PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	Imatinib Mesylate	0-8	sequestosome 1	Homo sapiens	89-92	
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	Imatinib Mesylate	0-8	sequestosome 1	Homo sapiens	102-116	
31789418-7	2020	In conclusion, HHT induced p62-mediated autophagy in imatinib-resistant CML K562G cells, thus promoting autophagic degradation of the BCR-ABL protein and providing a novel strategy for the treatment of TKI-resistant CML.	Imatinib Mesylate	53-61	sequestosome 1	Homo sapiens	27-30	
22262776-5	2012	Specifically, GSK3beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity.	Imatinib Mesylate	69-86	sequestosome 1	Homo sapiens	202-205