全文获取类型
收费全文 | 69篇 |
免费 | 11篇 |
出版年
2021年 | 1篇 |
2018年 | 1篇 |
2016年 | 2篇 |
2015年 | 2篇 |
2014年 | 7篇 |
2013年 | 5篇 |
2012年 | 2篇 |
2011年 | 3篇 |
2010年 | 5篇 |
2008年 | 2篇 |
2007年 | 1篇 |
2006年 | 3篇 |
2005年 | 3篇 |
2004年 | 2篇 |
2003年 | 3篇 |
2002年 | 1篇 |
2001年 | 4篇 |
2000年 | 3篇 |
1999年 | 6篇 |
1998年 | 1篇 |
1997年 | 1篇 |
1996年 | 1篇 |
1993年 | 1篇 |
1991年 | 1篇 |
1990年 | 2篇 |
1989年 | 3篇 |
1987年 | 2篇 |
1985年 | 3篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1981年 | 1篇 |
1980年 | 3篇 |
1978年 | 1篇 |
1976年 | 1篇 |
1960年 | 1篇 |
排序方式: 共有80条查询结果,搜索用时 281 毫秒
1.
Vittorio de Franciscis Vittorio E. Avvedimento Giulia Colletta Vincenzo Zimarino Valeria M. Ursini Fortunato Ciliberto Giancarlo Vecchio 《Experimental cell research》1987,171(2):483-491
We have exploited a recently characterized system of rat thyroid epithelial cells transformed by the wild-type (wt) and a temperature-sensitive (ts) mutant strain of the Kirsten murine sarcoma virus (Ki-MSV) in order to study the effects of the K-ras oncogene on the gene expression of differentiated thyroid epithelial cells. By using cDNAs isolated from normal thyroid glands as probes, we were able to identify three sets of cellular sequences whose expression is influenced by the v-K-ras oncogene. The first set of genes is irreversibly repressed by transformation with both the wt and the ts viruses. The second set of genes is repressed in the ts-Ki-MSV-transformed cells but not in the same cells grown at the nonpermissive temperature. A third set of genes is present at higher levels at the nonpermissive temperature than at the permissive temperature. This system has allowed us to isolate and characterize a number of cDNA clones belonging to each of these three sets of genes. These specific cDNAs are suitable probes to study phenotypical changes during transformation of epithelial cells. 相似文献
2.
3.
Membrane-bound cAMP-dependent protein kinase controls cAMP-induced differentiation in PC12 cells. 总被引:1,自引:0,他引:1
S Cassano A Di Lieto R Cerillo E V Avvedimento 《The Journal of biological chemistry》1999,274(46):32574-32579
4.
Feliciello A Cardone L Garbi C Ginsberg MD Varrone S Rubin CS Avvedimento EV Gottesman ME 《FEBS letters》1999,464(3):174-178
A yeast two-hybrid screen revealed that regulatory subunits (RII) of PKAII bind the Yotiao protein. Yotiao interacts with the NR1 subunit of the NMDA receptor. A purified C-terminal fragment of Yotiao binds PKAII, via an RII binding site constituted by amino acid residues 1452-1469, with a dissociation constant (K(d)) between 50 and 90 nM in vitro. A stable complex composed of Yotiao, RII and NR1 was immunoprecipitated from whole rat brain extracts. Immunostaining analysis disclosed that Yotiao, RIIbeta and NR1 colocalize in striatal and cerebellar neurons. Co-assembly of Yotiao/PKAII complexes with NR1 subunits may promote cAMP-dependent modulation of NMDA receptor activity at synapses, thereby influencing brain development and synaptic plasticity. 相似文献
5.
T de Cristofaro A Affaitati L Cariello E V Avvedimento S Varrone 《Biochemical and biophysical research communications》1999,260(1):150-158
A common feature of CAG-expansion neurodegenerative diseases is the presence of intranuclear aggregates in neuronal cells. We have used a synthetic fusion protein containing at the NH2 terminus the influenza hemoagglutinin epitope (HA), a polyglutamine stretch (polyQ) of various size (17, 36, 43 CAG) and a COOH tail encoding the green fluorescent protein (GFP). The fusion proteins were expressed in COS-7 and neuroblastoma SK-N-BE cells. We found that the formation of aggregates largely depends on the length of polyglutamine tracts and on the levels of expression of the fusion protein. Moreover, transglutaminase overexpression caused an increase of insoluble aggregates only in cells expressing the mutant expanded protein. Conversely, treatment of cells with cystamine, a transglutaminase inhibitor, reduced the percentage of aggregates. We found also that the inhibition of the proteasome ubiquitin-dependent degradation increased the formation of intranuclear aggregates. These data suggest that length of polyglutamine tract, its expression, unbalance between cellular transglutaminase activity, and the ubiquitin-degradation pathway are key factors in the formation of intranuclear aggregates. 相似文献
6.
7.
Affaitati A Cardone L de Cristofaro T Carlucci A Ginsberg MD Varrone S Gottesman ME Avvedimento EV Feliciello A 《The Journal of biological chemistry》2003,278(6):4286-4294
A-Kinase anchor proteins (AKAPs) immobilize and concentrate protein kinase A (PKA) isoforms at specific subcellular compartments. Intracellular targeting of PKA holoenzyme elicits rapid and efficient phosphorylation of target proteins, thereby increasing sensitivity of downstream effectors to cAMP action. AKAP121 targets PKA to the cytoplasmic surface of mitochondria. Here we show that conditional expression of AKAP121 in PC12 cells selectively enhances cAMP.PKA signaling to mitochondria. AKAP121 induction stimulates PKA-dependent phosphorylation of the proapoptotic protein BAD at Ser(155), inhibits release of cytochrome c from mitochondria, and protects cells from apoptosis. An AKAP121 derivative mutant that localizes on mitochondria but does not bind PKA down-regulates PKA signaling to the mitochondria and promotes apoptosis. These findings indicate that PKA anchored by AKAP121 transduces cAMP signals to the mitochondria, and it may play an important role in mitochondrial physiology. 相似文献
8.
9.
10.
D'Angiolella V Costanzo V Gottesman ME Avvedimento EV Gautier J Grieco D 《Current biology : CB》2001,11(15):1221-1226
Mitosis requires cyclin-dependent kinase (cdk) 1-cyclin B activity [1]. Exit from mitosis depends on the inactivation of the complex by the degradation of cyclin B [2]. Cdk2 is also active during mitosis [3, 4]. In Xenopus egg extracts, cdk2 is primarily in complex with cyclin E, which is stable [5]. At the end of mitosis, downregulation of cdk2-cyclin E activity is accompanied by inhibitory phosphorylation of cdk2 [6]. Here, we show that cdk2-cyclin E activity maintains cdk1-cyclin B during mitosis. At mitosis exit, cdk2 is inactivated prior to cdk1. The loss of cdk2 activity follows and depends upon an increase in protein kinase A (PKA) activity. Prematurely inactivating cdk2 advances the time of cyclin B degradation and cdk1 inactivation. Blocking PKA, instead, stabilizes cdk2 activity and inhibits cyclin B degradation and cdk1 inactivation. The stabilization of cdk1-cyclin B is also induced by a mutant cdk2-cyclin E complex that is resistant to inhibitory phosphorylation. P21-Cip1, which inhibits both wild-type and mutant cdk2-cyclin E, reverses mitotic arrest under either condition. Our findings indicate that the proteolysis-independent downregulation of cdk2 activity at the end of mitosis depends on PKA and is required to activate the proteolysis cascade that leads to mitosis exit. 相似文献