MCD BIO 165A Lecture 5: Paper 5 Notes
29 Nov 2016
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Dysfunction initiates effects of ethanol on golgi morphology. Found at punctate sites, cyto, localized at er. Removes hazardous asgp (terminal galactose, n-acetylgalactosamine, oligosaccs w/ sialic acid) Deficiency -> altered hepatic function, cancer viral hepatitis, cirrhosis content within decr after ethanol exposure. 20% found in rer, 50% in ser/curl, 30% in golgi. Disrupts golgi structure but sar1a expression is not affected. Ethanol impaired giantin function -> altered asgp-r trafficking. Sar1a dysfunction + copii vesicle formation alteration -> impaired golgi delivery of pdia3. Sar 1a silencing/ethanol treatment -> giantin dedimerization, pdia3 arresting in er, golgi architecture alterations. Alcohol treatment -> golgi to plasma membrane trafficking inhibited -> intracellular accumulation of proteins -> hepatocyte ballooning, hypertrophy. Alteration of cop ii vesicle formation -> golgi components cycling disrupted + Results: heaptic adh generated metabolites of ethanol is contributor of golgi fragmentation (fig 1) Ethanol treatment + pyrazole/adh inhibitor -> reduced fragmentation. Conclusion: ethanol metabolites are primary contributors to ethanol-induced.
