PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24091729-9	2013	Finally, the proteasome inhibitor bortezomib, which induces the expression of miR-29b, decreased global DNA methylation by a miR-29b-dependent mechanism and induced SOCS-1 promoter demethylation and protein upregulation.	Bortezomib	34-44	microRNA 29b-1	Homo sapiens	78-85	
24091729-9	2013	Finally, the proteasome inhibitor bortezomib, which induces the expression of miR-29b, decreased global DNA methylation by a miR-29b-dependent mechanism and induced SOCS-1 promoter demethylation and protein upregulation.	Bortezomib	34-44	microRNA 29b-1	Homo sapiens	125-132	
24091729-10	2013	In conclusion, our data indicate that miR-29b is endowed with epigenetic activity and mediates previously unknown functions of bortezomib in MM cells.	Bortezomib	127-137	microRNA 29b-1	Homo sapiens	38-45	
22566605-2	2012	Subsequent preclinical studies with bortezomib in AML cells have shown drug-induced miR-29b up-regulation, resulting in loss of transcriptional activation for several genes relevant to myeloid leukemogenesis, including DNA methyltransferases and receptor tyrosine kinases.	Bortezomib	36-46	microRNA 29b-1	Homo sapiens	84-91	
22566605-8	2012	Additional mechanistic studies showed that FLT3 down-regulation was due to bortezomib-induced miR-29b up-regulation; this led to SP1 down-regulation and destruction of the SP1/NF-kappaB complex that transactivated FLT3.	Bortezomib	75-85	microRNA 29b-1	Homo sapiens	94-101	
30967527-0	2019	Bortezomib-inducible long non-coding RNA myocardial infarction associated transcript is an oncogene in multiple myeloma that suppresses miR-29b.	Bortezomib	0-10	microRNA 29b-1	Homo sapiens	136-143	
25234165-0	2015	MiR-29b replacement inhibits proteasomes and disrupts aggresome+autophagosome formation to enhance the antimyeloma benefit of bortezomib.	Bortezomib	126-136	microRNA 29b-1	Homo sapiens	0-7	
25234165-5	2015	MiR-29b was significantly reduced in bortezomib-resistant cells as well as in cells resistant to second-generation PIs carfilzomib and ixazomib.	Bortezomib	37-47	microRNA 29b-1	Homo sapiens	0-7	
25234165-9	2015	Immunofluorescence studies revealed that miR-29b replacements enhanced the bortezomib-induced accumulation of ubiquitinated proteins but did not reveal aggresome or autophagosome formation.	Bortezomib	75-85	microRNA 29b-1	Homo sapiens	41-48	
25234165-10	2015	Taken together, our study identifies miR-29b replacements as the first-in-class miR-based PIs that also disrupt the autophagy pathway and highlight their potential to synergistically enhance the antimyeloma effect of bortezomib.	Bortezomib	217-227	microRNA 29b-1	Homo sapiens	37-44