PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33736531-4	2021	The effects of 5-Aza treatment on SHP-1 expression and methylation and STAT3 phosphorylation were investigated in MDS cells by methylation-specific PCR, reverse transcription PCR, and western blotting.	Azacitidine	15-20	nuclear receptor subfamily 0 group B member 2	Homo sapiens	34-39	
34075200-7	2021	In STAT3 mutated LGLL cells, DNA methyltransferase (DNMT) inhibitor azacitidine abrogated the activation of STAT3 via restored SHP1 expression.	Azacitidine	68-79	nuclear receptor subfamily 0 group B member 2	Homo sapiens	127-131	
33736531-7	2021	SHP-1 expression was significantly increased at mRNA and protein levels following 5-Aza treatment, while the phosphorylation of STAT3 protein was significantly decreased.	Azacitidine	82-87	nuclear receptor subfamily 0 group B member 2	Homo sapiens	0-5	
14976049-10	2004	Treatment with 5-azacytidine led to progressive demethylation of SHP1 on days 2 to 5, with consequent increasing reexpression of SHP1 as shown by reverse transcription-polymerase chain reaction (RT-PCR).	Azacitidine	15-28	nuclear receptor subfamily 0 group B member 2	Homo sapiens	65-69	
29572158-8	2018	Although no significant correlation was found between Syk and SHP-1 expression and the clinical response to combination therapy, in vitro studies repeatedly demonstrated that azacitidine-treated AML cells had an increased response to GO treatment.	Azacitidine	175-186	nuclear receptor subfamily 0 group B member 2	Homo sapiens	62-67	
14976049-10	2004	Treatment with 5-azacytidine led to progressive demethylation of SHP1 on days 2 to 5, with consequent increasing reexpression of SHP1 as shown by reverse transcription-polymerase chain reaction (RT-PCR).	Azacitidine	15-28	nuclear receptor subfamily 0 group B member 2	Homo sapiens	129-133