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191.
192.
K B Sprenger 《Clinical physiology and biochemistry》1985,3(4):208-220
In the pathogenesis of hypertension, the importance of intracellular calcium is increasing. Clinical and experimental studies of essential hypertension indicate a pathological increase of intracellular Ca2+ in this disease. In the past, changes in cellular Na+ and its transport mechanisms were considered the triggering factors and Na+-Ca2+ exchange was attributed a decisive influence on intracellular homeostasis. Recently, a reduced Ca2+-binding capacity of the cellular membrane was observed in hypertension, which could have been due to a defect of the Ca2+-ATPase or its control. It is therefore necessary to establish the hypothesis that changes in the cellular Ca2+ metabolism associated with an increase in the intracellular Ca2+ concentration may be the primary cause of hypertension. Disorders of Na+ transport can also be traced to the increase in intracellular Ca2+ and were thus a consequence but not the cause of the increased intracellular Ca2+ concentration. 相似文献
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The NADP(H)-dependent enzyme glucose-fructose oxidoreductase (GFOR) is a classic example of a redox protein that is translocated across a membrane in fully folded form. GFOR is synthesized in the cytoplasm with a 52-residue signal peptide, giving a precursor form, preGFOR, that is fully active and has its cofactor tightly bound. A twin-arginine motif in the signal peptide directs it to a Sec-independent pathway by which it is translocated, in fully folded form, into the periplasm where it functions to produce sorbitol for osmoprotection. We have determined the crystal structures of four different forms of preGFOR, (i) oxidized preGFOR, with succinate bound in the active site, (ii) oxidized preGFOR with glycerol bound, (iii) reduced preGFOR in 0.3 M glucose, and (iv) reduced preGFOR in 1.5 M sorbitol, at resolutions of 2.2, 2.05, 2.5, and 2.6 A, respectively. In all four crystal structures, the signal peptide is disordered, implying a flexibility that may be important for its interaction with the translocation apparatus; a factor contributing to this disorder may be the high positive charge of the protein surface in the region where the signal peptide emerges. This may disfavor a stable association between the signal peptide and the rest of the protein. The crystal structures show that the mature enzyme portion of preGFOR is identical to native GFOR, in structure and cofactor binding, explaining the enzymatic activity of the precursor form. In the glycerol complex, preGFOR(gll), a bound glycerol molecule models the binding of the glucose substrate, with its O1 atom hydrogen bonded to the essential acid/base catalyst, Tyr269, and C1 only 3 A from C4 of the nicotinamide. In the glucose-soaked structure, preGFOR(glu), we identify a conformational change of the nearby Lys181 that probably results from the oxidation of glucose to gluconolactone, and functions to prevent rebinding of glucose prior to the binding of fructose. In this conformational change, the Lys181 side chain moves closer to the nicotinamide ring, stabilized by its increased negative charge. 相似文献
195.