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61.
Bennett JA 《Science (New York, N.Y.)》1986,232(4754):1153
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Boucher TJ Okuse K Bennett DL Munson JB Wood JN McMahon SB 《Science (New York, N.Y.)》2000,290(5489):124-127
Neuropathic pain arises as a debilitating consequence of nerve injury. The etiology of such pain is poorly understood, and existing treatment is largely ineffective. We demonstrate here that glial cell line-derived neurotrophic factor (GDNF) both prevented and reversed sensory abnormalities that developed in neuropathic pain models, without affecting pain-related behavior in normal animals. GDNF reduces ectopic discharges within sensory neurons after nerve injury. This may arise as a consequence of the reversal by GDNF of the injury-induced plasticity of several sodium channel subunits. Together these findings provide a rational basis for the use of GDNF as a therapeutic treatment for neuropathic pain states. 相似文献
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Li R Mitra N Gratkowski H Vilaire G Litvinov R Nagasami C Weisel JW Lear JD DeGrado WF Bennett JS 《Science (New York, N.Y.)》2003,300(5620):795-798
Transmembrane helices of integrin alpha and beta subunits have been implicated in the regulation of integrin activity. Two mutations, glycine-708 to asparagine-708 (G708N)and methionine-701 to asparagine-701, in the transmembrane helix of the beta3 subunit enabled integrin alphaIIbbeta3 to constitutively bind soluble fibrinogen. Further characterization of the G708N mutant revealed that it induced alphaIIbbeta3 clustering and constitutive phosphorylation of focal adhesion kinase. This mutation also enhanced the tendency of the transmembrane helix to form homotrimers. These results suggest that homomeric associations involving transmembrane domains provide a driving force for integrin activation. They also suggest a structural basis for the coincidence of integrin activation and clustering. 相似文献
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Uhlmann WR Bennett R Botkin JR Botstein D Boughman JA Chakravarti A Clayton EW Kahn J Koenig B Murray TH Olson MV Rowley J Terry S Valle D 《Science (New York, N.Y.)》2003,299(5612):1515; author reply 1515
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An in situ microcosm study of the influence of surface-adhering bacteria on silicate diagenesis in a shallow petroleum-contaminated aquifer showed that minerals were colonized by indigenous bacteria and chemically weathered at a rate faster than theoretically predicted. Feldspar and quartz fragments were placed in anoxic, organic-rich ground water, left for 14 months, recovered, and compared to unreacted controls with scanning electron microscopy. Ground-water geochemistry was characterized before and after the experiment. Localized mineral etching probably occurred in a reaction zone at the bacteria-mineral interface where high concentrations of organic acids, formed by bacteria during metabolism of hydrocarbon, selectively mobilized silica and aluminum from the mineral surface. 相似文献
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A diminished response to insulin is exhibited by isolated fat cells obtained from rats that have been either starved, or treated with prednisone, or made diabetic by administration of streptozotocin. This decrease in response is not accompanied by changes in the quantity of insulin receptor of these cells or in the affinity of these receptors for insulin. Similarly, the decreased responsiveness to insulin of fat cells obtained from certain species (hamster, rabbit, mouse, guinea pig) is not explainable in terms of alterations of the insulin receptor. 相似文献
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Treusch S Hamamichi S Goodman JL Matlack KE Chung CY Baru V Shulman JM Parrado A Bevis BJ Valastyan JS Han H Lindhagen-Persson M Reiman EM Evans DA Bennett DA Olofsson A DeJager PL Tanzi RE Caldwell KA Caldwell GA Lindquist S 《Science (New York, N.Y.)》2011,334(6060):1241-1245
Aβ (beta-amyloid peptide) is an important contributor to Alzheimer's disease (AD). We modeled Aβ toxicity in yeast by directing the peptide to the secretory pathway. A genome-wide screen for toxicity modifiers identified the yeast homolog of phosphatidylinositol binding clathrin assembly protein (PICALM) and other endocytic factors connected to AD whose relationship to Aβ was previously unknown. The factors identified in yeast modified Aβ toxicity in glutamatergic neurons of Caenorhabditis elegans and in primary rat cortical neurons. In yeast, Aβ impaired the endocytic trafficking of a plasma membrane receptor, which was ameliorated by endocytic pathway factors identified in the yeast screen. Thus, links between Aβ, endocytosis, and human AD risk factors can be ascertained with yeast as a model system. 相似文献
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