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991.
Kumar P. S. Ling C. Y. Zhou Z. B. Dong Y. L. Sun C. L. Song Y. X. Wong N. K. Ju J. H. 《Microbiology》2020,89(4):483-492
Microbiology - Marine actinobacteria particularly from marine environments are believed to be inexhaustible sources of biologically active molecules for biomedical and industrial applications. We... 相似文献
992.
Jing Zhang Mingjian Zhou Zhenglin Ge Jie Shen Can Zhou Cecilia Gotor Luis C. Romero Xingliang Duan Xin Liu Deliang Wu Xianchao Yin Yanjie Xie 《Plant, cell & environment》2020,43(3):624-636
Recent studies have demonstrated that hydrogen sulfide (H2S) produced through the activity of l -cysteine desulfhydrase (DES1) is an important gaseous signaling molecule in plants that could participate in abscisic acid (ABA)-induced stomatal closure. However, the coupling of the DES1/H2S signaling pathways to guard cell movement has not been thoroughly elucidated. The results presented here provide genetic evidence for a physiologically relevant signaling pathway that governs guard cell in situ DES1/H2S function in stomatal closure. We discovered that ABA-activated DES1 produces H2S in guard cells. The impaired guard cell ABA phenotype of the des1 mutant can be fully complemented when DES1/H2S function has been specifically rescued in guard cells and epidermal cells, but not mesophyll cells. This research further characterized DES1/H2S function in the regulation of LONG HYPOCOTYL1 (HY1, a member of the heme oxygenase family) signaling. ABA-induced DES1 expression and H2S production are hyper-activated in the hy1 mutant, both of which can be fully abolished by the addition of H2S scavenger. Impaired guard cell ABA phenotype of des1/hy1 can be restored by H2S donors. Taken together, this research indicated that guard cell in situ DES1 function is involved in ABA-induced stomatal closure, which also acts as a pivotal hub in regulating HY1 signaling. 相似文献
993.
Xu Feng Peng Feng Huilin Yu Xingyu Yu Qi Sun Siyu Liu Thuy Nguyen Minh Jun Chen Di Wang Qing Zhang Lei Cao Changmei Zhou Qiang Li Jialei Xiao Shihua Zhong Aoxue Wang Lijuan Wang Hongyu Pan Xiaodong Ding 《Plant, cell & environment》2020,43(5):1192-1211
Although the function and regulation of SnRK1 have been studied in various plants, its molecular mechanisms in response to abiotic stresses are still elusive. In this work, we identified an AP2/ERF domain-containing protein (designated GsERF7) interacting with GsSnRK1 from a wild soybean cDNA library. GsERF7 gene expressed dominantly in wild soybean roots and was responsive to ethylene, salt, and alkaline. GsERF7 bound GCC cis-acting element and could be phosphorylated on S36 by GsSnRK1. GsERF7 phosphorylation facilitated its translocation from cytoplasm to nucleus and enhanced its transactivation activity. When coexpressed in the hairy roots of soybean seedlings, GsSnRK1(wt) and GsERF7(wt) promoted plants to generate higher tolerance to salt and alkaline stresses than their mutated species, suggesting that GsSnRK1 may function as a biochemical and genetic upstream kinase of GsERF7 to regulate plant adaptation to environmental stresses. Furthermore, the altered expression patterns of representative abiotic stress-responsive and hormone-synthetic genes were determined in transgenic soybean hairy roots after stress treatments. These results will aid our understanding of molecular mechanism of how SnRK1 kinase plays a cardinal role in regulating plant stress resistances through activating the biological functions of downstream factors. 相似文献
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996.
Li Zhibin Hua Zetian Dong Li Zhu Wei He Guangsheng Qu Lijun Qi Na Xu Zhengjin Wang Fang 《Journal of Plant Growth Regulation》2020,39(1):60-71
Journal of Plant Growth Regulation - RAD-seq method is a recently developed, cost-effective, and high-throughput approach for detecting genetic variability based on single-nucleotide polymorphisms... 相似文献
997.
Zhenyuan Gao Hairong Zhou Yaping Wang Juan Chen Yimei Ou 《Journal of cellular biochemistry》2020,121(1):332-343
This investigation was intended to elucidate whether long noncoding RNA (lncRNA)-activated by transforming growth factor-β (ATB) interacting with miR-200c could mediate colorectal cancer (CRC) progression, offering potential strategies for diagnosing and treating CRC. Here totally 315 patients with CRC were recruited, and their CRC tissues and adjacent normal tissues were gathered. Concurrently, four colon cancer cell lines (ie, SW620, Lovo, HCT116, and SW480) and the human colon mucosal epithelial cell line (NCM460) were also purchased. Moreover, si-ATB, si-NC, miR-200c mimic, miR-200c inhibitor, and miR-NC were prepared for transfection into the CRC cells, and their effects on CRC cell lines were evaluated based on the conduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, and flow cytometry assay. Eventually, the Luciferase reporter gene assay was carried out to judge if there existed a targeted relationship between ATB and miR-200c. The results of Cox regression analyses suggested that overexpressed lncRNA ATB, underexpressed miR-200c, poor tumor differentiation, lymph-vascular invasion, and perineural invasion were symbolic of shortened survival of the patients with CRC (all P < .05). Besides, transfection of pcDNA3.1-ATB and miR-200c inhibitor could boost the viability and proliferation of Lovo and SW620 cell lines (all P < .05). Meanwhile, the expressions of p53 and p21 were also reduced under treatments of pcDNA3.1-ATB and miR-200c inhibitor (P < .05). In addition, CDK2 seemed to reverse the contribution of miR-200c to intensifying viability and proliferation of Lovo and SW420 cell lines (P < .05). Furthermore, ATB might downregulate miR-200c expression by targeting it (P < .05), and CDK2 was subjected to dual regulation of both ATB and miR-200c (P < .05). In conclusion, the lncRNA ATB/miR-200c/CDK2 signaling was responsible for intensified proliferation and prohibited apoptosis of CRC cells, which might provide effective approaches for diagnosing and treating CRC. 相似文献
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999.
Shan Pan Jun Leng Xinzhou Deng Honggang Ruan Lu Zhou Muhammad Jamal Ruijing Xiao Jie Xiong Qian Yin Yingjie Wu Meng Wang Wen Yuan Liang Shao Qiuping Zhang 《Journal of cellular biochemistry》2020,121(1):574-586
The NAD-dependent deacetylase Sirtuin 1 (SIRT1) plays a vital role in leukemogenesis. Nicotinamide (NAM) is the principal NAD+ precursor and a noncompetitive inhibitor of SIRT1. In our study, we showed that NAM enhanced the sensitivity of chronic myeloid leukemia (CML) to doxorubicin (DOX) via SIRT1. We found that SIRT1 high expression in CML patients was associated with disease progression and drug resistance. Exogenous NAM efficiently repressed the deacetylation activity of SIRT1 and induced the apoptosis of DOX-resistant K562 cells (K562R) in a dose-dependent manner. Notably, the combination of NAM and DOX significantly inhibited tumor cell proliferation and induced cell apoptosis. The knockdown of SIRT1 in K562R cells enhanced NAM+DOX-induced apoptosis. SIRT1 rescue in K562R reduced the NAM+DOX-induced apoptosis. Mechanistically, the combinatory treatment significantly increased the cleavage of caspase-3 and PARP in K562R in vitro and in vivo. These results suggest the potential role of NAM in increasing the sensitivity of CML to DOX via the inhibition of SIRT1. 相似文献
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