全文获取类型
收费全文 | 78篇 |
免费 | 0篇 |
专业分类
现状及发展 | 31篇 |
研究方法 | 4篇 |
综合类 | 43篇 |
出版年
2012年 | 2篇 |
2011年 | 2篇 |
2010年 | 1篇 |
2009年 | 1篇 |
2008年 | 4篇 |
2007年 | 5篇 |
2006年 | 6篇 |
2005年 | 3篇 |
2004年 | 1篇 |
2003年 | 5篇 |
2002年 | 4篇 |
2001年 | 1篇 |
2000年 | 3篇 |
1999年 | 1篇 |
1998年 | 1篇 |
1993年 | 1篇 |
1992年 | 3篇 |
1990年 | 5篇 |
1989年 | 2篇 |
1988年 | 2篇 |
1987年 | 5篇 |
1985年 | 3篇 |
1984年 | 4篇 |
1975年 | 2篇 |
1971年 | 3篇 |
1969年 | 2篇 |
1968年 | 3篇 |
1967年 | 1篇 |
1966年 | 1篇 |
1958年 | 1篇 |
排序方式: 共有78条查询结果,搜索用时 31 毫秒
31.
Enhancement of chilling tolerance of a cyanobacterium by genetic manipulation of fatty acid desaturation 总被引:55,自引:0,他引:55
The sensitivity (or tolerance) of plants to chilling determines their choice of natural habitat and also limits the worldwide production of crops. Although the molecular mechanism for chilling sensitivity has long been debated, no definitive conclusion has so far been reached about its nature. A probable hypothesis, however, is that chilling injury is initiated by phase transition of lipids of cellular membranes, as demonstrated for cyanobacteria, which serve as a model system for the plant cells. Because the phase transition temperature depends on the degree of unsaturation of fatty acids of the membrane lipids, it is predicted that the chilling tolerance of plants can be altered by genetically manipulating fatty-acid desaturation by introducing double bonds into fatty acids of membrane lipids. Here we report the cloning of a gene for the plant-type desaturation (termed desA). The introduction of this gene from a chilling-resistant cyanobacterium, Synechocystis PCC6803, into a chilling-sensitive cyanobacterium, Anacystis nidulans, increases the tolerance of the recipient to low temperature. 相似文献
32.
We tested the activity of low-molecular-weight enzyme inhibitors with immunomodifying actions on the suppression of experimental allergic encephalomyelitis (EAE). Of the agents tested the inhibitors of alkaline phosphatase, aminopeptidase B and esterase gave significant protection against the clinical expression of EAE in guinea pigs. 相似文献
33.
Sequence and expression of a frog brain complementary DNA encoding a kainate-binding protein 总被引:11,自引:0,他引:11
K Wada C J Dechesne S Shimasaki R G King K Kusano A Buonanno D R Hampson C Banner R J Wenthold Y Nakatani 《Nature》1989,342(6250):684-689
Excitatory amino acids (EAAs) are important neurotransmitters in the vertebrate central nervous system. Electrophysiological and ligand-binding studies indicate that at least three different receptor subtypes for EAAs exist--N-methyl-D-aspartate, kainate and quisqualate receptor subtypes--on the basis of the preferred agonist of the receptors. We recently purified a kainate-binding protein (KBP) from frog (Rana pipiens berlandieri) brain by domoic acid (a high-affinity kainate analogue) affinity chromatography, and showed that the kainate-binding activity was associated with a protein of relative molecular mass 48,000 (Mr 48 K). The pharmacological properties and the anatomical distribution of KBP were consistent with those of a kainate receptor-ionophore complex. We have now isolated a complementary DNA encoding KBP of Mr 48 K. The deduced amino-acid sequence of the KBP has similar hydrophobic profiles to those found in other ligand-gated ion channel subunits, and shows some amino-acid sequence similarities to the corresponding regions of brain nicotinic acetylcholine receptor subunits. Localization of the KBP messenger RNAs by in situ hybridization histochemistry is compatible with the results of immunohistochemistry and receptor autoradiography studies. COS-7 cells transfected with the cDNA encoding the KBP show high-affinity kainate-binding activity with pharmacological properties similar to those of the biochemically purified KBP. These results provide the first molecular characterization of an EAA-binding site and raise the possibility that the KBP cDNA encodes a ligand-binding subunit of a kainate receptor-ionophore complex. 相似文献
34.
Primary structure and functional expression of the inositol 1,4,5-trisphosphate-binding protein P400 总被引:53,自引:0,他引:53
Cloning and expression of functional P400 protein from cerebellar Purkinje neurons shows that this protein is a receptor for inositol 1,4,5-trisphosphate, a second messenger that mediates the release of intracellular calcium. 相似文献
35.
36.
