PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28260091-5	2017	The cells treated with paclitaxel alone eventually acquired MDR along with the overexpression of and highly activated P-glycoprotein (Pgp), while the cells treated with the paclitaxel-TET combination were sensitive to chemotherapeutic drugs and expressed decreased levels of Pgp and less Pgp activity.	tet	184-187	ATP binding cassette subfamily B member 1	Homo sapiens	275-278	
28260091-5	2017	The cells treated with paclitaxel alone eventually acquired MDR along with the overexpression of and highly activated P-glycoprotein (Pgp), while the cells treated with the paclitaxel-TET combination were sensitive to chemotherapeutic drugs and expressed decreased levels of Pgp and less Pgp activity.	tet	184-187	ATP binding cassette subfamily B member 1	Homo sapiens	275-278	
28260091-9	2017	On the whole, our findings suggest that TET prevents paclitaxel-induced MDR by inhibiting Pgp overexpression through a mechanism that may involve the inhibition of NF-kappaB signaling in osteosarcoma.	tet	40-43	ATP binding cassette subfamily B member 1	Homo sapiens	90-93	
24520791-8	2014	Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05).	tet	89-92	ATP binding cassette subfamily B member 1	Homo sapiens	66-70	
24520791-8	2014	Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05).	tet	182-185	ATP binding cassette subfamily B member 1	Homo sapiens	66-70	
24520791-9	2014	CONCLUSION: TET could achieve MDR reversion in gastric cancer cells by down-regulating the expression of ZNF139, MRP-1, and MDR1.	tet	12-15	ATP binding cassette subfamily B member 1	Homo sapiens	124-128	
19840446-5	2009	It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells.	tet	25-28	ATP binding cassette subfamily B member 1	Homo sapiens	245-250	
19840446-5	2009	It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells.	tet	159-162	ATP binding cassette subfamily B member 1	Homo sapiens	245-250	
9625436-3	1998	TET (3.0 microM), FAN (3.0 microM) and VER (10.0 microM) reduced the paclitaxel (TAX) concentration required to achieve 50% inhibition of cell growth (EC50) to HCT15 (P-gp-positive) cells about 3100-, 1900- and 410-fold, and these compounds also reduced the EC50 value of actinomycin D (AMD) about 36.0-, 45.9- and 18.2-fold in the cells, respectively.	tet	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	167-171	
9625436-5	1998	On the other hand, TET (3.0 microM), FAN (3.0 microM) and VER (10.0 microM) similarly enhanced the accumulation rates of rhodamine 123, a well known P-gp substrate, in HCT15 cells (200-250%).	tet	19-22	ATP binding cassette subfamily B member 1	Homo sapiens	149-153	
9625436-8	1998	From the result, we conclude that TET and FAN enhanced the cytotoxicity of MDR-related drugs via modulation of P-gp.	tet	34-37	ATP binding cassette subfamily B member 1	Homo sapiens	111-115