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Evidence for a novel GTPase priming step in the SRP protein targeting pathway. 总被引:4,自引:0,他引:4 下载免费PDF全文
Y Lu H Y Qi J B Hyndman N D Ulbrandt A Teplyakov N Tomasevic H D Bernstein 《The EMBO journal》2001,20(23):6724-6734
Protein targeting by the signal recognition particle (SRP) pathway requires the interaction of two homologous GTPases that reciprocally regulate each other's GTPase activity, the SRP signal peptide- binding subunit (SRP54) and the SRP receptor alpha-subunit (SRalpha). The GTPase domain of both proteins abuts a unique 'N domain' that appears to facilitate external ligand binding. To examine the relationship between the unusual regulation and unique architecture of the SRP pathway GTPases, we mutated an invariant glycine in Escherichia coli SRP54 and SRalpha orthologs ('Ffh' and 'FtsY', respectively) that resides at the N-GTPase domain interface. A G257A mutation in Ffh produced a lethal phenotype. The mutation did not significantly affect Ffh function, but severely reduced interaction with FtsY. Likewise, mutation of FtsY Gly455 produced growth defects and inhibited interaction with Ffh. The data suggest that Ffh and FtsY interact only in a 'primed' conformation which requires interdomain communication. Based on these results, we propose that the distinctive features of the SRP pathway GTPases evolved to ensure that SRP and the SR engage external ligands before interacting with each other. 相似文献
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褐飞虱饲养于不同水稻品种、不同生育期以及不同种群密度条件下,5龄若虫翅芽长度与成虫翅型具有稳定的相关性:翅芽长于1.10mm羽化后为长翅型雌虫,介于0.96~1.09mm之间为长翅型雄虫或短翅型雌虫,小于0.95mm为短翅型雄虫。根据5龄若虫翅芽长度结合外生殖器特征,编制了成虫翅型检索表。由此,可在5龄若虫期预测成虫的翅型和种群盛衰的趋势。 相似文献
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1,1,2,2‐Tetrachloroethane (TeCA) as a Solvent Additive for Organic Hole Transport Materials and Its Application in Highly Efficient Solid‐State Dye‐Sensitized Solar Cells 下载免费PDF全文
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Rui‐Jie Dang Yan‐Mei Yang Lei Zhang Dian‐Chao Cui Bangxing Hong Ping Li Qiuxia Lin Yan Wang Qi‐Yu Wang Fengjun Xiao Ning Mao Changyong Wang Xiao‐Xia Jiang Ning Wen 《Journal of cellular and molecular medicine》2016,20(8):1550-1560
Mesenchymal stem cells (MSCs) possess an immunoregulatory capacity and are a therapeutic target for many inflammation‐related diseases. However, the detailed mechanisms of MSC‐mediated immunosuppression remain unclear. In this study, we provide new information to partly explain the molecular mechanisms of immunoregulation by MSCs. Specifically, we found that A20 expression was induced in MSCs by inflammatory cytokines. Knockdown of A20 in MSCs resulted in increased proliferation and reduced adipogenesis, and partly reversed the suppressive effect of MSCs on T cell proliferation in vitro and inhibited tumour growth in vivo. Mechanistic studies indicated that knockdown of A20 in MSCs inhibited activation of the p38 mitogen‐activated protein kinase (MAPK) pathway, which potently promoted the production of tumour necrosis factor (TNF)‐α and inhibited the production of interleukin (IL)‐10. Collectively, these data reveal a crucial role of A20 in regulating the immunomodulatory activities of MSCs by controlling the expression of TNF‐α and IL‐10 in an inflammatory environment. These findings provide novel insights into the pathogenesis of various inflammatory‐associated diseases, and are a new reference for the future development of treatments for such afflictions. 相似文献
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Diana M. Shih Zeneng Wang Richard Lee Yonghong Meng Nam Che Sarada Charugundla Hannah Qi Judy Wu Calvin Pan J. Mark Brown Thomas Vallim Brian J. Bennett Mark Graham Stanley L. Hazen Aldons J. Lusis 《Journal of lipid research》2015,56(1):22-37
We performed silencing and overexpression studies of flavin containing monooxygenase (FMO) 3 in hyperlipidemic mouse models to examine its effects on trimethylamine N-oxide (TMAO) levels and atherosclerosis. Knockdown of hepatic FMO3 in LDL receptor knockout mice using an antisense oligonucleotide resulted in decreased circulating TMAO levels and atherosclerosis. Surprisingly, we also observed significant decreases in hepatic lipids and in levels of plasma lipids, ketone bodies, glucose, and insulin. FMO3 overexpression in transgenic mice, on the other hand, increased hepatic and plasma lipids. Global gene expression analyses suggested that these effects of FMO3 on lipogenesis and gluconeogenesis may be mediated through the PPARα and Kruppel-like factor 15 pathways. In vivo and in vitro results were consistent with the concept that the effects were mediated directly by FMO3 rather than trimethylamine/TMAO; in particular, overexpression of FMO3 in the human hepatoma cell line, Hep3B, resulted in significantly increased glucose secretion and lipogenesis. Our results indicate a major role for FMO3 in modulating glucose and lipid homeostasis in vivo, and they suggest that pharmacologic inhibition of FMO3 to reduce TMAO levels would be confounded by metabolic interactions. 相似文献
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