全文获取类型
收费全文 | 68篇 |
免费 | 8篇 |
出版年
2023年 | 1篇 |
2022年 | 1篇 |
2019年 | 1篇 |
2018年 | 3篇 |
2017年 | 2篇 |
2016年 | 3篇 |
2015年 | 5篇 |
2014年 | 2篇 |
2013年 | 6篇 |
2012年 | 2篇 |
2011年 | 6篇 |
2010年 | 2篇 |
2009年 | 5篇 |
2008年 | 3篇 |
2007年 | 3篇 |
2006年 | 8篇 |
2005年 | 2篇 |
2004年 | 2篇 |
2002年 | 2篇 |
2001年 | 2篇 |
2000年 | 2篇 |
1999年 | 1篇 |
1992年 | 1篇 |
1990年 | 1篇 |
1989年 | 2篇 |
1988年 | 2篇 |
1987年 | 1篇 |
1985年 | 1篇 |
1982年 | 1篇 |
1979年 | 1篇 |
1973年 | 1篇 |
1971年 | 1篇 |
排序方式: 共有76条查询结果,搜索用时 31 毫秒
31.
32.
33.
34.
Characterization of the origins of replication of bacteriophage phi 29 DNA. 总被引:3,自引:1,他引:2 下载免费PDF全文
The origins of replication of phi 29 DNA have been studied by analyzing the activity as templates in the phi 29 in vitro replication system of E. coli recombinant plasmids and M13 derivatives containing phi 29 DNA terminal sequences. Plasmid pITR, containing the 6 bp long inverted terminal repeat of phi 29 DNA, was shown to be essentially inactive. The analysis of a series of deletion derivatives of plasmid pID13, that contains the 73 and 269 bp from the left and right phi 29 DNA ends, respectively, indicated that the minimal origins of replication are comprised within the mutagenesis at these sequences was carried out. Changes of the second or third A into a C completely abolished the template activity. In the case of changes at position from 4 to 12, only 3 out of 14 mutations reduced the template activity; these 3 mutations were double changes and 2 of them affected the inverted terminal repeat. The results suggest that the sequence requirement at the end-proximal region of the origin of replication is more strict than that at the distal region. 相似文献
35.
Site-directed mutagenesis in the DNA linking site of bacteriophage phi 29 terminal protein: isolation and characterization of a Ser232----Thr mutant. 总被引:2,自引:1,他引:1 下载免费PDF全文
By site-directed mutagenesis we have changed the serine residue 232 of the phi 29 terminal protein, involved in the covalent linkage to dAMP for the initiation of replication, into a threonine residue. The mutant terminal protein has been purified to homogeneity and shown to be inactive in the formation of the initiation complex; nevertheless, the mutant protein retains its ability to interact with the phi 29 DNA polymerase and with the DNA. The results obtained indicate a high specificity in the linking site of the terminal protein. 相似文献
36.
37.
Victoria Cano David Moranta Enrique Llobet-Brossa José Antonio Bengoechea Junkal Garmendia 《BMC microbiology》2009,9(1):156
Background
Klebsiella pneumoniae is a capsulated Gram negative bacterial pathogen and a frequent cause of nosocomial infections. Despite its clinical relevance, little is known about the features of the interaction between K. pneumoniae and lung epithelial cells on a cellular level, neither about the role of capsule polysaccharide, one of its best characterised virulence factors, in this interaction. 相似文献38.
The West Nile virus: its recent emergence in North America 总被引:6,自引:0,他引:6
Garmendia AE Van Kruiningen HJ French RA 《Microbes and infection / Institut Pasteur》2001,3(3):223-229
West Nile fever emerged in New York in the summer of 1999 when seven people, several horses and thousands of wild birds died. It was soon established that the human disease and the mortality of birds were related. Continued surveillance detected West Nile virus in mosquitoes, birds, horses, small mammals, bats and humans, and has shown its spread to several northeastern states. These events confirm the establishment of West Nile virus endemically in the United States. 相似文献
39.
40.
Characterization of TccP-mediated N-WASP activation during enterohaemorrhagic Escherichia coli infection 总被引:4,自引:1,他引:3
Subversion of the host cell cytoskeleton is the hallmark of enterohaemorrhagic Escherichia coli (EHEC) infection. EHEC translocates the trans -membrane receptor protein Tir (translocated intimin receptor), which links the extracellular bacterium to the eukaryotic cell actin cytoskeleton, triggering formation of actin-rich pedestals beneath adherent bacteria. Tir-mediated actin accretion by EHEC requires TccP (Tir cytoskeleton coupling protein), a recently discovered type III secretion system effector protein which, following translocation, binds and activates Wiskott–Aldrich syndrome protein (N-WASP), which in turn activates the actin-related protein 2/3 complex leading to localized polymerization of actin. In this study, truncated N-WASP and TccP derivatives were generated and tested in in vitro actin polymerization and epithelial cell infection assays. The C-terminal amino acids 253–276 of the GTPase binding domain (GBD) of N-WASP were identified as essential, although not sufficient, for TccP:N-WASP protein:protein interaction, TccP-mediated N-WASP activation and induction of actin polymerization. TccP from EHEC O157:H7 strain EDL933 consists of a unique N-terminal domain and six proline-rich repeats. Progressive deletions within the N-terminus of TccP revealed that residues 1–21 are necessary and sufficient for its translocation, while amino acids 1–181, encompassing the N-terminal translocation signal and two proline-rich repeats, are sufficient for triggering actin polymerization in EHEC-infected epithelial cells and in in vitro actin polymerization assays. This study defines the modular domain structure of TccP and the molecular basis of TccP-mediated N-WASP activation and EHEC-induced remodelling of the host actin cytoskeleton. 相似文献