Chronic ethanol consumption leads to destabilization of rat liver β-galactoside α2,6-sialyltransferase mRNA☆
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Cited by (19)
Alteration of protein glycosylation in liver diseases
2009, Journal of HepatologyCitation Excerpt :A decreased level of dolichol has been observed in rats fed ethanol [24]. The abnormal terminal sialylation can be explained by a decrease in β-galactoside α2,6 sialyltransferase (ST6GalI) mRNA and protein expression and/or an increase in hepatocyte membrane associated sialidase observed during chronic alcohol abuse [25–27]. Oxidation products of ethanol such as acetaldehyde interfere with the N-glycan biosynthesis and/or transfer by binding the involved enzymes.
Down-regulation of liver Galβ1, 4GlcNAc α2, 6-sialyltransferase gene by ethanol significantly correlates with alcoholic steatosis in humans
2008, Metabolism: Clinical and ExperimentalCitation Excerpt :The key enzyme that is responsible for the terminal sialylation of various glycoproteins is Galβl, 4GlcNAc α2, 6-sialyltransferase (ST6Gal1), which mediates the addition of α2, 6-linked sialic acid to glycoproteins and glycolipids in the Golgi compartment. In our ongoing studies in both rats and humans, we have shown that ST6Gal1 messenger RNA (mRNA) expression is markedly reduced in the long-term alcohol group compared with the control group [13-15]. We have shown that the concomitant decreased hepatic ST6Gal1 activity is due to its decreased synthetic rate [6], whereas the down-regulation of ST6Gal1 mRNA is due to its decreased stability [14].
Liver Galβ1,4GlcNAc α2,6-sialyltransferase is down-regulated in human alcoholics: possible cause for the appearance of asialoconjugates
2007, Metabolism: Clinical and ExperimentalCitation Excerpt :Accordingly, we have demonstrated that plasma SIJ is significantly decreased by 50% (P < .001) in human long-term alcoholics of both sexes compared with nondrinkers [14]. In our rat alcohol-feeding model, ST6GalI messenger RNA (mRNA) expression is reduced by as much as 59% by long-term alcohol treatment compared with the pair-fed control group in a dose-dependent manner [15,16]. We have shown that the concomitant decreased hepatic ST6GalI activity is due to its decreased synthetic rate [17], whereas the down-regulation of ST6GalI mRNA is due to its decreased stability [16].
Chronic ethanol consumption down-regulates CMP-NeuAc:GM<inf>3</inf> α2,8-sialyltransferase (ST8Sia-1) gene in the rat brain
2006, Neurochemistry InternationalChronic ethanol consumption upregulates the cytosolic and plasma membrane sialidase genes, but downregulates lysosomal membrane sialidase gene in rat liver
2006, Metabolism: Clinical and ExperimentalChronic ethanol feeding controls the activities of various sialidases by regulating their relative synthetic rates in the rat liver
2005, Metabolism: Clinical and Experimental
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Supported by National Institute for Alcoholism and Alcohol Abuse Grant No. AA08149 (M.R.L.).