全文获取类型
收费全文 | 61篇 |
免费 | 2篇 |
专业分类
63篇 |
出版年
2018年 | 1篇 |
2015年 | 3篇 |
2014年 | 1篇 |
2013年 | 2篇 |
2010年 | 2篇 |
2009年 | 1篇 |
2007年 | 1篇 |
2005年 | 3篇 |
2004年 | 1篇 |
2002年 | 1篇 |
2000年 | 2篇 |
1999年 | 2篇 |
1998年 | 5篇 |
1997年 | 1篇 |
1996年 | 4篇 |
1995年 | 2篇 |
1994年 | 2篇 |
1993年 | 4篇 |
1990年 | 1篇 |
1989年 | 3篇 |
1988年 | 1篇 |
1959年 | 2篇 |
1958年 | 3篇 |
1957年 | 2篇 |
1956年 | 1篇 |
1954年 | 1篇 |
1952年 | 1篇 |
1951年 | 2篇 |
1950年 | 2篇 |
1949年 | 5篇 |
1948年 | 1篇 |
排序方式: 共有63条查询结果,搜索用时 0 毫秒
1.
2.
3.
4.
5.
6.
alpha 1-Proteinase inhibitor (alpha 1-PI), a member of the serineproteinase inhibitor superfamily, has a primary role in controllingneutrophil elastase activity within the mammalian circulation. Severalstudies have indicated that the reactive center region of alpha 1-PI, theamino acid sequence of which is critical to recognition of and binding totarget proteinases, is highly divergent within and among species. Thisappears to be a consequence of accelerated rates of evolution that may havebeen driven by positive Darwinian selection. In order to examine this andother features of alpha 1-PI evolution in more detail, we have isolated andsequenced cDNAs representing alpha 1- PI mRNAs of the mouse species Mussaxicola and Mus minutoides and have compared these with a number of othermammalian alpha 1-PI mRNAs. Relative to other mammalian mRNAs, the extentof nonsynonymous substitution is generally high throughout the alpha 1-PImRNA molecule, indicating greater overall rates of amino acid substitution.Within and among mouse species, the 5'-half of the mRNA, but not the3'-half, has been homogenized by concerted evolution. Finally, the reactivecenter is under diversifying or positive Darwinian selection in muridrodents (rats, mice) and guinea pigs yet is under purifying selection inprimates and artiodactyls. The significance of these findings to alpha 1-PIfunction and the possible selective forces driving evolution of serpins ingeneral are discussed. 相似文献
7.
8.
9.
Gerd Reuter Roland Schauer Claudia Szeiki Johannis P Kamerling Johannes FG Vliegenthart 《Glycoconjugate journal》1989,6(1):35-44
Periodate oxidation of terminalN-acetyl- andN-glycoloylneuraminic acid residues in the mucins from edible bird nest substance and pig submandibular gland, respectively, can be carried out under conditions which exclusively give rise to the formation of the C-7 analogues of these sialic acids. In contrast, the C-8 compounds can be obtained in a maximum yield of about 40%. Under identical conditions,N-glycoloylneuraminic acid is oxidized about 1.5 times faster than theN-acetylated derivative. After release of the sialic acids by acid hydrolysis, the characterization of the oxidation products was carried out by TLC, by GLC and GLC-MS of the corresponding pertrimethylsilyl derivatives, and by 500-MHz1H-NMR spectroscopy. In addition, molar response factors for GLC analysis and extinction coefficients in the orcinol/Fe3+/HCl assay were determined. 相似文献
10.
Marieke Meijer Bernhard Dörr Hanna CA Lammertse Chrysanthi Blithikioti Jan RT van Weering Ruud FG Toonen Thomas H Söllner Matthijs Verhage 《The EMBO journal》2018,37(2):300-320
Tyrosine kinases are important regulators of synaptic strength. Here, we describe a key component of the synaptic vesicle release machinery, Munc18‐1, as a phosphorylation target for neuronal Src family kinases (SFKs). Phosphomimetic Y473D mutation of a SFK phosphorylation site previously identified by brain phospho‐proteomics abolished the stimulatory effect of Munc18‐1 on SNARE complex formation (“SNARE‐templating”) and membrane fusion in vitro. Furthermore, priming but not docking of synaptic vesicles was disrupted in hippocampal munc18‐1‐null neurons expressing Munc18‐1Y473D. Synaptic transmission was temporarily restored by high‐frequency stimulation, as well as by a Munc18‐1 mutation that results in helix 12 extension, a critical conformational step in vesicle priming. On the other hand, expression of non‐phosphorylatable Munc18‐1 supported normal synaptic transmission. We propose that SFK‐dependent Munc18‐1 phosphorylation may constitute a potent, previously unknown mechanism to shut down synaptic transmission, via direct occlusion of a Synaptobrevin/VAMP2 binding groove and subsequent hindrance of conformational changes in domain 3a responsible for vesicle priming. This would strongly interfere with the essential post‐docking SNARE‐templating role of Munc18‐1, resulting in a largely abolished pool of releasable synaptic vesicles. 相似文献