全文获取类型
收费全文 | 116篇 |
免费 | 30篇 |
出版年
2022年 | 2篇 |
2021年 | 2篇 |
2019年 | 1篇 |
2017年 | 4篇 |
2016年 | 1篇 |
2015年 | 3篇 |
2014年 | 7篇 |
2013年 | 11篇 |
2012年 | 4篇 |
2011年 | 7篇 |
2010年 | 9篇 |
2009年 | 7篇 |
2008年 | 7篇 |
2007年 | 7篇 |
2006年 | 8篇 |
2005年 | 7篇 |
2004年 | 5篇 |
2003年 | 9篇 |
2002年 | 6篇 |
2001年 | 8篇 |
2000年 | 3篇 |
1999年 | 5篇 |
1998年 | 1篇 |
1997年 | 1篇 |
1996年 | 3篇 |
1995年 | 2篇 |
1994年 | 3篇 |
1993年 | 1篇 |
1992年 | 2篇 |
1990年 | 2篇 |
1989年 | 3篇 |
1988年 | 1篇 |
1987年 | 1篇 |
1986年 | 1篇 |
1972年 | 1篇 |
1962年 | 1篇 |
排序方式: 共有146条查询结果,搜索用时 15 毫秒
1.
Mandy L. Roberts-Crowley Tora Mitra-Ganguli Liwang Liu Ann R. Rittenhouse 《Cell calcium》2009,45(6):589-601
Great skepticism has surrounded the question of whether modulation of voltage-gated Ca2+ channels (VGCCs) by the polyunsaturated free fatty acid arachidonic acid (AA) has any physiological basis. Here we synthesize findings from studies of both native and recombinant channels where micromolar concentrations of AA consistently inhibit both native and recombinant activity by stabilizing VGCCs in one or more closed states. Structural requirements for these inhibitory actions include a chain length of at least 18 carbons and multiple double bonds located near the fatty acid's carboxy terminus. Acting at a second site, AA increases the rate of VGCC activation kinetics, and in CaV2.2 channels, increases current amplitude. We present evidence that phosphatidylinositol 4,5-bisphosphate (PIP2), a palmitoylated accessory subunit (β2a) of VGCCs and AA appear to have overlapping sites of action giving rise to complex channel behavior. Their actions converge in a physiologically relevant manner during muscarinic modulation of VGCCs. We speculate that M1 muscarinic receptors may stimulate multiple lipases to break down the PIP2 associated with VGCCs and leave PIP2's freed fatty acid tails bound to the channels to confer modulation. This unexpectedly simple scheme gives rise to unanticipated predictions and redirects thinking about lipid regulation of VGCCs. 相似文献
2.
The cloned human oestrogen receptor contains a mutation which alters its hormone binding properties. 总被引:39,自引:7,他引:32 下载免费PDF全文
L Tora A Mullick D Metzger M Ponglikitmongkol I Park P Chambon 《The EMBO journal》1989,8(7):1981-1986
We demonstrate here that the human oestrogen receptor (hER) cDNA clone pOR8 obtained from MCF-7 cells contains an artefactual point mutation which results in the substitution of a valine for a glycine at amino acid position 400 (Gly-400----Val-400). This mutation in the hormone binding domain of the cloned hER destabilizes its structure and decreases its apparent affinity for oestradiol at 25 degrees C, but not at 4 degrees C, when compared with the wild-type hER with a Gly-400. 相似文献
3.
4.
Xiaojun Han Rita L. Civiello Charles M. Conway Deborah A. Cook Carl D. Davis Andrew P. Degnan Xiang-Jun Jiang Robert Macci Neil R. Mathias Paul Moench Sokhom S. Pin Richard Schartman Laura J. Signor George Thalody George Tora Valerie Whiterock Cen Xu John E. Macor Gene M. Dubowchik 《Bioorganic & medicinal chemistry letters》2013,23(12):3674
5.
6.
Leandro Moretti Jack Stalfort Thomas Harrison Barker Daniel Abebayehu 《The Journal of biological chemistry》2022,298(2)
Various forms of fibrosis, comprising tissue thickening and scarring, are involved in 40% of deaths across the world. Since the discovery of scarless functional healing in fetuses prior to a certain stage of development, scientists have attempted to replicate scarless wound healing in adults with little success. While the extracellular matrix (ECM), fibroblasts, and inflammatory mediators have been historically investigated as separate branches of biology, it has become increasingly necessary to consider them as parts of a complex and tightly regulated system that becomes dysregulated in fibrosis. With this new paradigm, revisiting fetal scarless wound healing provides a unique opportunity to better understand how this highly regulated system operates mechanistically. In the following review, we navigate the four stages of wound healing (hemostasis, inflammation, repair, and remodeling) against the backdrop of adult versus fetal wound healing, while also exploring the relationships between the ECM, effector cells, and signaling molecules. We conclude by singling out recent findings that offer promising leads to alter the dynamics between the ECM, fibroblasts, and inflammation to promote scarless healing. One factor that promises to be significant is fibroblast heterogeneity and how certain fibroblast subpopulations might be predisposed to scarless healing. Altogether, reconsidering fetal wound healing by examining the interplay of the various factors contributing to fibrosis provides new research directions that will hopefully help us better understand and address fibroproliferative diseases, such as idiopathic pulmonary fibrosis, liver cirrhosis, systemic sclerosis, progressive kidney disease, and cardiovascular fibrosis. 相似文献
7.
8.
9.
10.