全文获取类型
收费全文 | 22398篇 |
免费 | 1810篇 |
国内免费 | 1064篇 |
出版年
2024年 | 37篇 |
2023年 | 487篇 |
2022年 | 394篇 |
2021年 | 1101篇 |
2020年 | 1210篇 |
2019年 | 1639篇 |
2018年 | 1110篇 |
2017年 | 661篇 |
2016年 | 784篇 |
2015年 | 925篇 |
2014年 | 1475篇 |
2013年 | 1795篇 |
2012年 | 1093篇 |
2011年 | 1411篇 |
2010年 | 977篇 |
2009年 | 1054篇 |
2008年 | 1068篇 |
2007年 | 1087篇 |
2006年 | 979篇 |
2005年 | 912篇 |
2004年 | 812篇 |
2003年 | 698篇 |
2002年 | 634篇 |
2001年 | 383篇 |
2000年 | 326篇 |
1999年 | 311篇 |
1998年 | 248篇 |
1997年 | 196篇 |
1996年 | 156篇 |
1995年 | 137篇 |
1994年 | 137篇 |
1993年 | 122篇 |
1992年 | 85篇 |
1991年 | 75篇 |
1990年 | 64篇 |
1989年 | 50篇 |
1988年 | 59篇 |
1987年 | 46篇 |
1986年 | 45篇 |
1985年 | 49篇 |
1984年 | 70篇 |
1983年 | 45篇 |
1982年 | 54篇 |
1981年 | 37篇 |
1980年 | 55篇 |
1979年 | 43篇 |
1978年 | 28篇 |
1977年 | 24篇 |
1976年 | 29篇 |
1974年 | 18篇 |
排序方式: 共有10000条查询结果,搜索用时 140 毫秒
1.
Suzanne Camus Sergio Menéndez Kenneth Fernandes Nelly Kua Geng Liu Dimitris P. Xirodimas David P. Lane Jean-Christophe Bourdon 《Cell cycle (Georgetown, Tex.)》2012,11(8):1646-1655
The discovery that the single p53 gene encodes several different p53 protein isoforms has initiated a flurry of research into the function and regulation of these novel p53 proteins. Full-length p53 protein level is primarily regulated by the E3-ligase Mdm2, which promotes p53 ubiquitination and degradation. Here, we report that all of the novel p53 isoforms are ubiquitinated and degraded to varying degrees in an Mdm2-dependent and -independent manner, and that high-risk human papillomavirus can degrade some but not all of the novel isoforms, demonstrating that full-length p53 and the p53 isoforms are differentially regulated. In addition, we provide the first evidence that Mdm2 promotes the NEDDylation of p53β. Altogether, our data indicates that Mdm2 can distinguish between the p53 isoforms and modify them differently. 相似文献
2.
3.
Monica Driscoll 《Developmental neurobiology》1992,23(9):1327-1351
In C. elegans, cell death can be readily studied at the cellular, genetic, and molecular levels. Two types of death have been characterized in this nematode: (1) programmed cell death, which occurs as a normal component in development; and (2) pathological cell death which occurs aberrantly as a consequence of mutation. Analysis of mutations that disrupt programmed cell death in various ways has defined a genetic pathway for programmed cell death which includes genes that perform such functions as the determination of which cells die, the execution of cell death, the engulfment of cell corpses, and the digestion of DNA from dead cells. Molecular analysis is providing insightinto the nature of the molecules that function in these aspects of programmed cell death. Characterization of some genes that mutate to induce abnormal cell death has defined a novel gene family called degenerins that encode putative membrane proteins. Dominant alleles of at least two degenerin genes, mec-4 and deg-1, can cause cellular swelling and late onset neurodegeneration of specific groups of cells. © 1992 John Wiley & Sons, Inc. 相似文献
4.
《Cell reports》2020,30(3):725-738.e4
5.
6.
Towards a theory of the evolution of butterfly colour patterns under directional and disruptive selection 总被引:1,自引:0,他引:1
R. I. VANE-WRIGHT 《Biological journal of the Linnean Society. Linnean Society of London》1979,11(2):141-152
Two general models for the transspecific evolution of butterfly colour patterns are advanced: directional selection acting equally on both sexes, and disruptive selection involving periods of polymorphism. To consider possible outcomes of me latter process, a morphism notation based on an integrated classification for polymorphism and sexual dimorphism is developed. This notation is used to examine the properties of all morphism transformations possible from the minimal expressions of the nine morphism categories, as reached through defined minimum step changes. The significance of such pathway models is analysed in terms of general properties of butterfly polymorphism. The potential use of pathway models in evolutionary studies is briefly discussed, mainly with respect to phylogenetics, and ideas on the evolution of genetic dominance. 相似文献
7.
D E Bowman 《Biochemical and biophysical research communications》1979,87(1):78-84
The oxidized B chain of insulin was used as a simple model for further consideration of limited proteolysis with low substrate:enzyme ratios. With low B chain:trypsin ratios, the ordinarily slower cleavage rate of the -Lys29-Ala30 bond essentially equaled the cleavage saturation rate of the -Arg22-Gly23 bond. This led to the disappearance of octapeptide which ordinarily forms most rapidly. Heptapeptide and alanine, formed mainly by cleavage of the octapeptide, decreased somewhat at high enzyme relative levels. Trypsin added to B chain formed a single chromatographic peak. 相似文献
8.
Comment on: Rokavec M, et al. Mol Cell 2012; 45:777-89. 相似文献
9.
10.
《Journal of molecular biology》2021,433(4):166790
G protein coupled receptors signal through G proteins or arrestins. A long-standing mystery in the field is why vertebrates have two non-visual arrestins, arrestin-2 and arrestin-3. These isoforms are ~75% identical and 85% similar; each binds numerous receptors, and appear to have many redundant functions, as demonstrated by studies of knockout mice. We previously showed that arrestin-3 can be activated by inositol-hexakisphosphate (IP6). IP6 interacts with the receptor-binding surface of arrestin-3, induces arrestin-3 oligomerization, and this oligomer stabilizes the active conformation of arrestin-3. Here, we compared the impact of IP6 on oligomerization and conformational equilibrium of the highly homologous arrestin-2 and arrestin-3 and found that these two isoforms are regulated differently. In the presence of IP6, arrestin-2 forms “infinite” chains, where each promoter remains in the basal conformation. In contrast, full length and truncated arrestin-3 form trimers and higher-order oligomers in the presence of IP6; we showed previously that trimeric state induces arrestin-3 activation (Chen et al., 2017). Thus, in response to IP6, the two non-visual arrestins oligomerize in different ways in distinct conformations. We identified an insertion of eight residues that is conserved across arrestin-2 homologs, but absent in arrestin-3 that likely accounts for the differences in the IP6 effect. Because IP6 is ubiquitously present in cells, this suggests physiological consequences, including differences in arrestin-2/3 trafficking and JNK3 activation. The functional differences between two non-visual arrestins are in part determined by distinct modes of their oligomerization. The mode of oligomerization might regulate the function of other signaling proteins. 相似文献