PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15836624-0	2005	Interference of CREB-dependent transcriptional activation by expanded polyglutamine stretches--augmentation of transcriptional activation as a potential therapeutic strategy for polyglutamine diseases.	polyglutamine	70-83	cAMP responsive element binding protein 1	Mus musculus	16-20	
15836624-2	2005	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	175-188	cAMP responsive element binding protein 1	Mus musculus	23-62	
15836624-2	2005	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	175-188	cAMP responsive element binding protein 1	Mus musculus	64-68	
15836624-4	2005	Expanded polyglutamine-induced cytotoxicity was also substantially suppressed by augmenting CREB-dependent transcriptional activation with a high concentration of cAMP.	polyglutamine	9-22	cAMP responsive element binding protein 1	Mus musculus	92-96	
15836624-5	2005	FR901228, a histone deacetylase inhibitor, was also demonstrated as rescuing the expanded polyglutamine-induced suppression of CREB phosphorylation and c-Fos expression.	polyglutamine	90-103	cAMP responsive element binding protein 1	Mus musculus	127-131	
15836624-7	2005	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	135-148	cAMP responsive element binding protein 1	Mus musculus	39-43	
15836624-7	2005	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	135-148	cAMP responsive element binding protein 1	Mus musculus	289-293	
15836624-7	2005	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	221-234	cAMP responsive element binding protein 1	Mus musculus	39-43	
15836624-7	2005	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	221-234	cAMP responsive element binding protein 1	Mus musculus	289-293	
15836624-8	2005	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	102-115	cAMP responsive element binding protein 1	Mus musculus	48-52	
15836624-8	2005	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	102-115	cAMP responsive element binding protein 1	Mus musculus	228-232