Mycorrhizal roots of the deciduous trees European beech (Fagus sylvatica (L.)) and Sessile oak (Quercus petraea (MattuschkaLiebl.)) and the conifers Norway spruce (Picea abies (L.) H. Karst.) and European larch (Larix...Mycorrhizal roots of the deciduous trees European beech (Fagus sylvatica (L.)) and Sessile oak (Quercus petraea (MattuschkaLiebl.)) and the conifers Norway spruce (Picea abies (L.) H. Karst.) and European larch (Larix decidua (Mill.)) associated with the ectomycorrhizal fungi matt bolete (Xerocomus pruinatus (Fries 1835)) or bay bolete (X. badius (Fries 1818)) were analysed with respect to the occurrence of dihydrolipoyl dehydrogenase (EC 1.8.1.4) allozymes. In root tissues of the two deciduous trees, two gene loci could be visualized after cellulose acetate electrophoresis while three loci were expressed in root tissues of the two coniferous species. The two fungal species and further ectomycorrhizal fungi expressed exclusively one dihydrolipoyl dehydrogenase gene. In Xerocomus pruinatus and X. badius, the dihydrolipoyl dehydrogenase gene consists of 1460 bp and 1370 bp, respectively, including five introns each consisting of 52 bp. Their DNA sequences correspond to 70 to 90% to other fungal dihydrolipoyl dehydrogenase genes. One monomer of the dimeric dihydrolipoyl dehydrogenase enzyme consists of 486 (X. pruinatus) or 454 (X. badius) amino acids which sum up to a molecular mass of 55 kDa (X. pruinatus), respectively 52 kDa (X. badius). The number of positively charged amino acid residues makes 79 (X. pruinatus) and 68 (X. badius) and the number of negatively charged amino acid residues was calculated to make 46 (X. pruinatus) and 48 (X. badius);isoelectric points make 9.99 (X. pruinatus) and 9.68 (X. badius). Calculated three dimensional structures reveal a short NADH binding site being part of a larger FAD-binding site and a binding/dimerization domain.展开更多
Primary biliary cholangitis(PBC)is a chronic cholestatic progressive liver disease and one of the most important progressive cholangiopathies in adults.Damage to cholangiocytes triggers the development of intrahepatic...Primary biliary cholangitis(PBC)is a chronic cholestatic progressive liver disease and one of the most important progressive cholangiopathies in adults.Damage to cholangiocytes triggers the development of intrahepatic cholestasis,which progresses to cirrhosis in the terminal stage of the disease.Accumulating data indicate that damage to biliary epithelial cells[(BECs),cholangiocytes]is most likely associated with the intracellular accumulation of bile acids,which have potent detergent properties and damaging effects on cell membranes.The mechanisms underlying uncontrolled bile acid intake into BECs in PBC are associated with pH change in the bile duct lumen,which is controlled by the bicarbonate(HCO3-)buffer system“biliary HCO3-umbrella”.The impaired production and entry of HCO3-from BECs into the bile duct lumen is due to epigenetic changes in expression of the X-linked microRNA 506.Based on the growing body of knowledge on the molecular mechanisms of cholangiocyte damage in patients with PBC,we propose a hypothesis explaining the pathogenesis of the first morphologic(ductulopenia),immunologic(antimitochondrial autoantibodies)and clinical(weakness,malaise,rapid fatigue)signs of the disease in the asymptomatic stage.This review focuses on the consideration of these mechanisms.展开更多
文摘Mycorrhizal roots of the deciduous trees European beech (Fagus sylvatica (L.)) and Sessile oak (Quercus petraea (MattuschkaLiebl.)) and the conifers Norway spruce (Picea abies (L.) H. Karst.) and European larch (Larix decidua (Mill.)) associated with the ectomycorrhizal fungi matt bolete (Xerocomus pruinatus (Fries 1835)) or bay bolete (X. badius (Fries 1818)) were analysed with respect to the occurrence of dihydrolipoyl dehydrogenase (EC 1.8.1.4) allozymes. In root tissues of the two deciduous trees, two gene loci could be visualized after cellulose acetate electrophoresis while three loci were expressed in root tissues of the two coniferous species. The two fungal species and further ectomycorrhizal fungi expressed exclusively one dihydrolipoyl dehydrogenase gene. In Xerocomus pruinatus and X. badius, the dihydrolipoyl dehydrogenase gene consists of 1460 bp and 1370 bp, respectively, including five introns each consisting of 52 bp. Their DNA sequences correspond to 70 to 90% to other fungal dihydrolipoyl dehydrogenase genes. One monomer of the dimeric dihydrolipoyl dehydrogenase enzyme consists of 486 (X. pruinatus) or 454 (X. badius) amino acids which sum up to a molecular mass of 55 kDa (X. pruinatus), respectively 52 kDa (X. badius). The number of positively charged amino acid residues makes 79 (X. pruinatus) and 68 (X. badius) and the number of negatively charged amino acid residues was calculated to make 46 (X. pruinatus) and 48 (X. badius);isoelectric points make 9.99 (X. pruinatus) and 9.68 (X. badius). Calculated three dimensional structures reveal a short NADH binding site being part of a larger FAD-binding site and a binding/dimerization domain.
文摘Primary biliary cholangitis(PBC)is a chronic cholestatic progressive liver disease and one of the most important progressive cholangiopathies in adults.Damage to cholangiocytes triggers the development of intrahepatic cholestasis,which progresses to cirrhosis in the terminal stage of the disease.Accumulating data indicate that damage to biliary epithelial cells[(BECs),cholangiocytes]is most likely associated with the intracellular accumulation of bile acids,which have potent detergent properties and damaging effects on cell membranes.The mechanisms underlying uncontrolled bile acid intake into BECs in PBC are associated with pH change in the bile duct lumen,which is controlled by the bicarbonate(HCO3-)buffer system“biliary HCO3-umbrella”.The impaired production and entry of HCO3-from BECs into the bile duct lumen is due to epigenetic changes in expression of the X-linked microRNA 506.Based on the growing body of knowledge on the molecular mechanisms of cholangiocyte damage in patients with PBC,we propose a hypothesis explaining the pathogenesis of the first morphologic(ductulopenia),immunologic(antimitochondrial autoantibodies)and clinical(weakness,malaise,rapid fatigue)signs of the disease in the asymptomatic stage.This review focuses on the consideration of these mechanisms.
