PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16631597-0	2006	cAMP differentially regulates gamma-globin gene expression in erythroleukemic cells and primary erythroblasts through c-Myb expression.	Cyclic AMP	0-4	hemoglobin subunit gamma 1	Homo sapiens	30-42	
16631597-0	2006	cAMP differentially regulates gamma-globin gene expression in erythroleukemic cells and primary erythroblasts through c-Myb expression.	Cyclic AMP	0-4	MYB proto-oncogene, transcription factor	Homo sapiens	118-123	
16631597-1	2006	Our previous studies demonstrated roles of cyclic nucleotides in gamma-globin gene expression.	Nucleotides, Cyclic	43-61	hemoglobin subunit gamma 1	Homo sapiens	65-77	
16631597-2	2006	We recently found that, upon activation of the cAMP pathway, expression of the gamma-globin gene is inhibited in K562 cells but induced in adult erythroblasts.	Cyclic AMP	47-51	hemoglobin subunit gamma 1	Homo sapiens	79-91	
16631597-3	2006	Here we show that c-Myb, a proto-oncogene product that plays a role in cell growth and differentiation, is involved in the cAMP-mediated differential regulation of gamma-globin gene expression in K562 cells and primary erythroblasts.	Cyclic AMP	123-127	MYB proto-oncogene, transcription factor	Homo sapiens	18-23	
16631597-3	2006	Here we show that c-Myb, a proto-oncogene product that plays a role in cell growth and differentiation, is involved in the cAMP-mediated differential regulation of gamma-globin gene expression in K562 cells and primary erythroblasts.	Cyclic AMP	123-127	hemoglobin subunit gamma 1	Homo sapiens	164-176	
16631597-4	2006	Our studies found that c-Myb is expressed at a high level in K562 cells compared to primary erythroblasts, and that c-Myb expression is further increased following the treatment with forskolin, an adenylate cyclase activator.	Colforsin	183-192	MYB proto-oncogene, transcription factor	Homo sapiens	23-28	
16631597-4	2006	Our studies found that c-Myb is expressed at a high level in K562 cells compared to primary erythroblasts, and that c-Myb expression is further increased following the treatment with forskolin, an adenylate cyclase activator.	Colforsin	183-192	MYB proto-oncogene, transcription factor	Homo sapiens	116-121	
16631597-6	2006	Importantly, forskolin-induced erythroid differentiation in K562 cells, as determined by the expression of glycophorins and CD71, suggesting that high-level expression of c-Myb may not be sufficient to inhibit the differentiation of erythroid cells.	Colforsin	13-22	transferrin receptor	Homo sapiens	124-128	
16631597-6	2006	Importantly, forskolin-induced erythroid differentiation in K562 cells, as determined by the expression of glycophorins and CD71, suggesting that high-level expression of c-Myb may not be sufficient to inhibit the differentiation of erythroid cells.	Colforsin	13-22	MYB proto-oncogene, transcription factor	Homo sapiens	171-176	
16631597-8	2006	Together, these results show that the cAMP pathway blocks gamma-globin gene expression in K562 cells by increasing c-Myb expression and c-Myb plays a role in defining the mode of response of the gamma-globin gene to fetal hemoglobin inducers in erythroid cells.	Cyclic AMP	38-42	hemoglobin subunit gamma 1	Homo sapiens	58-70	
16631597-8	2006	Together, these results show that the cAMP pathway blocks gamma-globin gene expression in K562 cells by increasing c-Myb expression and c-Myb plays a role in defining the mode of response of the gamma-globin gene to fetal hemoglobin inducers in erythroid cells.	Cyclic AMP	38-42	MYB proto-oncogene, transcription factor	Homo sapiens	115-120	
16631597-8	2006	Together, these results show that the cAMP pathway blocks gamma-globin gene expression in K562 cells by increasing c-Myb expression and c-Myb plays a role in defining the mode of response of the gamma-globin gene to fetal hemoglobin inducers in erythroid cells.	Cyclic AMP	38-42	hemoglobin subunit gamma 1	Homo sapiens	195-207