PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25983101-0	2015	ANXA1 silencing increases the sensitivity of cancer cells to low-concentration arsenic trioxide treatment by inhibiting ERK MAPK activation.	Arsenic Trioxide	79-95	annexin A1	Homo sapiens	0-5	
25983101-8	2015	RESULTS: After verification of the mRNA and protein levels in 4 cancer cell lines, ANXA1 and lamin A/B were validated to have increased expression levels after low-concentration ATO treatment.	Arsenic Trioxide	178-181	annexin A1	Homo sapiens	83-88	
25983101-9	2015	Lower concentrations of ATO, which has no effect on proliferation of cancer cells, induced apoptosis after ANXA1 silencing.	Arsenic Trioxide	24-27	annexin A1	Homo sapiens	107-112	
25983101-10	2015	Furthermore, overexpression of ANXA1 induced by ATO resulted in activation of extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases (MAPKs), rendering cancer cells resistant to the agent.	Arsenic Trioxide	48-51	annexin A1	Homo sapiens	31-36	
25983101-12	2015	CONCLUSIONS: Taken together, these data indicate that overexpression of ANXA1 induced by low-concentration ATO makes cancer cells more resistant to the agent via activated ERK MAPKs.	Arsenic Trioxide	107-110	annexin A1	Homo sapiens	72-77	
25983101-13	2015	Specific silencing of ANXA1 increased the sensitivity of cancer cells to ATO treatment.	Arsenic Trioxide	73-76	annexin A1	Homo sapiens	22-27	
18081892-0	2008	Arsenic trioxide induces de novo protein synthesis of annexin-1 in neutrophils: association with a heat shock-like response and not apoptosis.	Arsenic Trioxide	0-16	annexin A1	Homo sapiens	54-63	
18081892-3	2008	AnxA1 was detected at the cell membrane of ATO-induced neutrophils as well as in the supernatants.	Arsenic Trioxide	43-46	annexin A1	Homo sapiens	0-5	
18081892-7	2008	We conclude that ATO-induced neutrophil apoptosis by an AnxA1-independent mechanism.	Arsenic Trioxide	17-20	annexin A1	Homo sapiens	56-61