PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32469087-7	2020	Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors.	bafilomycin A1	307-321	high mobility group box 1	Homo sapiens	14-19	
30686534-5	2019	In contrast, genetic ablation (using ATG5-/- or ATG7-/- cells) or pharmacologic inhibition (the administration of bafilomycin A1 or chloroquine) of autophagy was found to block ferroptosis activator-induced HMGB1 release.	bafilomycin A1	114-128	high mobility group box 1	Homo sapiens	207-212