ArticleGenes & nutrition2010
Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences.
Article in Genes & nutrition, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The trial behind it
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Alcohol and Prostate Cancer: Time to Draw Conclusions.Biomolecules · 2022Review
- Alcohol-Induced Liver Injury: Down-regulation and Redistribution of Rab3D Results in Atypical Protein Trafficking.Hepatology communications · 2022Article
- cAMP Signaling in Pathobiology of Alcohol Associated Liver Disease.Biomolecules · 2020Review
- Identifying Differentially Expressed MicroRNAs, Target Genes, and Key Pathways Deregulated in Patients with Liver Diseases.International journal of molecular sciences · 2020Article
- Alcohol-induced microtubule acetylation leads to the accumulation of large, immobile lipid droplets.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- The cell biology of the hepatocyte: A membrane trafficking machine.The Journal of cell biology · 2019Review
- Ethanol metabolism by alcohol dehydrogenase or cytochrome PAmerican journal of physiology. Gastrointestinal and liver physiology · 2017Article
- The role of Rab6a and phosphorylation of non-muscle myosin IIA tailpiece in alcohol-induced Golgi disorganization.Scientific reports · 2016Article
- Metabolic derivatives of alcohol and the molecular culprits of fibro-hepatocarcinogenesis: Allies or enemies?World journal of gastroenterology · 2016Review
- Downregulation of the small GTPase SAR1A: a key event underlying alcohol-induced Golgi fragmentation in hepatocytes.Scientific reports · 2015Article
- The Altered Hepatic Tubulin Code in Alcoholic Liver Disease.Biomolecules · 2015Review
- Hepatic microtubule acetylation and stability induced by chronic alcohol exposure impair nuclear translocation of STAT3 and STAT5B, but not Smad2/3.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Alcohol and lipid traffic don't mix.Hepatology (Baltimore, Md.) · 2011Article
- Proteomic analysis of endocytic vesicles: Rab1a regulates motility of early endocytic vesicles.Journal of cell science · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alcoholic liver disease is a major biomedical health concern in the United States. Despite considerable research efforts aimed at understanding the progression of the disease, the specific mechanisms leading to alcohol-induced damage remain elusive. Numerous proteins are known to have alcohol-induced alterations in their dynamics. Defining these defects in protein trafficking is an active area of research. In general, two trafficking pathways are affected: transport of newly synthesized secretory or membrane glycoproteins from the Golgi to the basolateral membrane and clathrin-mediated endocytosis from the sinusoidal surface. Both impaired secretion and internalization require ethanol metabolism and are likely mediated by acetaldehyde. Although the mechanisms by which ethanol exposure impairs protein trafficking are not fully understood, recent work implicates alcohol-induced modifications on tubulin or components of the clathrin machinery as potential mediators. Furthermore, the physiological ramifications of impaired protein trafficking are not fully understood. In this review, we will list and discuss the proteins whose trafficking patterns are known to be impaired by ethanol exposure. We will then describe what is known about the possible mechanisms leading to impaired protein trafficking and how disrupted protein trafficking alters liver function and may explain clinical features of the alcoholic patient.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.