Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aminotransferases catalyze the reversible pyridoxal phosphate-dependent transfer of amino groups from amino acids to oxo acids and play important roles for the balance between carbon and nitrogen metabolism. In this report, four aminotransferases (Ap1-Ap4) from a halotolerant cyanobacterium Aphanothece halophytica were examined. The results revealed that Ap1 and Ap2 exhibited the aspartate:2-oxoglutarate aminotransferase (AspAT) activity whereas Ap2 catalyzed further aminotransferase activities with alanine (AlaAT) and LL-diaminopimelate (an intermediate for the synthesis of Lys/peptidoglycan) as amino donors. Ap4 exhibited bifunctional aminotransferase with phosphoserine (PSAT) and glycine (GGAT) as amino donors. No activity was observed for Ap3. We identified third gene encoding phosphoserine phosphatase (PSP) in phosphorylate serine biosynthetic pathway. The levels of mRNA for Ap2 and ApMurE encoding UDP-N-acetylmuramoyl-L-alanyl-D-glutamate-2,6-diaminopimelate ligase were increased after salt stress. These results suggest the link among photorespiratory metabolite (serine, glycine, glyoxylate), phosphorylate serine biosynthetic pathway and aspartate metabolism via aminotransferases for the synthesis of peptidoglycan and betaine under salt stress conditions.
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PMID:Functional characterization of aminotransferase involved in serine and aspartate metabolism in a halotolerant cyanobacterium, Aphanothece halophytica. 3134 53

The aim of present study was to investigate hematological, biochemical and oxidative state parameters in cattle spontaneously infected with bovine leukemia virus (BLV). A total 500 cattle were examined for BLV infection by enzyme linked immunosorbent assay (ELISA). Eighty (16%) animals were positive for BLV infection. Biochemical and oxidative stress markers revealed significant increases in liver enzymes Alanine Transaminase, Aspartate Transaminase and Alkaline Phosphatase (ALT, AST and ALP) activities, creatinine level and superoxide dismutase (SOD) activity associated with a significant decrease in calcium level in seropositive cattle in comparison with seronegative cattle. Meanwhile, non-significant changes were reported in levels of malondialdehyde (MDA), Nitric oxide (NO), reduced glutathione (GSH) and hematological parameters in seropositive cattle in comparison with seronegative cattle.
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PMID:Oxidative state markers and clinicopathological findings associated with bovine leukemia virus infection in cattle. 3140 Apr 42

Familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is a rare genetic disease characterized by low HDL-C levels, low plasma cholesterol esterification, and the formation of Lipoprotein-X (Lp-X), an abnormal cholesterol-rich lipoprotein particle. LCAT deficiency causes corneal opacities, normochromic normocytic anemia, and progressive renal disease due to Lp-X deposition in the glomeruli. Recombinant LCAT is being investigated as a potential therapy for this disorder. Several hepatic disorders, namely primary biliary cirrhosis, primary sclerosing cholangitis, cholestatic liver disease, and chronic alcoholism also develop Lp-X, which may contribute to the complications of these disorders. We aimed to test the hypothesis that an increase in plasma LCAT could prevent the formation of Lp-X in other diseases besides FLD. We generated a murine model of intrahepatic cholestasis in LCAT-deficient (KO), wild type (WT), and LCAT-transgenic (Tg) mice by gavaging mice with alpha-naphthylisothiocyanate (ANIT), a drug well known to induce intrahepatic cholestasis. Three days after the treatment, all mice developed hyperbilirubinemia and elevated liver function markers (ALT, AST, Alkaline Phosphatase). The presence of high levels of LCAT in the LCAT-Tg mice, however, prevented the formation of Lp-X and other plasma lipid abnormalities in WT and LCAT-KO mice. In addition, we demonstrated that multiple injections of recombinant human LCAT can prevent significant accumulation of Lp-X after ANIT treatment in WT mice. In summary, LCAT can protect against the formation of Lp-X in a murine model of cholestasis and thus recombinant LCAT could be a potential therapy to prevent the formation of Lp-X in other diseases besides FLD.
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PMID:LCAT protects against Lipoprotein-X formation in a murine model of drug-induced intrahepatic cholestasis. 3189 24

