全文获取类型
收费全文 | 486篇 |
免费 | 17篇 |
专业分类
503篇 |
出版年
2019年 | 2篇 |
2018年 | 3篇 |
2017年 | 9篇 |
2016年 | 8篇 |
2015年 | 5篇 |
2014年 | 12篇 |
2013年 | 20篇 |
2012年 | 18篇 |
2011年 | 23篇 |
2010年 | 11篇 |
2009年 | 9篇 |
2008年 | 29篇 |
2007年 | 29篇 |
2006年 | 22篇 |
2005年 | 24篇 |
2004年 | 26篇 |
2003年 | 30篇 |
2002年 | 16篇 |
2001年 | 21篇 |
2000年 | 19篇 |
1999年 | 18篇 |
1998年 | 10篇 |
1997年 | 11篇 |
1996年 | 2篇 |
1995年 | 5篇 |
1994年 | 2篇 |
1993年 | 4篇 |
1992年 | 7篇 |
1991年 | 6篇 |
1990年 | 4篇 |
1989年 | 8篇 |
1988年 | 2篇 |
1987年 | 6篇 |
1986年 | 2篇 |
1985年 | 9篇 |
1984年 | 4篇 |
1983年 | 8篇 |
1982年 | 4篇 |
1981年 | 2篇 |
1980年 | 6篇 |
1979年 | 7篇 |
1978年 | 3篇 |
1976年 | 4篇 |
1975年 | 3篇 |
1974年 | 7篇 |
1973年 | 2篇 |
1972年 | 5篇 |
1970年 | 5篇 |
1969年 | 2篇 |
1967年 | 2篇 |
排序方式: 共有503条查询结果,搜索用时 0 毫秒
501.
502.
A novel sulfotransferase activity was discovered in fetal bovine serum using pig skin dermatan sulfate as an acceptor and [35S]3'-phosphoadenosine 5'-phosphosulfate as a sulfate donor. The enzyme was separated from chondroitin:GalNAc 6-O-sulfotransferase by chromatographic techniques. Enzymatic analysis of the reaction products demonstrated that the enzyme transferred sulfate to the C6 position of the GalNAc residue in the sequence -iduronic acid alpha1-3GalNAc beta1-4iduronic acid-. Thus, the enzyme has been identified as a hitherto unreported dermatan sulfate:GalNAc 6-O-sulfotransferase. The finding is in sharp contrast to the current concept that in dermatan sulfate biosynthesis GalNAc 4-O-sulfation is a prerequisite for iduronic acid formation by C5 epimerase. 相似文献
503.
Identification of cell-binding site of angiomodulin (AGM/TAF/Mac25) that interacts with heparan sulfates on cell surface. 总被引:3,自引:0,他引:3
J Sato S Hasegawa K Akaogi H Yasumitsu S Yamada K Sugahara K Miyazaki 《Journal of cellular biochemistry》1999,75(2):187-195
Angiomodulin (AGM/TAF/mac25) is a 30-kDa glycoprotein that was identified as an integrin-independent cell adhesion protein secreted by human bladder carcinoma cells. AGM is highly accumulated in small blood vessels of tumor tissues. In the present study, we attempted to identify the cell surface receptor and the cell-binding site of AGM using ECV-304 human vascular endothelial cells and BALB/c3T3 mouse fibroblasts. Heparin, heparan sulfate, and dextran sulfate, but not chondroitin sulfate, inhibited both adhesion of the two cell lines to AGM-coated plates and binding of AGM to these cells. Treatment of cells with heparinase, but not chondroitinase, inhibited both cell adhesion to AGM and AGM binding to cells. These results strongly suggested that heparan sulfates are the major receptor for AGM. Furthermore, we determined a 20-amino acid sequence within AGM molecule as its major cell-binding site. The synthetic peptide for the cell-binding sequence showed cell adhesion activity comparable to that of AGM, and the activity was inhibited by heparin and heparan sulfate. The peptide competitively inhibited cell adhesion to AGM and the binding of AGM to cells. These results indicated that AGM binds to cells through interaction of the identified cell-binding sequence with heparan sulfates on cell surface. It was also found that the heparan sulfate-binding peptide inhibited the formation of capillary tube-like structures of vascular endothelial cells in culture. 相似文献