首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   471篇
  免费   27篇
  2021年   6篇
  2017年   6篇
  2016年   6篇
  2015年   13篇
  2014年   16篇
  2013年   14篇
  2012年   19篇
  2011年   21篇
  2010年   14篇
  2009年   13篇
  2008年   11篇
  2007年   14篇
  2006年   7篇
  2005年   12篇
  2003年   15篇
  2002年   11篇
  2001年   9篇
  2000年   10篇
  1999年   15篇
  1998年   5篇
  1997年   6篇
  1996年   5篇
  1995年   5篇
  1994年   4篇
  1993年   7篇
  1992年   5篇
  1991年   9篇
  1990年   8篇
  1989年   7篇
  1988年   8篇
  1987年   6篇
  1986年   12篇
  1985年   5篇
  1984年   6篇
  1983年   5篇
  1982年   6篇
  1981年   11篇
  1980年   4篇
  1979年   20篇
  1978年   14篇
  1977年   10篇
  1976年   11篇
  1975年   7篇
  1974年   11篇
  1973年   6篇
  1971年   12篇
  1969年   6篇
  1968年   5篇
  1967年   4篇
  1966年   4篇
排序方式: 共有498条查询结果,搜索用时 187 毫秒
71.
72.
73.
74.
75.
76.
77.
78.
79.
Detecting the phosphorylation substrates of multiple kinases in a single experiment is a challenge, and new techniques are being developed to overcome this challenge. Here, we used a multiplexed assay for kinase specificity (MAKS) to identify the substrates directly and to map the phosphorylation site(s) of plant symbiotic receptor‐like kinases. The symbiotic receptor‐like kinases nodulation receptor‐like kinase (NORK) and lysin motif domain‐containing receptor‐like kinase 3 (LYK3) are indispensable for the establishment of root nodule symbiosis. Although some interacting proteins have been identified for these symbiotic receptor‐like kinases, very little is known about their phosphorylation substrates. Using this high‐throughput approach, we identified several other potential phosphorylation targets for both these symbiotic receptor‐like kinases. In particular, we also discovered the phosphorylation of LYK3 by NORK itself, which was also confirmed by pairwise kinase assays. Motif analysis of potential targets for these kinases revealed that the acidic motif xxxsDxxx was common to both of them. In summary, this high‐throughput technique catalogs the potential phosphorylation substrates of multiple kinases in a single efficient experiment, the biological characterization of which should provide a better understanding of phosphorylation signaling cascade in symbiosis.  相似文献   
80.
Perry  CT  Kench  PS  Smithers  SG  Riegl  BR  Gulliver  P  Daniells  JJ 《Coral reefs (Online)》2017,36(3):1013-1021

Low-lying coral reef islands are considered highly vulnerable to climate change, necessitating an improved understanding of when and why they form, and how the timing of formation varies within and among regions. Several testable models have been proposed that explain inter-regional variability as a function of sea-level history and, more recently, a reef platform size model has been proposed from the Maldives (central Indian Ocean) to explain intra-regional (intra-atoll) variability. Here we present chronostratigraphic data from Pipon Island, northern Great Barrier Reef (GBR), enabling us to test the applicability of existing regional island evolution models, and the platform size control hypothesis in a Pacific context. We show that reef platform infilling occurred rapidly (~4–5 mm yr−1) under a “bucket-fill” type scenario. Unusually, this infilling was dominated by terrigenous sedimentation, with platform filling and subsequent reef flat formation complete by ~5000 calibrated years BP (cal BP). Reef flat exposure as sea levels slowly fell post highstand facilitated a shift towards intertidal and subaerial-dominated sedimentation. Our data suggest, however, a lag of ~1500 yr before island initiation (at ~3200 cal BP), i.e. later than that reported from smaller and more evolutionarily mature reef platforms in the region. Our data thus support: (1) the hypothesis that platform size acts to influence the timing of platform filling and subsequent island development at intra-regional scales; and (2) the hypothesis that the low wooded islands of the northern GBR conform to a model of island formation above an elevated reef flat under falling sea levels.

  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号