全文获取类型
收费全文 | 547篇 |
免费 | 30篇 |
国内免费 | 19篇 |
专业分类
596篇 |
出版年
2024年 | 1篇 |
2023年 | 14篇 |
2022年 | 19篇 |
2021年 | 31篇 |
2020年 | 22篇 |
2019年 | 27篇 |
2018年 | 28篇 |
2017年 | 18篇 |
2016年 | 11篇 |
2015年 | 24篇 |
2014年 | 38篇 |
2013年 | 68篇 |
2012年 | 34篇 |
2011年 | 21篇 |
2010年 | 11篇 |
2009年 | 19篇 |
2008年 | 13篇 |
2007年 | 10篇 |
2006年 | 9篇 |
2005年 | 15篇 |
2004年 | 18篇 |
2003年 | 9篇 |
2002年 | 9篇 |
2001年 | 5篇 |
2000年 | 9篇 |
1999年 | 11篇 |
1998年 | 5篇 |
1997年 | 8篇 |
1996年 | 5篇 |
1995年 | 11篇 |
1994年 | 8篇 |
1993年 | 5篇 |
1992年 | 9篇 |
1991年 | 6篇 |
1990年 | 10篇 |
1989年 | 9篇 |
1988年 | 6篇 |
1987年 | 9篇 |
1986年 | 7篇 |
1985年 | 2篇 |
1984年 | 1篇 |
1982年 | 1篇 |
排序方式: 共有596条查询结果,搜索用时 0 毫秒
1.
《Developmental cell》2022,57(2):212-227.e8
2.
3.
Rat kidney (NRK) cells infected with a temperature-sensitive mutant of the Kirsten sarcoma virus were arrested in the G0/G1 phase of their cell cycle by incubation in serum-deficient medium at a p21-inactivating temperature of 41 degrees C. These quiescent ts K-NRK cells were then stimulated to transit G1 and initiate DNA replication by lowering the temperature to 36 degrees C, which rapidly reactivated p21. Reactivating the viral Ki-RAS protein by temperature shift led to an increase in adenylate cyclase activity in early G1 phase. The Ki-RAS protein increased the sensitivity of adenylate cyclase to guanyl nucleotides by a mechanism that seemed to involve inactivation of the enzyme's inhibitory G1 regulatory protein. 相似文献
4.
B Groner 《Journal of cellular biochemistry》1992,49(2):128-136
Mouse strains which develop tumors at a high incidence with characteristics very similar to human cancers have been derived over the last 8 years. The tumors are caused by defined genetic alterations in the mouse genome. Three areas of research have contributed to the derivation of these mouse strains: (1) Molecular analysis of human tumors has shown that distinct oncogenes and tumor suppressor genes are consistently involved in a high percentage of primary tumors. (2) Regulatory enhancer-promoter sequences have been identified which direct gene expression to specific target cells, preferentially mammary epithelial cells. (3) The introduction of recombinant DNA molecules into fertilized mouse eggs by microinjection and integration of the injected DNA into the genome of injected cells has given rise to mutant mouse strains with unique and defined genetic alterations. Studies with different promoter-oncogene combinations introduced into transgenic mouse strains have led to the following general conclusions: (1) Oncogenes expressed in mammary gland cells predispose transgenic mice to mammary tumors. (2) The oncogenic potential of individual oncogenes in mammary epithelial cells differs. (3) Oncogene expression initially often causes a preneoplastic state affecting growth and differentiation parameters of cells. (4) The expression of different oncogenes synergizes to reduce tumor latency. Synergism can also be observed with physiological growth signals like estrogen or growth hormone. The oncogenes with a role in mammary carcinomas which have been investigated in transgenic mice will be described here. The phenotypic consequences of oncogene expression and the implications for the multistep carcinogenesis model will be discussed. 相似文献
5.
6.
Ras interaction with the GTPase-activating protein (GAP) 总被引:18,自引:0,他引:18
M D Schaber V M Garsky D Boylan W S Hill E M Scolnick M S Marshall I S Sigal J B Gibbs 《Proteins》1989,6(3):306-315
Biologically active forms of Ras complexed to GTP can bind to the GTPase-activating protein (GAP), which has been implicated as possible target of Ras in mammalian cells. In order to study the structural features of Ras required for this interaction, we have evaluated a series of mutant ras proteins for the ability to bind GAP and a series of Ras peptides for the ability to interfere with this interaction. Point mutations in the putative effector region of Ras (residues 32-40) that inhibit biological activity also impair Ras binding to GAP. An apparent exception is the Thr to Ser substitution at residue 35; [Ser-35]Ras binds to GAP as effectively as wild-type Ras even though this mutant is biologically weak in both mammalian and S. cerevisiae cells. In vitro, [Ser-35]Ras can also efficiently stimulate the S. cerevisiae target of Ras, adenylyl cyclase, indicating that other factors may influence Ras/protein interactions in vivo. Peptides having Ras residues 17-44 and 17-32 competed with the binding of Ras to E. coli-expressed GAP with IC50 values of 2.4 and 0.9 microM, respectively, whereas Ras peptide 17-26 was without effect up to 400 microM. A related peptide from the yeast GTP-binding protein YPT1 analogous to Ras peptide 17-32 competed with an IC50 value of 19 microM even though the YPT1 protein itself is unable to bind to GAP. These results suggest that determinants within Ras peptide 17-32 may be important for Ras binding to GAP. 相似文献
7.
8.
Eric Hbert Michel Monsigny 《Biology of the cell / under the auspices of the European Cell Biology Organization》1994,81(1):73-76
Summary— The increase in galectin-3 lectin content observed in tumours or in in vitro transformed cells suggests that this lectin is important in the transformation process. In the present study, we investigated the mRNA expression level of the galectin-3, galectin-I and macrophage mannose receptor in normal and ras-transformed NIH 3T3 cells in relation to their transformation state. The galectin3 mRNA content in ras-transformed cells is increased in fully transformed cells, with a maximum in ras-transformed cells that have lost their growth anchorage-dependence. Under the same conditions, the galectin-1 mRNA level which was high in normal cells, increased slightly in transformed cells. The mRNA for the macrophage mannose receptor was not detected in 3T3 cells or in their ras-transformed counterparts. 相似文献
9.
10.