全文获取类型
收费全文 | 1406篇 |
免费 | 190篇 |
出版年
2022年 | 11篇 |
2021年 | 23篇 |
2020年 | 12篇 |
2019年 | 20篇 |
2018年 | 23篇 |
2017年 | 13篇 |
2016年 | 13篇 |
2015年 | 35篇 |
2014年 | 41篇 |
2013年 | 57篇 |
2012年 | 68篇 |
2011年 | 81篇 |
2010年 | 57篇 |
2009年 | 46篇 |
2008年 | 69篇 |
2007年 | 54篇 |
2006年 | 51篇 |
2005年 | 57篇 |
2004年 | 43篇 |
2003年 | 59篇 |
2002年 | 58篇 |
2001年 | 46篇 |
2000年 | 39篇 |
1999年 | 27篇 |
1998年 | 23篇 |
1997年 | 10篇 |
1996年 | 15篇 |
1994年 | 13篇 |
1992年 | 29篇 |
1991年 | 29篇 |
1990年 | 11篇 |
1989年 | 22篇 |
1988年 | 21篇 |
1987年 | 30篇 |
1986年 | 18篇 |
1983年 | 14篇 |
1982年 | 19篇 |
1981年 | 13篇 |
1980年 | 10篇 |
1979年 | 11篇 |
1978年 | 10篇 |
1977年 | 13篇 |
1975年 | 13篇 |
1974年 | 10篇 |
1973年 | 14篇 |
1945年 | 11篇 |
1939年 | 17篇 |
1938年 | 12篇 |
1937年 | 10篇 |
1916年 | 10篇 |
排序方式: 共有1596条查询结果,搜索用时 15 毫秒
71.
72.
73.
Maria Carolina Florian Hanna Leins Michael Gobs Yang Han Gina Marka Karin Soller Angelika Vollmer Vadim Sakk Kalpana J. Nattamai Ahmad Rayes Xueheng Zhao Kenneth Setchell Medhanie Mulaw Wolfgang Wagner Yi Zheng Hartmut Geiger 《Aging cell》2020,19(9)
Cdc42 is a small RhoGTPase regulating multiple functions in eukaryotic cells. The activity of Cdc42 is significantly elevated in several tissues of aged mice, while the Cdc42 gain‐of‐activity mouse model presents with a premature aging‐like phenotype and with decreased lifespan. These data suggest a causal connection between elevated activity of Cdc42, aging, and reduced lifespan. Here, we demonstrate that systemic treatment of aged (75‐week‐old) female C57BL/6 mice with a Cdc42 activity‐specific inhibitor (CASIN) for 4 consecutive days significantly extends average and maximum lifespan. Moreover, aged CASIN‐treated animals displayed a youthful level of the aging‐associated cytokines IL‐1β, IL‐1α, and INFγ in serum and a significantly younger epigenetic clock as based on DNA methylation levels in blood cells. Overall, our data show that systemic administration of CASIN to reduce Cdc42 activity in aged mice extends murine lifespan. 相似文献
74.
Manfred Schartl Susanne Kneitz Jenny Ormanns Cornelia Schmidt Jennifer L. Anderson Angel Amores Julian Catchen Catherine Wilson Dietmar Geiger Kang Du Mateo Garcia-Olazábal Sudha Sudaram Christoph Winkler Rainer Hedrich Wesley C. Warren Ronald Walter Axel Meyer John H. Postlethwait 《Current biology : CB》2021,31(5):911-922.e4
75.
76.
Yulia Mostovoy Feyza Yilmaz Stephen K Chow Catherine Chu Chin Lin Elizabeth A Geiger Naomi J L Meeks Kathryn C Chatfield Curtis R Coughlin II Urvashi Surti Pui-Yan Kwok Tamim H Shaikh 《Genetics》2021,217(2)
Segmental duplications (SDs) are a class of long, repetitive DNA elements whose paralogs share a high level of sequence similarity with each other. SDs mediate chromosomal rearrangements that lead to structural variation in the general population as well as genomic disorders associated with multiple congenital anomalies, including the 7q11.23 (Williams–Beuren Syndrome, WBS), 15q13.3, and 16p12.2 microdeletion syndromes. Population-level characterization of SDs has generally been lacking because most techniques used for analyzing these complex regions are both labor and cost intensive. In this study, we have used a high-throughput technique to genotype complex structural variation with a single molecule, long-range optical mapping approach. We characterized SDs and identified novel structural variants (SVs) at 7q11.23, 15q13.3, and 16p12.2 using optical mapping data from 154 phenotypically normal individuals from 26 populations comprising five super-populations. We detected several novel SVs for each locus, some of which had significantly different prevalence between populations. Additionally, we localized the microdeletion breakpoints to specific paralogous duplicons located within complex SDs in two patients with WBS, one patient with 15q13.3, and one patient with 16p12.2 microdeletion syndromes. The population-level data presented here highlights the extreme diversity of large and complex SVs within SD-containing regions. The approach we outline will greatly facilitate the investigation of the role of inter-SD structural variation as a driver of chromosomal rearrangements and genomic disorders. 相似文献
77.
Albert Geiger Ane Lester Jörg Kleiber Henrik Ørum 《Nucleosides, nucleotides & nucleic acids》2013,32(9-11):1717-1724
Abstract A comparative study using immobilised DNA and PNA oligomers demonstrates the suitability of PNA molecules as sequence specific capture probes in the detection of single point mutations in a DNA analyte and in the analysis of complex analyte mixtures. 相似文献
78.
79.
Patrick Mumm Dennis Imes Enrico Martinoia Khaled A.S. AI-Rasheid Dietmar Geiger Irene Marten Rainer Hedrich 《植物生理与分子生物学学报》2013,(5):1550-1563
Anion transporters in plants play a fundamental role in volume regulation and signaling. Currently, two plasma membrane-located anion channel familiesmSLAC/SLAH and ALMTmare known. Among the ALMT family, the root-expressed ALuminium-activated Malate Transporter 1 was identified by comparison of aluminum-tolerant and Al3+-sensitive wheat cultivars and was subsequently shown to mediate voltage-independent malate currents. In con- trast, ALMT12/QUAC1 (QUickly activating Anion Channel1) is expressed in guard cells transporting malate in an Al3+- insensitive and highly voltage-dependent manner. So far, no information is available about the structure and mechanism of voltage-dependent gating with the QUAC1 channel protein. Here, we analyzed gating of QUACl-type currents in the plasma membrane of guard cells and QUACl-expressing oocytes revealing similar voltage dependencies and activation- deactivation kinetics. In the heterologous expression system, QUAC1 was electrophysiologically characterized at increas- ing extra- and intracellular malate concentrations. Thereby, malate additively stimulated the voltage-dependent QUAC1 activity. In search of structural determinants of the gating process, we could not identify transmembrane domains com- mon for voltage-sensitive channels. However, site-directed mutations and deletions at the C-terminus of QUAC1 resulted in altered voltage-dependent channel activity. Interestingly, the replacement of a single glutamate residue, which is con- served in ALMT channels from different clades, by an alanine disrupted QUAC1 activity. Together with C- and N-terminal tagging, these results indicate that the cytosolic C-terminus is involved in the voltage-dependent gating mechanism of QUAC1. 相似文献
80.