全文获取类型
收费全文 | 24417篇 |
免费 | 1958篇 |
国内免费 | 1812篇 |
出版年
2024年 | 34篇 |
2023年 | 252篇 |
2022年 | 790篇 |
2021年 | 1279篇 |
2020年 | 885篇 |
2019年 | 1039篇 |
2018年 | 1032篇 |
2017年 | 751篇 |
2016年 | 1071篇 |
2015年 | 1470篇 |
2014年 | 1729篇 |
2013年 | 1898篇 |
2012年 | 2254篇 |
2011年 | 1932篇 |
2010年 | 1168篇 |
2009年 | 1020篇 |
2008年 | 1208篇 |
2007年 | 1065篇 |
2006年 | 932篇 |
2005年 | 813篇 |
2004年 | 697篇 |
2003年 | 630篇 |
2002年 | 544篇 |
2001年 | 481篇 |
2000年 | 417篇 |
1999年 | 405篇 |
1998年 | 256篇 |
1997年 | 270篇 |
1996年 | 260篇 |
1995年 | 242篇 |
1994年 | 222篇 |
1993年 | 136篇 |
1992年 | 206篇 |
1991年 | 145篇 |
1990年 | 130篇 |
1989年 | 109篇 |
1988年 | 73篇 |
1987年 | 94篇 |
1986年 | 56篇 |
1985年 | 56篇 |
1984年 | 43篇 |
1983年 | 30篇 |
1982年 | 30篇 |
1981年 | 19篇 |
1980年 | 8篇 |
1979年 | 6篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
971.
FUNDC1 regulates mitochondrial dynamics at the ER–mitochondrial contact site under hypoxic conditions 下载免费PDF全文
Wen Li Haixia Zhuang Xingliang Zhang Hao Chen Shupeng Li Yue Yang Yue Lu Jingjing Wang Runzhi Zhu Liangqing Zhang Senfang Sui Ning Tan Bin Zhao Jingjing Zhang Longxuan Li Du Feng 《The EMBO journal》2016,35(13):1368-1384
In hypoxic cells, dysfunctional mitochondria are selectively removed by a specialized autophagic process called mitophagy. The ER–mitochondrial contact site (MAM) is essential for fission of mitochondria prior to engulfment, and the outer mitochondrial membrane protein FUNDC1 interacts with LC3 to recruit autophagosomes, but the mechanisms integrating these processes are poorly understood. Here, we describe a new pathway mediating mitochondrial fission and subsequent mitophagy under hypoxic conditions. FUNDC1 accumulates at the MAM by associating with the ER membrane protein calnexin. As mitophagy proceeds, FUNDC1/calnexin association attenuates and the exposed cytosolic loop of FUNDC1 interacts with DRP1 instead. DRP1 is thereby recruited to the MAM, and mitochondrial fission then occurs. Knockdown of FUNDC1, DRP1, or calnexin prevents fission and mitophagy under hypoxic conditions. Thus, FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under hypoxic conditions in mammalian cells. 相似文献
972.
973.
974.
Transcriptome‐wide sequencing provides insights into geocarpy in peanut (Arachis hypogaea L.) 下载免费PDF全文
Xiaoping Chen Qingli Yang Haifen Li Heying Li Yanbin Hong Lijuan Pan Na Chen Fanghe Zhu Xiaoyuan Chi Wei Zhu Mingna Chen Haiyan Liu Zhen Yang Erhua Zhang Tong Wang Ni Zhong Mian Wang Hong Liu Shijie Wen Xingyu Li Guiyuan Zhou Shaoxiong Li Hong Wu Rajeev Varshney Xuanqiang Liang Shanlin Yu 《Plant biotechnology journal》2016,14(5):1215-1224
975.
Transcriptome analysis reveals a comprehensive insect resistance response mechanism in cotton to infestation by the phloem feeding insect Bemisia tabaci (whitefly) 总被引:1,自引:0,他引:1 下载免费PDF全文
Jianying Li Lizhen Zhu J. Joe Hull Sijia Liang Henry Daniell Shuangxia Jin Xianlong Zhang 《Plant biotechnology journal》2016,14(10):1956-1975
976.
