全文获取类型
收费全文 | 109篇 |
免费 | 4篇 |
专业分类
113篇 |
出版年
2023年 | 1篇 |
2022年 | 3篇 |
2021年 | 4篇 |
2020年 | 3篇 |
2019年 | 4篇 |
2018年 | 4篇 |
2017年 | 2篇 |
2016年 | 8篇 |
2015年 | 5篇 |
2014年 | 6篇 |
2013年 | 8篇 |
2012年 | 9篇 |
2011年 | 7篇 |
2009年 | 2篇 |
2008年 | 5篇 |
2007年 | 2篇 |
2006年 | 3篇 |
2005年 | 2篇 |
2004年 | 2篇 |
2003年 | 2篇 |
2002年 | 1篇 |
2001年 | 1篇 |
2000年 | 2篇 |
1999年 | 2篇 |
1998年 | 3篇 |
1997年 | 1篇 |
1996年 | 1篇 |
1993年 | 1篇 |
1992年 | 1篇 |
1991年 | 2篇 |
1989年 | 3篇 |
1987年 | 1篇 |
1986年 | 2篇 |
1985年 | 1篇 |
1984年 | 3篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1980年 | 1篇 |
1977年 | 1篇 |
1966年 | 2篇 |
排序方式: 共有113条查询结果,搜索用时 15 毫秒
1.
Eleven temperature-sensitive mutants of adenovirus type 12, capable of forming plaques in human cells at 33 C but not at 39.5 C, were isolated from a stock of a wild-type strain after treatment with either nitrous acid or hydroxyl-amine. Complementation tests in doubly infected human cells permitted a tentative assignment of eight of these mutants to six complementation groups. Temperature-shift experiments revealed that one mutant is affected early and most of the other mutants are affected late. Only the early mutant, H12ts505, was temperature sensitive in viral DNA replication. Infectious virions of all the mutants except H12ts505 and two of the late mutants produced at 33 C, appeared to be more heat labile than those of the wild type. Only H12ts505 was temperature sensitive for the establishment of transformation of rat 3Y1 cells. One of the late mutants (H12ts504) had an increased transforming ability at the permissive temperature. Results of temperature-shift transformation experiments suggest that a viral function affected in H12ts505 is required for “initiation” of transformation. Some of the growth properties of H12ts505-transformed cells were also temperature dependent, suggesting that a functional expression of a gene mutated in H12ts505 is required to maintain at least some aspects of the transformed state. 相似文献
2.
Koji Yamada Masafuni Sasaki Genki Kimura 《In vitro cellular & developmental biology. Plant》1986,22(4):212-216
Summary We examined cellular protein content in four temperature-sensitive (ts) mutants of rat 3Y1 fibroblasts (3Y1tsD123, 3Y1tsF121,
3Y1tsG125, and 3Y1tsH203) under various conditions of culture that affect cell proliferation. When proliferation of the ts
mutants was inhibited at a nonpermissive temperature (39.8°C) in the G1 phase, prominent accumulation of cellular protein occurred in three mutants (3Y1tsF121, 3Y1tsG125, and 3Y1tsH203) but not
in 3Y1tsD123. The over-accumulation of protein at 39.8°C in the former three mutants was inhibited at high cell densities.
At low cell densities there was an upper limit in the protein accumulation at 39.8°C. When the three mutants, proliferation-arrested
at high cell densities at 33.8°C, were replated sparsely in fresh medium and shifted to 39.8°C, proliferation was completely
inhibited whereas over-accumulation of protein occurred. These results indicating dissociation of protein accumulation and
cell proliferation suggest that the two events are regulated by different mechanisms.
This work was supported in part by a Grant-in-Aid for Encouragement of Young Scientists (1984) to K. Y. from the Ministry
of Education, Science, and Culture, Japan. 相似文献
3.
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
4.
Temperature-sensitive (ts) mutants of rat 3Y1 fibroblasts representing four separate complementation groups (3Y1tsD123, 3Y1tsF121, 3Y1tsG125, and 3Y1tsH203) are arrested mainly in the G1 phase when cells of randomly proliferating population at 33.8 degrees C are shifted to 39.8 degrees C (temperature arrest). We examined the time lag of the cellular entry into the S phase after release at 33.8 degrees C, both from the temperature arrest and from the arrest at 33.8 degrees C at a confluent cell density (density arrest). In the temperature-arrested cells, as the duration of temperature arrest increased, the time lag of entry into S phase after shift down to 33.8 degrees C was prolonged, in all four mutants. These observations suggest that the four different functional lesions, each causing arrest in the G1 phase, are also responsible for prolongation of the time lag of entry into the S phase in cells arrested in the G1 phase. The prolongation of the time lag in the temperature-arrested cultures was accelerated at a higher cell density, in medium supplemented with a lower concentration of serum, and at a higher restrictive temperature. In the density-arrested cells, as the duration of pre-exposure to 39.8 degrees C was increased, the time lag of entry into S phase at 33.8 degrees C after release from the arrest was drastically prolonged, in all four mutants. In 3Y1tsF121, 3Y1tsG125, and 3Y1tsH203, when the density-arrested cells were prestimulated by serum at 39.8 degrees C for various periods of time, the time lag of entry into S phase after release from the density arrest at 33.8 degrees C was initially shortened, and then, prolonged progressively as the period of prestimulation increased. These findings, taken together with other data, show that all four ts defects affect cells in states ranging from the deeper resting to mid- or late-G1 phase. It is suggested that events represented by these four mutants are required for entry into the S phase and normally operate in parallel but not in sequence in cells in states ranging from the deeper resting to the mid- or late-G1 phases, though they may affect each other. 相似文献
5.
