Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genes encoding aspartate kinase (ask), homoserine dehydrogenase (hom), homoserine kinase (thrB) and threonine synthase (thrC) from the obligate methylotroph Methylobacillus flagellatus were cloned. In maxicells hom and thrC directed synthesis of 51 and 48 kDa polypeptides, respectively. The hom, thrB and thrC genes and adjacent DNA areas were sequenced. Of the threonine biosynthesis genes, only hom and thrC were tightly linked in the order hom-thrC. The gene for thymidylate synthase (thyA) followed thrC and the gene for aspartate aminotransferase (aspC) preceded hom. All four genes (aspC-hom-thrC-thyA) were transcribed in the same direction. mRNA analysis indicated that hom-thrC are apparently transcribed in one 7.5 kb transcript in M. flagellatus. Promoter analysis showed the presence of a functional promoter between aspC and hom. No functional promoter was found to be associated with the DNA stretch between hom and thrC. The thrB gene encoded an unusual type of homoserine kinase and was not linked to other threonine biosynthesis genes.
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PMID:Organization of threonine biosynthesis genes from the obligate methylotroph Methylobacillus flagellatus. 1058 37

Alcohol is a globally well-established cause of fatty liver disease (FLD). Increased salt consumption is associated with an increased prevalence of adipocyte hypertrophy and liver injury. In this study, high dietary salt potentiated chronic alcohol-induced hepatic damage. We explored the physiological mechanism of alcoholic FLD in the gastrointestinal tract. Male C57BL/6J mice (8-week-old) were fed a high-salt diet (HSD; 4% NaCl) with or without chronic ethanol (CE) for 1 month. The fecal microbiota, serum biochemical indices, intestinal permeability, level of liver damage, and liver mitochondria were evaluated. The HSD, CE, and their combination (HSDE) significantly changed the gut microbiota's structure, and the HSDE mice contained more probiotic species (e.g., Bifidobacterium and Lactobacillus). The serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels were increased, and the lipid was accumulated in the liver tissues in the CE, HSD, and HSDE groups, which indicated liver damage, especially in the HSDE group. The increased intestinal permeability and mitochondrial dysfunction in the liver cells caused greater injury in the HSDE group than in the other groups. Thus, consuming HSD with alcohol contributes to FLD development and progression.
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PMID:Combination of Chronic Alcohol Consumption and High-Salt Intake Elicits Gut Microbial Alterations and Liver Steatosis in Mice. 3197 84