Disordered glucose and lipid metabolism contributes to the progression of several liver diseases, while the upregulation of phosphatase and tensin homology deleted on chromosome ten (PTEN), a well-known tumour suppressor gene, can improve the condition through metabolic programming. This study first characterized the metabolic profiles and the involvement of PTEN in the hepatic fibrosis induced by Schistosoma japonicum (S. japonicum) to provide a novel clue for metabolism-targeted treatment. Compared with control mice, infected mice showed infiltrated immune cells in their livers, increased levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and decreased glucose levels in their sera. The expression of key enzymes in the glycolytic pathway was significantly increased, and the expression of gluconeogenic genes was distinctly decreased. Moreover, the infection upregulated the hepatic expression of enzymes involved in fatty acid oxidation, which was consistent with the decreased number of lipid droplets in livers and the lowered levels of triglyceride in sera. Consistently, PTEN and its downstream signalling were significantly inhibited. In vitro, soluble egg antigen (SEA) downregulated the expression of PTEN in both the macrophage RAW264.7 cell line and the murine hepatocellular carcinoma HEP1-6 cell line, and induced a metabolic phenotype similar to the in vivo results. Overall, this study showed that S. japonicum infection induced the reprogramming of glucose and lipid metabolism in mice during the period of liver fibrosis and that SEA could act as a modulator to trigger such a metabolic switch in macrophages and hepatocytes. PTEN might play an essential role in mediating these metabolic reprogramming events.
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PMID:The Metabolic Reprogramming Profiles in the Liver Fibrosis of Mice Infected with Schistosoma japonicum. 3190 86

Saskatoon berry (Amelanchier alnifolia) is a potential functional food containing anthocyanins and flavonols, as well as ellagitannins and phenolic acids. We have determined the potential therapeutic effects of Saskatoon berry in diet-induced metabolic syndrome. Nine- to ten-week-old male Wistar rats were randomly assigned to four groups. Two groups were fed on control diets, either corn starch (C) or high-carbohydrate, high-fat diet (H) respectively, for 16 weeks. Two further groups were fed on C or H diet for 16 weeks with Saskatoon berry powder added to the diet for the final 8 weeks (CSSK, HSSK). After 16 weeks, H rats showed symptoms of metabolic syndrome, including increased body weight, visceral adiposity, systolic blood pressure, cardiac fibrosis, plasma concentrations of triglycerides and non-esterified fatty acids, and plasma activities of alanine transaminase and aspartate transaminase. Saskatoon berry intervention normalised body weight and adiposity, improved glucose tolerance, decreased systolic blood pressure, improved heart and liver structure and function with decreased infiltration of inflammatory cells, and decreased plasma total cholesterol. Further, Saskatoon berry normalised liver expression of hexokinase 1 and glycogen phosphorylase and increased glucose 6-phosphatase relative to H rats. These results suggest that Saskatoon berry regulates glycolysis, gluconeogenesis and glycogenesis to improve metabolic syndrome.
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PMID:Saskatoon Berry Amelanchier alnifolia Regulates Glucose Metabolism and Improves Cardiovascular and Liver Signs of Diet-Induced Metabolic Syndrome in Rats. 3223 Sep 55

In this study, we demonstrated the involvement of matrix metalloproteinases (MMPs) in hepatic ischemia/reperfusion (I/R) injury. Our aim is to evaluate the impact of reperfusion on I/R-related changes in RECK, an MMP modulator, and mitogen-activated protein kinase (MAPKs) pathways (ERK, p38, and JNK). Male Wistar rats were either subjected to 60 min partial-hepatic ischemia or sham-operated. After a 60 min or 120 min reperfusion, liver samples were collected for analysis of MMP-2 and MMP-9 by zymography and RECK, TIMP-1, and TIMP-2 content, MAPKs activation (ERK1/2, JNK1/2, and p38), as well as iNOS and eNOS by Western blot. Serum enzymes AST, ALT, and alkaline-phosphatase were quantified. A transitory decrease in hepatic RECK and TIMPs was associated with a transitory increase in both MMP-2 and MMP-9 activity and a robust activation of ERK1/2, JNK1/2, and p38 were detected at 60 min reperfusion. Hepatic expression of iNOS was maximally upregulated at 120 min reperfusion. An increase in eNOS was detected at 120 min reperfusion. I/R evoked significant hepatic injury in a time-dependent manner. These findings provide new insights into the underlying molecular mechanisms of reperfusion in inducing hepatic injury: a transitory decrease in RECK and TIMPs and increases in both MAPK and MMP activity suggest their role as triggering factors of the organ dysfunction.
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PMID:Transient Expression of Reck Under Hepatic Ischemia/Reperfusion Conditions Is Associated with Mapk Signaling Pathways. 3240 97


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