全文获取类型
收费全文 | 444篇 |
免费 | 35篇 |
出版年
2023年 | 3篇 |
2022年 | 5篇 |
2021年 | 20篇 |
2020年 | 12篇 |
2019年 | 8篇 |
2018年 | 11篇 |
2017年 | 12篇 |
2016年 | 16篇 |
2015年 | 25篇 |
2014年 | 33篇 |
2013年 | 32篇 |
2012年 | 35篇 |
2011年 | 28篇 |
2010年 | 16篇 |
2009年 | 7篇 |
2008年 | 24篇 |
2007年 | 18篇 |
2006年 | 11篇 |
2005年 | 19篇 |
2004年 | 11篇 |
2003年 | 11篇 |
2002年 | 10篇 |
2001年 | 9篇 |
2000年 | 7篇 |
1999年 | 14篇 |
1998年 | 7篇 |
1997年 | 5篇 |
1996年 | 3篇 |
1995年 | 1篇 |
1994年 | 5篇 |
1993年 | 1篇 |
1992年 | 7篇 |
1991年 | 9篇 |
1990年 | 6篇 |
1989年 | 6篇 |
1988年 | 5篇 |
1987年 | 6篇 |
1986年 | 3篇 |
1985年 | 3篇 |
1984年 | 3篇 |
1983年 | 2篇 |
1980年 | 3篇 |
1979年 | 2篇 |
1978年 | 2篇 |
1976年 | 2篇 |
1975年 | 1篇 |
排序方式: 共有479条查询结果,搜索用时 15 毫秒
1.
2.
Sequestration analysis for RNA polymerase I transcription factors with various deletion and point mutations reveals different functional regions of the mouse rRNA gene promoter. 总被引:7,自引:3,他引:4
下载免费PDF全文
![点击此处可从《Molecular and cellular biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
M Nagamine T Kishimoto J Aono H Kato R Kominami M Muramatsu 《Molecular and cellular biology》1987,7(4):1486-1495
3.
J Nakagawa D von der Ahe D Pearson B A Hemmings S Shibahara Y Nagamine 《The Journal of biological chemistry》1988,263(5):2460-2468
4.
Induction and desensitization of plasminogen activator gene expression by tumor promoters 总被引:15,自引:0,他引:15
J L Degen R D Estensen Y Nagamine E Reich 《The Journal of biological chemistry》1985,260(23):12426-12433
5.
A distinct basic fibroblast growth factor (FGF-2)/FGF receptor interaction distinguishes urokinase-type plasminogen activator induction from mitogenicity in endothelial cells. 总被引:2,自引:2,他引:0
下载免费PDF全文
![点击此处可从《Molecular biology of the cell》网站下载免费的PDF全文](/ch/ext_images/free.gif)
M Rusnati P Dell'Era C Urbinati E Tanghetti M L Massardi Y Nagamine E Monti M Presta 《Molecular biology of the cell》1996,7(3):369-381
Basic fibroblast growth factor (FGF-2) induces cell proliferation and urokinase-type plasminogen activator (uPA) production in fetal bovine aortic endothelial GM 7373 cells. In the present paper we investigated the role of the interaction of FGF-2 with tyrosine-kinase (TK) FGF receptors (FGFRs) in mediating uPA up-regulation in these cells. The results show that FGF-2 antagonists suramin, protamine, heparin, the synthetic peptide FGF-2(112-155), and a soluble form of FGFR-1 do not inhibit FGF-2-mediated uPA up-regulation at concentrations that affect growth factor binding to cell surface receptors and mitogenic activity. In contrast, tyrosine phosphorylation inhibitors and overexpression of a dominant negative TK- mutant of FGFR-1 abolish the uPA-inducing activity of FGF-2, indicating that FGFR and its TK activity are essential in mediating uPA induction. Accordingly, FGF-2 induces uPA up-regulation in Chinese hamster ovary cells transfected with wild-type FGFR-1, -2, -3, or -4 but not with TK- FGFR-1 mutant. Small unilamellar phosphatidyl choline:cholesterol vesicles loaded with FGF-2 increased uPA production in GM 7373 cells in the absence of a mitogenic response. Liposome-encapsulated FGF-2 showed a limited but significant capacity, relative to free FGF-2, to interact with FGFR both at 4 degrees C and 37 degrees C and to be internalized within the cell. uPA up-regulation by liposome-encapsulated FGF-2 was quenched by neutralizing anti-FGF-2 antibodies, indicating that the activity of liposome-delivered FGF-2 is mediated by an extracellular action of the growth factor. Taken together, the data indicate that a distinct interaction of FGF-2 with FGFR, quantitatively and/or qualitatively different from the one that leads to mitogenicity, is responsible for the uPA-inducing activity of the growth factor. 相似文献
6.