CLUSTERED PRIMARY BRANCH 1, a new allele of DWARF11, controls panicle architecture and seed size in rice 总被引:2,自引:0,他引:2 下载免费PDF全文
Yongzhen Wu Yongcai Fu Shuangshuang Zhao Ping Gu Zuofeng Zhu Chuanqing Sun Lubin Tan 《Plant biotechnology journal》2016,14(1):377-386
Panicle architecture and seed size are important agronomic traits that directly determine grain yield in rice (Oryza sativa L.). Although a number of key genes controlling panicle architecture and seed size have been cloned and characterized in recent years, their genetic and molecular mechanisms remain unclear. In this study, we identified a mutant that produced panicles with fascicled primary branching and reduced seeds in size. We isolated the underlying CLUSTERED PRIMARY BRANCH 1 (CPB1) gene, a new allele of DWARF11 (D11) encoding a cytochrome P450 protein involved in brassinosteroid (BR) biosynthesis pathway. Genetic transformation experiments confirmed that a His360Leu amino acid substitution residing in the highly conserved region of CPB1/D11 was responsible for the panicle architecture and seed size changes in the cpb1 mutants. Overexpression of CPB1/D11 under the background of cpb1 mutant not only rescued normal panicle architecture and plant height, but also had a larger leaf angle and seed size than the controls. Furthermore, the CPB1/D11 transgenic plants driven by panicle‐specific promoters can enlarge seed size and enhance grain yield without affecting other favourable agronomic traits. These results demonstrated that the specific mutation in CPB1/D11 influenced development of panicle architecture and seed size, and manipulation of CPB1/D11 expression using the panicle‐specific promoter could be used to increase seed size, leading to grain yield improvement in rice. 相似文献
977.
Baomin Feng Shisong Ma Sixue Chen Ning Zhu Shuxin Zhang Bin Yu Yu Yu Brandon Le Xuemei Chen Savithramma P Dinesh‐Kumar Libo Shan Ping He 《EMBO reports》2016,17(12):1799-1813
Protein poly(ADP‐ribosyl)ation (PARylation) primarily catalyzed by poly(ADP‐ribose) polymerases (PARPs) plays a crucial role in controlling various cellular responses. However, PARylation targets and their functions remain largely elusive. Here, we deployed an Arabidopsis protein microarray coupled with in vitro PARylation assays to globally identify PARylation targets in plants. Consistent with the essential role of PARylation in plant immunity, the forkhead‐associated (FHA) domain protein DAWDLE (DDL), one of PARP2 targets, positively regulates plant defense to both adapted and non‐adapted pathogens. Arabidopsis PARP2 interacts with and PARylates DDL, which was enhanced upon treatment of bacterial flagellin. Mass spectrometry and mutagenesis analysis identified multiple PARylation sites of DDL by PARP2. Genetic complementation assays indicate that DDL PARylation is required for its function in plant immunity. In contrast, DDL PARylation appears to be dispensable for its previously reported function in plant development partially mediated by the regulation of microRNA biogenesis. Our study uncovers many previously unknown PARylation targets and points to the distinct functions of DDL in plant immunity and development mediated by protein PARylation and small RNA biogenesis, respectively. 相似文献
978.
Mikolaj B. Ogrodnik Tamar Pirtskhalava Nassir M. Thalji Michael Hagler Diana Jurk Leslie A. Smith Grace Casaclang‐Verzosa Yi Zhu Marissa J. Schafer Tamara Tchkonia James L. Kirkland Jordan D. Miller 《Aging cell》2016,15(5):973-977
While reports suggest a single dose of senolytics may improve vasomotor function, the structural and functional impact of long‐term senolytic treatment is unknown. To determine whether long‐term senolytic treatment improves vasomotor function, vascular stiffness, and intimal plaque size and composition in aged or hypercholesterolemic mice with established disease. Senolytic treatment (intermittent treatment with Dasatinib + Quercetin via oral gavage) resulted in significant reductions in senescent cell markers (TAF+ cells) in the medial layer of aorta from aged and hypercholesterolemic mice, but not in intimal atherosclerotic plaques. While senolytic treatment significantly improved vasomotor function (isolated organ chamber baths) in both groups of mice, this was due to increases in nitric oxide bioavailability in aged mice and increases in sensitivity to NO donors in hypercholesterolemic mice. Genetic clearance of senescent cells in aged normocholesterolemic INK‐ATTAC mice phenocopied changes elicited by D+Q. Senolytics tended to reduce aortic calcification (alizarin red) and osteogenic signaling (qRT–PCR, immunohistochemistry) in aged mice, but both were significantly reduced by senolytic treatment in hypercholesterolemic mice. Intimal plaque fibrosis (picrosirius red) was not changed appreciably by chronic senolytic treatment. This is the first study to demonstrate that chronic clearance of senescent cells improves established vascular phenotypes associated with aging and chronic hypercholesterolemia, and may be a viable therapeutic intervention to reduce morbidity and mortality from cardiovascular diseases. 相似文献
979.
980.
DNA damage is a relatively common event in eukaryotic cell and may lead to genetic mutation and even cancer. DNA damage induces cellular responses that enable the cell either to repair the damaged DNA or cope with the damage in an appropriate way. Histone proteins are also the fundamental building blocks of eukaryotic chromatin besides DNA, and many types of post-translational modifications often occur on tails of histones. Although the function of these modifications has remained elusive, there is ever-growing studies suggest that histone modifications play vital roles in several chromatin-based processes, such as DNA damage response. In this review, we will discuss the main histone modifications, and their functions in DNA damage response. 相似文献