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Marlène Dreux Viet Loan Dao Thi Judith Fresquet Maryse Guérin Zélie Julia Géraldine Verney David Durantel Fabien Zoulim Dimitri Lavillette Fran?ois-Lo?c Cosset Birke Bartosch 《PLoS pathogens》2009,5(2)
HCV entry into cells is a multi-step and slow process. It is believed that the
initial capture of HCV particles by glycosaminoglycans and/or lipoprotein
receptors is followed by coordinated interactions with the scavenger receptor
class B type I (SR-BI), a major receptor of high-density lipoprotein (HDL), the
CD81 tetraspanin, and the tight junction protein Claudin-1, ultimately leading
to uptake and cellular penetration of HCV via low-pH endosomes.
Several reports have indicated that HDL promotes HCV entry through interaction
with SR-BI. This pathway remains largely elusive, although it was shown that HDL
neither associates with HCV particles nor modulates HCV binding to SR-BI. In
contrast to CD81 and Claudin-1, the importance of SR-BI has only been addressed
indirectly because of lack of cells in which functional complementation assays
with mutant receptors could be performed. Here we identified for the first time
two cell types that supported HCVpp and HCVcc entry upon ectopic SR-BI
expression. Remarkably, the undetectable expression of SR-BI in rat hepatoma
cells allowed unambiguous investigation of human SR-BI functions during HCV
entry. By expressing different SR-BI mutants in either cell line, our results
revealed features of SR-BI intracellular domains that influence HCV infectivity
without affecting receptor binding and stimulation of HCV entry induced by
HDL/SR-BI interaction. Conversely, we identified positions of SR-BI ectodomain
that, by altering HCV binding, inhibit entry. Finally, we characterized
alternative ectodomain determinants that, by reducing SR-BI cholesterol uptake
and efflux functions, abolish HDL-mediated infection-enhancement. Altogether, we
demonstrate that SR-BI is an essential HCV entry factor. Moreover, our results
highlight specific SR-BI determinants required during HCV entry and
physiological lipid transfer functions hijacked by HCV to favor infection. 相似文献
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Macoritto M Nguyen-Yamamoto L Huang DC Samuel S Yang XF Wang TT White JH Kremer R 《The Journal of biological chemistry》2008,283(8):4943-4956
46.
Yeast RNA polymerase I enhancer is dispensable for transcription of the chromosomal rRNA gene and cell growth, and its apparent transcription enhancement from ectopic promoters requires Fob1 protein. 下载免费PDF全文
47.
We investigated the cytotoxic and apoptotic effects of a methanol extract of Centaurea nerimaniae, a plant endemic in Turkey, on HeLa and MDA-MB-231 cells. Eight concentrations of C. nerimaniae extract were applied to cells, and cytotoxic effects were measured using the xCELLigence system. The TUNEL assay was used to assess apoptotic cell death and immunohistochemistry was used to determine active caspase-3 using the effective cytotoxic doses of the extract. Doses of 1.42 mg/ml C. nerimaniae inhibited the growth of HeLa cells and 3.67 mg/ml C. nerimaniae inhibited the growth of MDA-MB-231 cells in a dose- and time-dependent manner. The apoptotic indexes for HeLa and MDA-MB-231 cells were increased significantly compared to control groups. Immunohistochemistry showed that the number of caspase-3 immunostained cells increased in the extract treatment groups for both HeLa and MDA-MB-231 cells. In the MDA-MB-231 cell line, caspase-3 immunostaining was observed in nuclei and/or cytoplasm in the extract treated group. Caspase-3 activation was greater in HeLa cells than in MDA-MB-231 cells. We found that the extract of C. nerimaniae had a strong antiproliferative effect and induced apoptosis via caspase-3; MDA-MB-231 cancer cells were more resistant than HeLa cells. 相似文献
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