The active site of Bacillus macerans cyclodextrin glucanotransferase (CGTase) was examined by use of derivatives of phenyl alpha-maltopentaoside and phenyl alpha-glucoside as the substrates and acceptors, respectively. The active site of this enzyme is considered to be composed of tandem subsites (S4, S3, S2, S1, S1', S2', etc.) geometrically complementary to several glucose residues, and the alpha-1,4-glycosidic linkage of a substrate is split between S1 and S1'. The features of subsites S3 and S4 of the glycon binding site were estimated from the modes of the enzymatic action on phenyl alpha-maltopentaoside (G-G-G-G-G-phi; G, glucose residue; phi, phenyl residue; -, alpha-1,4-glycosidic bond) and its derivatives in which the CH2OH groups of the non-reducing-end glucose residues were converted to CH2I (IG-G-G-G-G-phi; IG, 6-deoxy-6-iodo-D-glucose residue), CH2NH2 (AG-G-G-G-G-phi; AG, 6-amino-6-deoxy-D-glucose residue), or COOH (CG-G-G-G-G-phi; CG, glucuronic acid residue). p-Nitrophenyl alpha-glucopyranoside (G-P; P, p-nitrophenyl residue) was used as an acceptor. HPLC analysis of the digests revealed that the CG residue of CG-G-G-G-G-phi was excluded from subsite S3, while it was accommodated in subsite S4. The Km and Vmax values for CG-G-G-G-G-phi were remarkably larger and smaller, respectively, than those for any other substrates.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
7.
8.
9.
10.
Ayaka Komatsu Izumi Iida Yusuke Nasu Genki Ito Fumiko Harada Sari Kishikawa Stephen J. Moss Takeyasu Maeda Miho Terunuma 《The Journal of biological chemistry》2022,298(5)
Hyperammonemia is known to cause various neurological dysfunctions such as seizures and cognitive impairment. Several studies have suggested that hyperammonemia may also be linked to the development of Alzheimer’s disease (AD). However, the direct evidence for a role of ammonia in the pathophysiology of AD remains to be discovered. Herein, we report that hyperammonemia increases the amount of mature amyloid precursor protein (mAPP) in astrocytes, the largest and most prevalent type of glial cells in the central nervous system that are capable of metabolizing glutamate and ammonia, and promotes amyloid beta (Aβ) production. We demonstrate the accumulation of mAPP in astrocytes was primarily due to enhanced endocytosis of mAPP from the plasma membrane. A large proportion of internalized mAPP was targeted not to the lysosome, but to the endoplasmic reticulum, where processing enzymes β-secretase BACE1 (beta-site APP cleaving enzyme 1) and γ-secretase presenilin-1 are expressed, and mAPP is cleaved to produce Aβ. Finally, we show the ammonia-induced production of Aβ in astrocytic endoplasmic reticulum was specific to Aβ42, a principal component of senile plaques in AD patients. Our studies uncover a novel mechanism of Aβ42 production in astrocytes and also provide the first evidence that ammonia induces the pathogenesis of AD by regulating astrocyte function. 相似文献