全文获取类型
收费全文 | 167篇 |
免费 | 12篇 |
国内免费 | 2篇 |
专业分类
耳鼻咽喉 | 1篇 |
儿科学 | 5篇 |
妇产科学 | 1篇 |
基础医学 | 17篇 |
口腔科学 | 1篇 |
临床医学 | 7篇 |
内科学 | 16篇 |
神经病学 | 18篇 |
特种医学 | 10篇 |
外科学 | 37篇 |
综合类 | 11篇 |
预防医学 | 4篇 |
眼科学 | 1篇 |
药学 | 20篇 |
中国医学 | 4篇 |
肿瘤学 | 28篇 |
出版年
2023年 | 2篇 |
2022年 | 8篇 |
2021年 | 7篇 |
2020年 | 6篇 |
2019年 | 7篇 |
2018年 | 8篇 |
2017年 | 6篇 |
2016年 | 5篇 |
2015年 | 16篇 |
2014年 | 15篇 |
2013年 | 14篇 |
2012年 | 3篇 |
2011年 | 6篇 |
2010年 | 3篇 |
2009年 | 15篇 |
2008年 | 8篇 |
2007年 | 8篇 |
2006年 | 6篇 |
2005年 | 6篇 |
2004年 | 4篇 |
2003年 | 3篇 |
2002年 | 7篇 |
2001年 | 2篇 |
2000年 | 3篇 |
1999年 | 2篇 |
1998年 | 1篇 |
1996年 | 1篇 |
1994年 | 1篇 |
1993年 | 2篇 |
1985年 | 1篇 |
1983年 | 1篇 |
1982年 | 2篇 |
1981年 | 2篇 |
排序方式: 共有181条查询结果,搜索用时 31 毫秒
1.
2.
3.
Pol32 is a subunit of Saccharomyces cerevisiae DNA polymerase δ required in DNA replication and repair. To gain insight into the function of Pol32 and to determine in which
repair pathway POL32 may be involved, we extended the analysis of the pol32Δ mutant with respect to UV and methylation sensitivity, UV-induced mutagenesis; and we performed an epistasis analysis of
UV sensitivity by combining the pol32Δ with mutations in several genes for postreplication repair (RAD6 group), nucleotide excision repair (RAD3 group) and recombinational repair (RAD52 group). These studies showed that pol32Δ is deficient in UV-induced mutagenesis and place POL32 in the error-prone RAD6/REV3 pathway. We also found that the increase in the CAN1 spontaneous forward mutation of different rad mutators relies entirely or partially on a functional POL32 gene. Moreover, in a two-hybrid screen, we observed that Pol32 interacts with Srs2, a DNA helicase required for DNA replication
and mutagenesis. Simultaneous deletion of POL32 and SRS2 dramatically decreases cellular viability at 15 °C and greatly increases cellular sensitivity to hydroxyurea at the permissive
temperature. Based on these findings, we propose that POL32 defines a link between the DNA polymerase and helicase activities, and plays a role in the mutagenic bypass repair pathway.
Received: 25 May 2000 / Accepted: 3 July 2000 相似文献
4.
The peptide melittin, the main constituent of bee venom is a potent stimulus for the generation of an eosinophil chemotactic factor (ECF) from human polymorphonuclear neutrophils, rat mast cells and rat peritoneal cells depleted in mast cells. Optimal EFC induction required a sublytic activation of the cells. With each cell type the kinetics of ECF generation were similar in that after an early rise in activity a steep fall off occurred at later times of incubation suggesting a mechanism of inactivation. The induction of ECF by melittin is increased in the presence of calcium. The polar portion of the melittin molecule (aminoacids 20–26) is responsible for the generation of the chemotactic activity. Other peptides of honey bee venom such as the mast cell degranulating peptide (MCD) or apamine do not initiate ECF release. It appears that melittin leads to ECF induction via the phospholipase A2-arachidonic acid dependent pathway of cell activation. Our data suggests that the lipid mediator ECF can be obtained from phagocytes and mast cells thus indicating the interdependence of inflammatory reactions. 相似文献
5.
6.
7.
8.
9.
10.