PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
12624953-4	2003	Transcriptional activity and expression of p53 proved to depend on the proportion between p53 and GSE22.	gse22	98-103	tumor protein p53	Homo sapiens	43-46
15735711-2	2005	HMEC immortalized by a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and ZNF217, and/or dominant negative p53 genetic suppressor element GSE22) displayed marked upregulation (10-15 fold) of the telomere-binding protein, TRF2.	gse22	166-171	tumor protein p53	Homo sapiens	135-138
15735711-2	2005	HMEC immortalized by a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and ZNF217, and/or dominant negative p53 genetic suppressor element GSE22) displayed marked upregulation (10-15 fold) of the telomere-binding protein, TRF2.	gse22	166-171	telomeric repeat binding factor 2	Homo sapiens	249-253
12624953-5	2003	The dominant-negative effect was observed only when GSE22 was in a multifold excess to p53.	gse22	52-57	tumor protein p53	Homo sapiens	87-90
12624953-6	2003	GSE22 was shown to be suitable for complete reversible inactivation of p53.	gse22	0-5	tumor protein p53	Homo sapiens	71-74
10779915-4	2000	Similar effects were observed upon transduction of the p53-GSE22 genetic suppressor element, known to reduce p53 transcriptional activity.	gse22	59-64	tumor protein p53	Homo sapiens	55-58
10779915-4	2000	Similar effects were observed upon transduction of the p53-GSE22 genetic suppressor element, known to reduce p53 transcriptional activity.	gse22	59-64	tumor protein p53	Homo sapiens	109-112
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	tumor protein p53	Homo sapiens	31-34
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	tumor protein p53	Homo sapiens	92-95
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	tumor protein p53	Homo sapiens	92-95