Summary Artificial bright light cycles (LD 816) of about 5000 lux during the light period were applied to two subjects in a temporal isolation unit, who had shown free-running circadian rhythms in sleep-wakefulness and rectal temperature. The circadian rhythms were successfully entrained by the artificial light cycle, but the phase relation of the rhythms to the light cycle was substantially different between the two subjects. The result indicated that the artificial bright lights are able to reset human circadian rhythms. 相似文献
37.
Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1beta production 总被引:1,自引:0,他引:1
Saitoh T Fujita N Jang MH Uematsu S Yang BG Satoh T Omori H Noda T Yamamoto N Komatsu M Tanaka K Kawai T Tsujimura T Takeuchi O Yoshimori T Akira S 《Nature》2008,456(7219):264-268
Systems for protein degradation are essential for tight control of the inflammatory immune response. Autophagy, a bulk degradation system that delivers cytoplasmic constituents into autolysosomes, controls degradation of long-lived proteins, insoluble protein aggregates and invading microbes, and is suggested to be involved in the regulation of inflammation. However, the mechanism underlying the regulation of inflammatory response by autophagy is poorly understood. Here we show that Atg16L1 (autophagy-related 16-like 1), which is implicated in Crohn's disease, regulates endotoxin-induced inflammasome activation in mice. Atg16L1-deficiency disrupts the recruitment of the Atg12-Atg5 conjugate to the isolation membrane, resulting in a loss of microtubule-associated protein 1 light chain 3 (LC3) conjugation to phosphatidylethanolamine. Consequently, both autophagosome formation and degradation of long-lived proteins are severely impaired in Atg16L1-deficient cells. Following stimulation with lipopolysaccharide, a ligand for Toll-like receptor 4 (refs 8, 9), Atg16L1-deficient macrophages produce high amounts of the inflammatory cytokines IL-1beta and IL-18. In lipopolysaccharide-stimulated macrophages, Atg16L1-deficiency causes Toll/IL-1 receptor domain-containing adaptor inducing IFN-beta (TRIF)-dependent activation of caspase-1, leading to increased production of IL-1beta. Mice lacking Atg16L1 in haematopoietic cells are highly susceptible to dextran sulphate sodium-induced acute colitis, which is alleviated by injection of anti-IL-1beta and IL-18 antibodies, indicating the importance of Atg16L1 in the suppression of intestinal inflammation. These results demonstrate that Atg16L1 is an essential component of the autophagic machinery responsible for control of the endotoxin-induced inflammatory immune response. 相似文献
38.
Tomita S Adesnik H Sekiguchi M Zhang W Wada K Howe JR Nicoll RA Bredt DS 《Nature》2005,435(7045):1052-1058
AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors mediate fast excitatory synaptic transmission in the brain. These ion channels rapidly deactivate and desensitize, which determine the time course of synaptic transmission. Here, we find that the AMPA receptor interacting protein, stargazin, not only mediates AMPA receptor trafficking but also shapes synaptic responses by slowing channel deactivation and desensitization. The cytoplasmic tail of stargazin determines receptor trafficking, whereas the ectodomain controls channel properties. Stargazin alters AMPA receptor kinetics by increasing the rate of channel opening. Disrupting the interaction of stargazin ectodomain with hippocampal AMPA receptors alters the amplitude and shape of synaptic responses, establishing a crucial function for stargazin in controlling the efficacy of synaptic transmission in the brain. 相似文献
39.
T. Sakata K. Fukagawa K. Fujimoto H. Yoshimatsu T. Shiraishi H. Wada 《Cellular and molecular life sciences : CMLS》1988,44(3):216-218
Summary Histamine antagonists were infused into the third ventricle of the cerebrum in rats. All the H1-, but none of the H2-antagonists tested, induced initial feeding during the early portion of the light phase when histamine level was highest. No periprandial drinking was observed. Ambulation increased during feeding. The effect on feeding was attenuated when brain histamine was normally low during the early portion of the dark phase, or was decreased by -fluoromethylhistidine. Hypothalamic neuronal histamine may suppress food intake through H1-receptors, and diurnal fluctuations of food intake may mirror neuronal histamine levels. 相似文献
40.
D. Robinette S. Wada T. Arroll M. G. Levy W. L. Miller E. J. Noga 《Cellular and molecular life sciences : CMLS》1998,54(5):467-475
Three antibacterial proteins were isolated from acid extracts of channel catfish (Ictalurus punctatus) skin by cation exchange chromatography and reverse-phase high-pressure liquid chromatography. The molecular masses of the
proteins were 15.5, 15.5 and 30 kD as determined by SDS-polyacrylamide gel electrophoresis. Mass spectrometry, amino acid
composition and amino acid sequence data suggest that the most abundant protein is closely related to histone H2B. The H2B-like
protein was inhibitory to Aeromonas hydrophila and Saprolegnia spp., which are important bacterial and fungal pathogens of fish. These findings suggest that histones may be important defensive
molecules in fish.
Received 22 December 1997; received after revision 5 March 1998; accepted 5 March 1998 相似文献