PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23769318-10	2013	Erlotinib treatment at clinically relevant concentrations induced autophagy (increased LC3II expression, Atg-5/Atg12 conjugation, formation of AVO and p62 degradation) in sensitive NSCLC cell lines, via p53 nuclear translocation, AMPK activation and mTOR suppression.	Erlotinib Hydrochloride	0-9	autophagy related 5	Homo sapiens	105-110	
23917044-6	2013	Inhibition of autophagy by chloroquine and knockdown of autophagy pathway genes Beclin-1 and Atg5 sensitized both cell lines to erlotinib-induced cytotoxicity, suggesting that autophagy may serve as a protective mechanism.	Erlotinib Hydrochloride	128-137	autophagy related 5	Homo sapiens	93-97	
26797786-8	2016	Then, through siRNA technology and WB, we found that erlotinib-induced autophagy is mediated by ATG5 but not Beclin1.	Erlotinib Hydrochloride	53-62	autophagy related 5	Homo sapiens	96-100	
26797786-9	2016	Also, knockdown of ATG5 significantly decreased the erlotinib resistance and knockdown of Beclin1 did not affect the sensitivity to erlotinib in TSCCs.	Erlotinib Hydrochloride	52-61	autophagy related 5	Homo sapiens	19-23	
23769318-12	2013	Similarly, silencing of Atg5 or Beclin-1 significantly increased sensitivity to erlotinib in both sensitive cell lines.	Erlotinib Hydrochloride	80-89	autophagy related 5	Homo sapiens	24-28	
21655094-6	2011	Moreover, cytotoxicity induced by gefitinib or erlotinib was greatly enhanced after autophagy inhibition by the pharmacological inhibitor chloroquine (CQ) and siRNAs targeting ATG5 and ATG7, the most important components for the formation of autophagosome.	Erlotinib Hydrochloride	47-56	autophagy related 5	Homo sapiens	176-180