全文获取类型
收费全文 | 96篇 |
免费 | 10篇 |
出版年
2022年 | 1篇 |
2021年 | 3篇 |
2020年 | 1篇 |
2019年 | 1篇 |
2018年 | 2篇 |
2017年 | 1篇 |
2015年 | 4篇 |
2014年 | 4篇 |
2013年 | 1篇 |
2012年 | 3篇 |
2011年 | 4篇 |
2010年 | 3篇 |
2009年 | 3篇 |
2008年 | 1篇 |
2007年 | 5篇 |
2006年 | 4篇 |
2005年 | 5篇 |
2004年 | 7篇 |
2003年 | 1篇 |
2002年 | 4篇 |
2001年 | 5篇 |
2000年 | 3篇 |
1999年 | 9篇 |
1998年 | 10篇 |
1997年 | 3篇 |
1996年 | 2篇 |
1995年 | 2篇 |
1994年 | 4篇 |
1993年 | 4篇 |
1989年 | 1篇 |
1986年 | 1篇 |
1985年 | 1篇 |
1984年 | 2篇 |
1977年 | 1篇 |
排序方式: 共有106条查询结果,搜索用时 15 毫秒
31.
Cell-to-cell transfer of glial proteins to the squid giant axon: The glia- neuron protein transfer hypothesis
下载免费PDF全文
![点击此处可从《The Journal of cell biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
The hypothesis that glial cells synthesize proteins which are transferred to adjacent neurons was evaluated in the giant fiber of the squid (Loligo pealei). When giant fibers are separated from their neuron cell bodies and incubated in the presence of radioactive amino acids, labeled proteins appear in the glial cells and axoplasm. Labeled axonal proteins were detected by three methods: extrusion of the axoplasm from the giant fiber, autoradiography, and perfusion of the giant fiber. This protein synthesis is completely inhibited by puromycin but is not affected by chloramphenicol. The following evidence indicates that the labeled axonal proteins are not synthesized within the axon itself. (a) The axon does not contain a significant amount of ribosomes or ribosomal RNA. (b) Isolated axoplasm did not incorporate [(3)H]leucine into proteins. (c) Injection of Rnase into the giant axon did not reduce the appearance of newly synthesized proteins in the axoplasm of the giant fiber. These findings, coupled with other evidence, have led us to conclude that the adaxonal glial cells synthesize a class of proteins which are transferred to the giant axon. Analysis of the kinetics of this phenomenon indicates that some proteins are transferred to the axon within minutes of their synthesis in the glial cells. One or more of the steps in the transfer process appear to involve Ca++, since replacement of extracellular Ca++ by either Mg++ or Co++ significantly reduces the appearance of labeled proteins in the axon. A substantial fraction of newly synthesized glial proteins, possibly as much as 40 percent, are transferred to the giant axon. These proteins are heterogeneous and range in size from 12,000 to greater than 200,000 daltons. Comparisons of the amount of amino acid incorporation in glia cells and neuron cell bodies raise the possibility that the adaxonal glial cells may provide an important source of axonal proteins which is supplemental to that provided by axonal transport from the cell body. These findings are discussed with reference to a possible trophic effect of glia on neurons and metabolic cooperation between adaxonal glia and the axon. 相似文献
32.
Groot Nanda de Kuik‐Romeijn Petra van Lee Sang He de Boer Herman A. 《Transgenic research》1999,8(4):319-319
Transgenic Research - 相似文献
33.
Gorski MM Romeijn RJ Eeken JC de Jong AW van Veen BL Szuhai K Mullenders LH Ferro W Pastink A 《DNA Repair》2004,3(6):603-615
The Rad50/Mre11/Nbs1 protein complex has a crucial role in DNA metabolism, in particular in double-strand break (DSB) repair through homologous recombination (HR). To elucidate the role of the Rad50 protein complex in DSB repair in a multicellular eukaryote, we generated a Rad50 deficient Drosophila strain by P-element mediated mutagenesis. Disruption of Rad50 causes retarded development and pupal lethality. To investigate the mechanism of pupal death, brains and wing imaginal discs from third instar larvae were studied in more detail. Wing imaginal discs from Rad50 mutant larvae displayed a 3.5-fold increase in the induction of spontaneous apoptotic cells in comparison to their heterozygous siblings. This finding correlates with increased levels of phosphorylated histone H2Av, indicating an accumulation of DSBs in Rad50 mutant larvae. A 45-fold increase in the frequency of anaphase bridges was detected in the brains of Rad50 deficient larvae, consistent with a role for Rad50 in telomere maintenance and/or replication of DNA. The induction of DSBs and defects in chromosome segregation are in agreement with a role of Drosophila Rad50 in repairing the DSBs that arise during replication. 相似文献
34.
Kujala P Raymond CR Romeijn M Godsave SF van Kasteren SI Wille H Prusiner SB Mabbott NA Peters PJ 《PLoS pathogens》2011,7(12):e1002449
After oral exposure, prions are thought to enter Peyer's patches via M cells and accumulate first upon follicular dendritic cells (FDCs) before spreading to the nervous system. How prions are actually initially acquired from the gut lumen is not known. Using high-resolution immunofluorescence and cryo-immunogold electron microscopy, we report the trafficking of the prion protein (PrP) toward Peyer's patches of wild-type and PrP-deficient mice. PrP was transiently detectable at 1 day post feeding (dpf) within large multivesicular LAMP1-positive endosomes of enterocytes in the follicle-associated epithelium (FAE) and at much lower levels within M cells. Subsequently, PrP was detected on vesicles in the late endosomal compartments of macrophages in the subepithelial dome. At 7-21 dpf, increased PrP labelling was observed on the plasma membranes of FDCs in germinal centres of Peyer's patches from wild-type mice only, identifying FDCs as the first sites of PrP conversion and replication. Detection of PrP on extracellular vesicles displaying FAE enterocyte-derived A33 protein implied transport towards FDCs in association with FAE-derived vesicles. By 21 dpf, PrP was observed on the plasma membranes of neurons within neighbouring myenteric plexi. Together, these data identify a novel potential M cell-independent mechanism for prion transport, mediated by FAE enterocytes, which acts to initiate conversion and replication upon FDCs and subsequent infection of enteric nerves. 相似文献
35.
Pauline?AaltenEmail author Inez?HGB?Ramakers Geert?Jan?Biessels Peter?Paul?de Deyn Huiberdina?L?Koek Marcel?GM?OldeRikkert Ania?M?Oleksik Edo?Richard Lieke?L?Smits John?C?van Swieten Laura?K?Teune Aad?van der Lugt Frederik?Barkhof Charlotte?E?Teunissen Nico?Rozendaal Frans?RJ?Verhey Wiesje?M?van der Flier 《BMC neurology》2014,14(1):254
36.
37.
38.
39.
40.
Forbidden synonymous substitutions in coding regions 总被引:2,自引:0,他引:2
In the evolution of highly conserved genes, a few "synonymous"
substitutions at third bases that would not alter the protein sequence are
forbidden or very rare, presumably as a result of functional requirements
of the gene or the messenger RNA. Another 10% or 20% of codons are
significantly less variable by synonymous substitution than are the
majority of codons. The changes that occur at the majority of third bases
are subject to codon usage restrictions. These usage restrictions control
sequence similarities between very distant genes. For example, 70% of third
bases are identical in calmodulin genes of man and trypanosome. Third-base
similarities of distant genes for conserved proteins are mathematically
predicted, on the basis of the G+C composition of third bases. These
observations indicate the need for reexamination of methods used to
calculate synonymous substitutions.
相似文献