PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32846959-4	2020	In a dox-induced senescence/polyploidization state, the accumulation of autophagy protein markers, such as LC3B II and p62/SQSTM1, was observed.	Doxorubicin	5-8	sequestosome 1	Homo sapiens	119-122	
32846959-4	2020	In a dox-induced senescence/polyploidization state, the accumulation of autophagy protein markers, such as LC3B II and p62/SQSTM1, was observed.	Doxorubicin	5-8	sequestosome 1	Homo sapiens	123-129	
22412944-8	2012	The 2D-DIGE/MS analysis identified that sequestosome 1 (SQSTM1/p62) had a significant increase in pre-DOX and LMB-treated cells (P<0.05).	Doxorubicin	102-105	sequestosome 1	Homo sapiens	40-54	
27735842-6	2016	DOXO induced hCPC apoptosis with reduction of SMP30 (regucalcin) and autophagosome marker LC3, as well as remarkable induction of the autophagy-related markers, Beclin-1, APG7, and P62/SQSTM1 and induction of calcium-related molecules, CaM (Calmodulin) and CaMKII (Calmodulin kinase II).	Doxorubicin	0-4	sequestosome 1	Homo sapiens	181-184	
27735842-6	2016	DOXO induced hCPC apoptosis with reduction of SMP30 (regucalcin) and autophagosome marker LC3, as well as remarkable induction of the autophagy-related markers, Beclin-1, APG7, and P62/SQSTM1 and induction of calcium-related molecules, CaM (Calmodulin) and CaMKII (Calmodulin kinase II).	Doxorubicin	0-4	sequestosome 1	Homo sapiens	185-191	
26961006-8	2016	Both colchicine and doxorubicin increased the expression of the master regulator of autophagy TFEB, the autophagy linker p62/SQSTM1 and the autophagosome component LC3.	Doxorubicin	20-31	sequestosome 1	Homo sapiens	121-124	
26961006-8	2016	Both colchicine and doxorubicin increased the expression of the master regulator of autophagy TFEB, the autophagy linker p62/SQSTM1 and the autophagosome component LC3.	Doxorubicin	20-31	sequestosome 1	Homo sapiens	125-131	
22412944-8	2012	The 2D-DIGE/MS analysis identified that sequestosome 1 (SQSTM1/p62) had a significant increase in pre-DOX and LMB-treated cells (P<0.05).	Doxorubicin	102-105	sequestosome 1	Homo sapiens	56-62	
22412944-8	2012	The 2D-DIGE/MS analysis identified that sequestosome 1 (SQSTM1/p62) had a significant increase in pre-DOX and LMB-treated cells (P<0.05).	Doxorubicin	102-105	sequestosome 1	Homo sapiens	63-66	
22412944-9	2012	In conclusion, our results suggest that drug-resistant lung cancer cells with p53 wild type could be sensitized to cell death by scheduled combination treatment of DOX and LMB through activating and restoring p53 as well as potentially other signaling pathway(s) involving sequestosome 1.	Doxorubicin	164-167	sequestosome 1	Homo sapiens	273-287	
1325792-4	1992	Protein phosphorylation experiments in intact cells revealed that HL60/ADR, the adriamycin-resistant variant, showed a higher overall phosphorylation of nuclear proteins than the drug-sensitive parental HL60, and that phorbol ester (protein kinase C activator) and calyculin A appeared to more specifically stimulate phosphorylation of p66 and p60, respectively.	Doxorubicin	80-90	sequestosome 1	Homo sapiens	344-347