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   11751篇
  免费   101篇
  国内免费   63篇
系统科学   126篇
丛书文集   113篇
教育与普及   19篇
理论与方法论   32篇
现状及发展   5498篇
研究方法   607篇
综合类   5396篇
自然研究   124篇
  2016年   79篇
  2012年   190篇
  2011年   330篇
  2010年   102篇
  2009年   83篇
  2008年   272篇
  2007年   287篇
  2006年   245篇
  2005年   241篇
  2004年   352篇
  2003年   224篇
  2002年   218篇
  2001年   391篇
  2000年   402篇
  1999年   275篇
  1992年   199篇
  1991年   166篇
  1990年   152篇
  1989年   140篇
  1988年   135篇
  1987年   165篇
  1986年   155篇
  1985年   216篇
  1984年   189篇
  1983年   133篇
  1982年   126篇
  1981年   151篇
  1980年   174篇
  1979年   345篇
  1978年   266篇
  1977年   274篇
  1976年   195篇
  1975年   227篇
  1974年   309篇
  1973年   265篇
  1972年   275篇
  1971年   312篇
  1970年   405篇
  1969年   325篇
  1968年   316篇
  1967年   315篇
  1966年   298篇
  1965年   225篇
  1959年   83篇
  1958年   154篇
  1957年   120篇
  1956年   126篇
  1955年   89篇
  1954年   104篇
  1948年   88篇
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
Linkage of Mls genes to endogenous mammary tumour viruses of inbred mice.   总被引:35,自引:0,他引:35  
W N Frankel  C Rudy  J M Coffin  B T Huber 《Nature》1991,349(6309):526-528
T cells that recognize self antigen are clonally deleted in the thymus--a maturation process that occurs in the context of histocompatibility molecules and the T-cell receptor. The minor lymphocyte stimulation antigens (Mls) effect these deletions through interactions with the V beta portion of the T-cell receptor, thus mimicking bacterial 'superantigens'. Intrigued by the fact that each known Mls gene maps to the same chromosomal region as an endogenous mouse mammary tumour virus (Mtv), we reevaluated the linkage relationships between the two gene families. Here we report perfect concordance in inbred and recombinant inbred mice between the presence of four Mtv proviruses with the expression of Mls gene products. These data suggest a general model in which mammary tumour virus gene products themselves are the ligands that shape a considerable portion of the immunological repertoire of common laboratory mice.  相似文献   
992.
Pyridoxal 5′-phosphate is a coenzyme for a number of enzymes which catalyse reactions at Cα of amino acid substrates including transaminases, decarboxylases and serine hydroxymethyltransferase. Using the X-ray coordinates for a transaminase, aspartate aminotransferase, and the results of stereochemical and mechanistic studies for decarboxylases and serine hydroxymethyltransferase, an active-site structure for the decarboxylase group is constructed. The structure of the active-site is further refined through active-site pyridoxyllysine peptide sequence comparison and a 3-D catalytic mechanism for the L-α-amino acid decarboxylases is proposed. The chemistry of serine hydroxymethyltransferase is re-examined in the light of the proposed decarboxylase mechanism.  相似文献   
993.
994.
The developmental gene Knotted-1 is a member of a maize homeobox gene family.   总被引:51,自引:0,他引:51  
E Vollbrecht  B Veit  N Sinha  S Hake 《Nature》1991,350(6315):241-243
  相似文献   
995.
D M Smith  N R Thomas  D Gani 《Experientia》1991,47(11-12):1104-1118
Pyridoxal 5'-phosphate is a coenzyme for a number of enzymes which catalyse reactions at C alpha of amino acid substrates including transaminases, decarboxylases and serine hydroxymethyltransferase. Using the X-ray coordinates for a transaminase, aspartate aminotransferase, and the results of stereochemical and mechanistic studies for decarboxylases and serine hydroxymethyltransferase, an active-site structure for the decarboxylase group is constructed. The structure of the active-site is further refined through active-site pyridoxyllysine peptide sequence comparison and a 3-D catalytic mechanism for the L-alpha-amino acid decarboxylases is proposed. The chemistry of serine hydroxymethyltransferase is re-examined in the light of the proposed decarboxylase mechanism.  相似文献   
996.
D H MacLennan  C J Brandl  B Korczak  N M Green 《Nature》1985,316(6030):696-700
We have cloned and sequenced complementary DNA encoding a Ca2+-ATPase of rabbit muscle sarcoplasmic reticulum. We propose a model of the protein which has 3 cytoplasmic domains joined to a set of 10 transmembrane helices by a narrow, penta-helical stalk. In this model, ATP bound to one cytoplasmic domain would phosphorylate an aspartate in an adjoining cytoplasmic domain, inducing translocation of Ca2+ from binding sites on the stalk.  相似文献   
997.
The distribution pattern of muscarinic receptors in N1E 115 mouse neuroblastoma cells after linear and non-linear gradient centrifugation was investigated. In untreated cells, at least two forms of the receptors, with different densities, were found.  相似文献   
998.
Summary During the first 40 days of life the rate of incorporation of32P into total phospholipids and into phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin, diphosphatidylglycerol, phosphatidic acid and phosphatidylinositol of mouse kidney was by some 25–35% higher than in older animals. Results suggest a different involvement of cellular membranes during of normal and compensatory renal growth.  相似文献   
999.
J M Lowenstein  O A Ryder 《Experientia》1985,41(9):1192-1193
It has been debated whether the extinct quagga was a distinct fourth species of African zebra or whether it was merely the southern variant of the Plains zebra (Equus burchelli). Using a radioimmunoassay (RIA) technique, we have shown that proteins remaining in quagga skins from museums are much more similar to serum proteins of the Plains zebra than to those of the other two extant zebras.  相似文献   
1000.
Cancer predisposition in hereditary non-polyposis colon cancer (HNPCC) is caused by defects in DNA mismatch repair (MMR). Mismatch recognition is attributed to two heterodimeric protein complexes: MutSalpha (refs 2, 3, 4, 5), a dimer of MutS homologues MSH2 and MSH6; and MutSbeta (refs 2,7), a dimer of MSH2 and MSH3. These complexes have specific and redundant mismatch recognition capacity. Whereas MSH2 deficiency ablates the activity of both dimers, causing strong cancer predisposition in mice and men, loss of MSH3 or MSH6 (also known as GTBP) function causes a partial MMR defect. This may explain the rarity of MSH6 and absence of MSH3 germline mutations in HNPCC families. To test this, we have inactivated the mouse genes Msh3 (formerly Rep3 ) and Msh6 (formerly Gtmbp). Msh6-deficient mice were prone to cancer; most animals developed lymphomas or epithelial tumours originating from the skin and uterus but only rarely from the intestine. Msh3 deficiency did not cause cancer predisposition, but in an Msh6 -deficient background, loss of Msh3 accelerated intestinal tumorigenesis. Lymphomagenesis was not affected. Furthermore, mismatch-directed anti-recombination and sensitivity to methylating agents required Msh2 and Msh6, but not Msh3. Thus, loss of MMR functions specific to Msh2/Msh6 is sufficient for lymphoma development in mice, whereas predisposition to intestinal cancer requires loss of function of both Msh2/Msh6 and Msh2/Msh3.  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