PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31484706-0	2019	Fenretinide via NOXA Induction, Enhanced Activity of the BCL-2 Inhibitor Venetoclax in High BCL-2-Expressing Neuroblastoma Preclinical Models.	Fenretinide	0-11	BCL2 apoptosis regulator	Homo sapiens	57-62	
31484706-10	2019	Thus, fenretinide + venetoclax is a synergistic combination that warrants clinical testing in high BCL-2-expressing neuroblastoma.	Fenretinide	6-17	BCL2 apoptosis regulator	Homo sapiens	99-104	
31484706-2	2019	Fenretinide (4-HPR) is a cytotoxic retinoid with clinical activity in recurrent neuroblastoma and venetoclax (ABT-199) is a selective inhibitor of the antiapoptotic protein B-cell lymphoma-2 (BCL-2).	Fenretinide	0-11	BCL2 apoptosis regulator	Homo sapiens	173-190	
31484706-2	2019	Fenretinide (4-HPR) is a cytotoxic retinoid with clinical activity in recurrent neuroblastoma and venetoclax (ABT-199) is a selective inhibitor of the antiapoptotic protein B-cell lymphoma-2 (BCL-2).	Fenretinide	0-11	BCL2 apoptosis regulator	Homo sapiens	192-197	
31839811-0	2019	Fenretinide-induced Apoptosis of Acute Myeloid Leukemia Cells via NR4A1 Translocation into Mitochondria and Bcl-2 Transformation.	Fenretinide	0-11	BCL2 apoptosis regulator	Homo sapiens	108-113	
31839811-14	2019	At the same time, fenretinide promoted NR4A1 translocation from nuclei into mitochondria, and enhanced the interaction between NR4A1 and Bcl-2, thereby exposing the BH3 domain of Bcl-2 to exert the anti-apoptotic effect.	Fenretinide	18-29	BCL2 apoptosis regulator	Homo sapiens	137-142	
31839811-14	2019	At the same time, fenretinide promoted NR4A1 translocation from nuclei into mitochondria, and enhanced the interaction between NR4A1 and Bcl-2, thereby exposing the BH3 domain of Bcl-2 to exert the anti-apoptotic effect.	Fenretinide	18-29	BCL2 apoptosis regulator	Homo sapiens	179-184	
17159502-6	2007	Western blot analysis further showed down-regulation of procaspase-3, X-linked inhibitor of apoptosis protein and poly(ADP-ribose) polymerase cleavage in Bel-7402 cells treated with 15 mumol/l fenretinide for 48 h. Overexpression of p53 was observed in a time-dependent manner, along with a decrease in the Bcl-2/Bax ratio.	Fenretinide	193-204	BCL2 apoptosis regulator	Homo sapiens	307-312	
15326375-6	2004	4HPR-induced apoptosis in these cells was associated with stimulation of reactive oxygen species generation, decreased levels of Bcl-2 protein, release of cytochrome c into the cytosol, increased caspase-3 activity, and poly(ADP-ribose) polymerase cleavage.	Fenretinide	0-4	BCL2 apoptosis regulator	Homo sapiens	129-134	
14645667-2	2003	The stress-inducible transcription factor known as growth and DNA damage (GADD)-inducible transcription factor 153 is induced in response to fenretinide and in other cell types modulates apoptosis via pro- and antiapoptotic members of the BCL2 family.	Fenretinide	141-152	BCL2 apoptosis regulator	Homo sapiens	239-243	
14645667-3	2003	Because BCL2-family proteins are important in apoptosis induced by chemotherapeutic drugs, GADD153 may be a key mediator of synergy between fenretinide and chemotherapeutic drugs.	Fenretinide	140-151	BCL2 apoptosis regulator	Homo sapiens	8-12	
13679861-0	2003	The chemopreventive agent N-(4-hydroxyphenyl)retinamide induces apoptosis through a mitochondrial pathway regulated by proteins from the Bcl-2 family.	Fenretinide	26-55	BCL2 apoptosis regulator	Homo sapiens	137-142