全文获取类型
收费全文 | 35733篇 |
免费 | 108篇 |
国内免费 | 150篇 |
专业分类
系统科学 | 149篇 |
丛书文集 | 516篇 |
教育与普及 | 66篇 |
理论与方法论 | 126篇 |
现状及发展 | 15938篇 |
研究方法 | 1491篇 |
综合类 | 17109篇 |
自然研究 | 596篇 |
出版年
2013年 | 275篇 |
2012年 | 518篇 |
2011年 | 1100篇 |
2010年 | 229篇 |
2008年 | 604篇 |
2007年 | 726篇 |
2006年 | 645篇 |
2005年 | 692篇 |
2004年 | 748篇 |
2003年 | 640篇 |
2002年 | 652篇 |
2001年 | 1053篇 |
2000年 | 1008篇 |
1999年 | 709篇 |
1992年 | 691篇 |
1991年 | 500篇 |
1990年 | 562篇 |
1989年 | 538篇 |
1988年 | 543篇 |
1987年 | 542篇 |
1986年 | 556篇 |
1985年 | 726篇 |
1984年 | 521篇 |
1983年 | 437篇 |
1982年 | 418篇 |
1981年 | 414篇 |
1980年 | 498篇 |
1979年 | 1125篇 |
1978年 | 887篇 |
1977年 | 865篇 |
1976年 | 709篇 |
1975年 | 736篇 |
1974年 | 995篇 |
1973年 | 874篇 |
1972年 | 957篇 |
1971年 | 1030篇 |
1970年 | 1393篇 |
1969年 | 1106篇 |
1968年 | 1006篇 |
1967年 | 1022篇 |
1966年 | 939篇 |
1965年 | 684篇 |
1964年 | 217篇 |
1959年 | 353篇 |
1958年 | 682篇 |
1957年 | 477篇 |
1956年 | 380篇 |
1955年 | 339篇 |
1954年 | 365篇 |
1948年 | 253篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
992.
A structural change in the kinesin motor protein that drives motility 总被引:34,自引:0,他引:34
Rice S Lin AW Safer D Hart CL Naber N Carragher BO Cain SM Pechatnikova E Wilson-Kubalek EM Whittaker M Pate E Cooke R Taylor EW Milligan RA Vale RD 《Nature》1999,402(6763):778-784
Kinesin motors power many motile processes by converting ATP energy into unidirectional motion along microtubules. The force-generating and enzymatic properties of conventional kinesin have been extensively studied; however, the structural basis of movement is unknown. Here we have detected and visualized a large conformational change of an approximately 15-amino-acid region (the neck linker) in kinesin using electron paramagnetic resonance, fluorescence resonance energy transfer, pre-steady state kinetics and cryo-electron microscopy. This region becomes immobilized and extended towards the microtubule 'plus' end when kinesin binds microtubules and ATP, and reverts to a more mobile conformation when gamma-phosphate is released after nucleotide hydrolysis. This conformational change explains both the direction of kinesin motion and processive movement by the kinesin dimer. 相似文献
993.
994.
995.
996.
997.
998.
999.
1000.
Huntington disease (HD), an autosomal dominant, progressive neurodegenerative disorder, is caused by an expanded CAG repeat sequence leading to an increase in the number of glutamine residues in the encoded protein. The normal CAG repeat range is 5-36, whereas 38 or more repeats are found in the diseased state; the severity of disease is roughly proportional to the number of CAG repeats. HD shows anticipation, in which subsequent generations display earlier disease onsets due to intergenerational repeat expansion. For longer repeat lengths, somatic instability of the repeat size has been observed both in human cases at autopsy and in transgenic mouse models containing either a genomic fragment of human HD exon 1 (ref. 9) or an expanded repeat inserted into the endogenous mouse gene Hdh (ref. 10). With increasing repeat number, the protein changes conformation and becomes increasingly prone to aggregation, suggesting important functional correlations between repeat length and pathology. Because dinucleotide repeat instability is known to increase when the mismatch repair enzyme MSH2 is missing, we examined instability of the HD CAG repeat by crossing transgenic mice carrying exon 1 of human HD (ref. 16) with Msh2-/- mice. Our results show that Msh2 is required for somatic instability of the CAG repeat. 相似文献