PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	Imatinib Mesylate	26-43	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	135-139	
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	Imatinib Mesylate	45-52	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	135-139	
19276246-1	2009	PURPOSE: Imatinib, a BCR-ABL tyrosine kinase inhibitor, is a substrate of the efflux transporters P-glycoprotein (P-gp; ABCB1) and ABCG2 (breast cancer resistance protein), and its brain accumulation is restricted by both transporters.	Imatinib Mesylate	9-17	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	120-125	
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	Imatinib Mesylate	17-25	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	83-88	
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	Imatinib Mesylate	156-164	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	83-88	
15805252-3	2005	Imatinib is transported in vitro and in vivo by P-glycoprotein (P-gp; ABCB1), which thereby limits its distribution into the brain in mice.	Imatinib Mesylate	0-8	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	70-75	
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	Imatinib Mesylate	236-244	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	175-179	
19591692-0	2009	Influence of the dual ABCB1 and ABCG2 inhibitor tariquidar on the disposition of oral imatinib in mice.	Imatinib Mesylate	86-94	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	22-27	
19591692-1	2009	BACKGROUND: Imatinib, a tyrosine kinase inhibitor currently approved for treatment of several malignancies, has been shown to be a substrate for multiple efflux-transporter proteins, including ABCB1 (P-glycoprotein) and ABCG2 (BCRP).	Imatinib Mesylate	12-20	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	193-198