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排序方式: 共有804条查询结果,搜索用时 15 毫秒
61.
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Shaw FW 《Science (New York, N.Y.)》1929,70(1819):454-455
63.
Arkin IT Xu H Jensen MØ Arbely E Bennett ER Bowers KJ Chow E Dror RO Eastwood MP Flitman-Tene R Gregersen BA Klepeis JL Kolossváry I Shan Y Shaw DE 《Science (New York, N.Y.)》2007,317(5839):799-803
Na+/H+ antiporters are central to cellular salt and pH homeostasis. The structure of Escherichia coli NhaA was recently determined, but its mechanisms of transport and pH regulation remain elusive. We performed molecular dynamics simulations of NhaA that, with existing experimental data, enabled us to propose an atomically detailed model of antiporter function. Three conserved aspartates are key to our proposed mechanism: Asp164 (D164) is the Na+-binding site, D163 controls the alternating accessibility of this binding site to the cytoplasm or periplasm, and D133 is crucial for pH regulation. Consistent with experimental stoichiometry, two protons are required to transport a single Na+ ion: D163 protonates to reveal the Na+-binding site to the periplasm, and subsequent protonation of D164 releases Na+. Additional mutagenesis experiments further validated the model. 相似文献
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Experiments in our laboratory have demonstrated that white rats fed only fresh whole milk secured enough minerals from their cages to prevent anemia. Animals consuming large amounts of milk became anemic more quickly than those limited to small amounts. Access to feces delayed somewhat the onset of anemia. These results probably explain some of the conflicting data reported in the literature and also raise a question regarding the correctness of conclusions drawn from experiments in which recognition was not given the factors shown in this study to be important. 相似文献
66.
Shaw EH 《Science (New York, N.Y.)》1930,71(1844):460-461
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Shaw WR 《Science (New York, N.Y.)》1918,48(1228):45-46
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Sreedharan J Blair IP Tripathi VB Hu X Vance C Rogelj B Ackerley S Durnall JC Williams KL Buratti E Baralle F de Belleroche J Mitchell JD Leigh PN Al-Chalabi A Miller CC Nicholson G Shaw CE 《Science (New York, N.Y.)》2008,319(5870):1668-1672
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder characterized pathologically by ubiquitinated TAR DNA binding protein (TDP-43) inclusions. The function of TDP-43 in the nervous system is uncertain, and a mechanistic role in neurodegeneration remains speculative. We identified neighboring mutations in a highly conserved region of TARDBP in sporadic and familial ALS cases. TARDBPM337V segregated with disease within one kindred and a genome-wide scan confirmed that linkage was restricted to chromosome 1p36, which contains the TARDBP locus. Mutant forms of TDP-43 fragmented in vitro more readily than wild type and, in vivo, caused neural apoptosis and developmental delay in the chick embryo. Our evidence suggests a pathophysiological link between TDP-43 and ALS. 相似文献