Pub. Date : 2005 May
PMID : 15836624
11 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | Interference of CREB-dependent transcriptional activation by expanded polyglutamine stretches--augmentation of transcriptional activation as a potential therapeutic strategy for polyglutamine diseases. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
2 | The phosphorylation of cAMP-responsive element binding protein (CREB) and induction of c-Fos in response to cAMP were strongly suppressed in Neuro2a cells expressing expanded polyglutamine. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
3 | The phosphorylation of cAMP-responsive element binding protein (CREB) and induction of c-Fos in response to cAMP were strongly suppressed in Neuro2a cells expressing expanded polyglutamine. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
4 | Expanded polyglutamine-induced cytotoxicity was also substantially suppressed by augmenting CREB-dependent transcriptional activation with a high concentration of cAMP. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
5 | FR901228, a histone deacetylase inhibitor, was also demonstrated as rescuing the expanded polyglutamine-induced suppression of CREB phosphorylation and c-Fos expression. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
6 | The co-expression of dominant-negative CREB vectors considerably abrogated the suppressive effect of cAMP and FR901228 on the expanded polyglutamine-induced nuclear fragmentation, suggesting that these compounds suppress polyglutamine-induced cytotoxicity, largely, via the enhancement of CREB-dependent transcriptional activation. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
7 | The co-expression of dominant-negative CREB vectors considerably abrogated the suppressive effect of cAMP and FR901228 on the expanded polyglutamine-induced nuclear fragmentation, suggesting that these compounds suppress polyglutamine-induced cytotoxicity, largely, via the enhancement of CREB-dependent transcriptional activation. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
8 | The co-expression of dominant-negative CREB vectors considerably abrogated the suppressive effect of cAMP and FR901228 on the expanded polyglutamine-induced nuclear fragmentation, suggesting that these compounds suppress polyglutamine-induced cytotoxicity, largely, via the enhancement of CREB-dependent transcriptional activation. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
9 | The co-expression of dominant-negative CREB vectors considerably abrogated the suppressive effect of cAMP and FR901228 on the expanded polyglutamine-induced nuclear fragmentation, suggesting that these compounds suppress polyglutamine-induced cytotoxicity, largely, via the enhancement of CREB-dependent transcriptional activation. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
10 | These findings suggest that the interference of CREB-dependent transcriptional activation by expanded polyglutamine stretches is involved in the pathogenetic mechanisms underlying neurodegeneration, and that the augmentation of CREB-dependent transcriptional activation is a potential strategy in treating polyglutamine diseases. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |
11 | These findings suggest that the interference of CREB-dependent transcriptional activation by expanded polyglutamine stretches is involved in the pathogenetic mechanisms underlying neurodegeneration, and that the augmentation of CREB-dependent transcriptional activation is a potential strategy in treating polyglutamine diseases. | polyglutamine | cAMP responsive element binding protein 1 | Mus musculus |