5 or ABCG8 impede dimerization of the gene expression products, sterolin 1 or 2, respectively, resulting in prevention of expression at the cellular lumen of canalicular hepatocytes and intestinal brush border enterocytes, where they normally function as efflux pumps to extrude phytosterols into bile for eventual incorporation into chylomicrons and subsequent elimination. 26,27 Diagnosis is validated via plasma sterol profiling by gas chromatography to determine levels of sitosterol, campesterol and stigmasterol. [2][3][4] Only few case reports in patients where sitosterolemia was recognized as a cause of PHT2HC have been previously reported including three Japanese reports of two unrelated subjects and one pair of sisters, [19][20][21] and one report on two unrelated Chinese patients, 22 with a history of xanthoma development during childhood.…”
mentioning
confidence: 99%
“…As principais rotas de efluxo do colesterol hepático são o colesterol livre secretado na bile, o colesterol convertido em sais e ácidos biliares e o secretado por meio do VLDLc (HARVEY e FERRIER, 2012;HSIEH et al 2014;YU et al, 2014).…”
Section: Metabolismo Do Colesterolunclassified
“…(ABCG5) e G8 (ABCG8) inibe a absorção de colesterol e esteróis vegetais da dieta mediando o efluxo destes esteróis a partir dos enterócitos de volta ao lúmen intestinal e promovendo a secreção eficiente de colesterol e esteróis vegetais de hepatócitos para a bile (YU et al, 2014 Ésteres de colesterol são, então, conduzidos à biogênese dos quilomícrons (WANG, 2007;HARVEY e FERRIER, 2012;CASTRO-TORRES et al, 2014).…”
Section: Metabolismo Do Colesterolunclassified