PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30719230-0	2019	ATF4 contributes to autophagy and survival in sunitinib treated brain tumor initiating cells (BTICs).	Sunitinib	46-55	activating transcription factor 4	Homo sapiens	0-4	
30552230-5	2019	Here, we report that the ER-associated protein degradation (ERAD) inhibitor eeyarestatin sensitized MTC cells to the TKIs, sunitinib and vandetanib, thereby leading to synergistic upregulation of ATF4 expression, accumulation of reactive oxygen species, and subsequent cell death.	Sunitinib	123-132	activating transcription factor 4	Homo sapiens	196-200	
30719230-5	2019	We found that the ATF4/p-eIF2alpha pathway is activated in response to Sunitinib in primary tumor initiating progenitor cell cultures (BTICs).	Sunitinib	71-80	activating transcription factor 4	Homo sapiens	18-22	
30719230-7	2019	In case of Sunitinib treated cells, autophagy is additionally increased by ATF4 mediated upregulation of autophagy genes.	Sunitinib	11-20	activating transcription factor 4	Homo sapiens	75-79	
30719230-8	2019	Inhibition of ATF4 by small interfering RNA (siRNA) reduced autophagy and cell proliferation after Sunitinib treatment in a subset of BTIC cultures.	Sunitinib	99-108	activating transcription factor 4	Homo sapiens	14-18