PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8471424-5	1993	Induction of differentiation inversely correlated with the levels of c-myc proto-oncogene expression: after a 2 week culture dexamethasone-treated cells showed the highest c-myc expression and N,N-dimethylformamide-treated cells the lowest.	Dimethylformamide	197-214	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	69-74	
8471424-8	1993	Therefore dexamethasone and N,N-dimethylformamide, both causing a decreased growth rate, showed opposing actions on myogenic differentiation and on c-myc proto-oncogene expression of human rhabdomyosarcoma cells.	Dimethylformamide	28-49	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	148-153	
3164710-2	1988	In the present report, Northern analysis indicates that addition of the maturational agent N,N-dimethylformamide (DMF) (1.0%) to proliferating HCT 116 and MOSER cells resulted in a repression of c-myc proto-oncogene expression; retinoic acid (1.0 microM) was less effective in this regard.	Dimethylformamide	91-112	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	195-200	
1637683-8	1992	All four agents inhibited myc oncoprotein expression reversibly (1% DMSO greater than 0.5% DMF greater than 10 microM RA greater than 10 ng ml-1 TGF-beta 1) and in time-dependent manner.	Dimethylformamide	91-94	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	26-29	
1540946-4	1992	When c-myc levels and responses to serum induction were analyzed in the presence of inducers of differentiation, i.e., dimethylformamide, retinoic acid, sodium butyrate and TGF-beta, distinct patterns of sensitivity and resistance emerged.	Dimethylformamide	119-136	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	5-10	
1540946-5	1992	Nuclear c-myc levels were reduced in all the colon cell phenotypes treated with dimethylformamide or sodium butyrate.	Dimethylformamide	80-97	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	8-13	
3164710-2	1988	In the present report, Northern analysis indicates that addition of the maturational agent N,N-dimethylformamide (DMF) (1.0%) to proliferating HCT 116 and MOSER cells resulted in a repression of c-myc proto-oncogene expression; retinoic acid (1.0 microM) was less effective in this regard.	Dimethylformamide	114-117	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	195-200	
3164710-3	1988	Repression of c-myc expression by DMF was observed in MOSER and HCT 116 cells, whether it was added to proliferating or late log phase cultures, and was associated with a corresponding reduction in cellular proliferation.	Dimethylformamide	34-37	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-19	
3164710-4	1988	The reduction in c-myc expression by DMF did not require new protein synthesis and occurred within a few minutes after its addition, resulting in a 70% reduction within approximately 2 hr.	Dimethylformamide	37-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	17-22