Jun-ichi Tsuboi Kentaro Morita Yusuke Koseki Shinsuke Endo Genki Sahashi Daisuke Kishi Takeshi Kikko Daisuke Ishizaki Masanori Nunokawa Yoichiro Kanno 《Oikos》2020,129(6):924-937
Animal populations are spatially structured in heterogeneous landscapes, in which local patches with differing vital rates are connected by dispersal of individuals to varying degrees. Although there is evidence that vital rates differ among local populations, much less is understood about how vital rates covary among local patches in spatially heterogeneous landscapes. In this study, we conducted a nine-year annual mark–recapture survey to characterize spatial covariation of survival and growth for two Japanese native salmonids, white-spotted charr Salvelinus leucomaenis japonicus and red-spotted masu salmon Oncorhynchus masou ishikawae, in a headwater stream network composed of distinctly different tributary and mainstem habitats. Spatial structure of survival and growth differed by species and age class, but results provided support for negative covariation between vital rates, where survival was higher in the tributary habitat but growth was higher in the mainstem habitat. Thus, neither habitat was apparently more important than the other, and local habitats with complementary vital rates may make this spatially structured population less vulnerable to environmental change (i.e. portfolio effect). Despite the spatial structure of vital rates and possibilities that fish can exploit spatially distributed resources, movement of fish was limited due partly to a series of low-head dams that prevented upstream movement of fish in the study area. This study shows that spatial structure of vital rates can be complex and depend on species and age class, and this knowledge is likely paramount to elucidating dynamics of spatially structured populations. 相似文献
6.
Molecular Biology Reports - Generally, the gene flow of marine organisms is well maintained, but some local populations of coastal species are genetically differentiated even on a small scale... 相似文献
7.
Murayama R Akanuma G Makino Y Nanamiya H Kawamura F 《Bioscience, biotechnology, and biochemistry》2004,68(8):1672-1680
Using a simple semi-synthetic competence and sporulation medium (CSM), we found evidence that Bacillus subtilis cells transformed in the competence phase can sporulate, indicating that genetic information acquired during the competence phase is inherited by the next generation after germination of the transformed spores. Moreover, the results from mixed cell culture experiments suggest that spontaneous genetic transformation can occur between competent cells and DNA released from lysed cells in the natural environment. We also found evidence that the spontaneous transformation system can be used for genetic mapping in B. subtilis. 相似文献
8.
In CAPRI Rounds 1 and 2, we assumed that because there are many ionic charges that weaken electrostatic interaction forces in living cells, the hydrophobic interaction force might be important entropically. As a result of Rounds 1 and 2, the predictions for binding sites and geometric centers were acceptable, but those of the binding axes were poor, because only the largest benzene cluster was used for generating the initial docking structures. These were generated by fitting of benzene clusters formed on the surface of receptor and ligand. In CAPRI Rounds 3-5, the grid-scoring sum on the protein-protein interaction surface and the pairwise potential of the amino acid residues, which were indicated as coming easily into the protein-protein interaction regions, were used as the calculation methods, along with the smaller benzene clusters that participated in benzene cluster fitting. Good predicted models were obtained for Targets 11 and 12. When the modeled receptor proteins were superimposed on the experimental structures, the smallest ligand root-mean-square deviation (RMSD) values corresponding to the RMSD between the model and experimental structures were 6.2 A and 7.3 A, respectively. 相似文献
9.
Liberation of zinc-containing L31 (RpmE) from ribosomes by its paralogous gene product, YtiA, in Bacillus subtilis
下载免费PDF全文
![点击此处可从《Journal of bacteriology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
We have found that alternative localization of two types of L31 ribosomal protein, RpmE and YtiA, is controlled by the intracellular concentration of zinc in Bacillus subtilis. The detailed mechanisms for the alternation of L31 proteins under zinc-deficient conditions were previously unknown. To obtain further information about this regulatory mechanism, we have studied the stability of RpmE in vivo and the binding affinity of these proteins to ribosomes in vitro, and we have found that liberation of RpmE from ribosomes is triggered by the expression of ytiA, which is induced by the derepression of Zur under zinc-deficient conditions. 相似文献
10.
Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis 总被引:1,自引:0,他引:1
Jordan CT Cao L Roberson ED Duan S Helms CA Nair RP Duffin KC Stuart PE Goldgar D Hayashi G Olfson EH Feng BJ Pullinger CR Kane JP Wise CA Goldbach-Mansky R Lowes MA Peddle L Chandran V Liao W Rahman P Krueger GG Gladman D Elder JT Menter A Bowcock AM 《American journal of human genetics》2012,90(5):796-808