PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Vorinostat	19-29	autophagy related 5	Homo sapiens	275-279	
20962572-6	2010	Inhibition of autophagy by 3-MA or Atg5 knockout reduced SAHA-induced cytotoxicity, indicating that SAHA-induced autophagy led to cell death.	Vorinostat	57-61	autophagy related 5	Homo sapiens	35-39	
20962572-6	2010	Inhibition of autophagy by 3-MA or Atg5 knockout reduced SAHA-induced cytotoxicity, indicating that SAHA-induced autophagy led to cell death.	Vorinostat	100-104	autophagy related 5	Homo sapiens	35-39	
18787411-7	2008	In a CD95-, FADD- and PERK-dependent fashion, sorafenib and vorinostat increased expression of ATG5 that was responsible for enhanced autophagy.	Vorinostat	60-70	autophagy related 5	Homo sapiens	95-99	
18787411-9	2008	Suppression of PERK function reduced sorafenib and vorinostat lethality whereas suppression of ATG5 levels elevated sorafenib and vorinostat lethality.	Vorinostat	130-140	autophagy related 5	Homo sapiens	95-99	
20543569-4	2010	Moreover, SAHA treatment upregulated expression of Beclin 1 and Atg7 and promoted formation of the Atg12-Atg5 conjugate.	Vorinostat	10-14	autophagy related 5	Homo sapiens	105-109