PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26459009-0	2015	Downregulation of P-gp, Ras and p-ERK1/2 contributes to the arsenic trioxide-induced reduction in drug resistance towards doxorubicin in gastric cancer cell lines.	Arsenic Trioxide	60-76	mitogen-activated protein kinase 3	Homo sapiens	34-40	
26459009-11	2015	As2O3 decreased the levels of Ras and p-ERK1/2 (P<0.01).	Arsenic Trioxide	0-5	mitogen-activated protein kinase 3	Homo sapiens	40-46	
26459009-14	2015	Non- and mildly-toxic doses of As2O3 reduced MDR to DOX through Ras/p-ERK1/2 signaling.	Arsenic Trioxide	31-36	mitogen-activated protein kinase 3	Homo sapiens	70-76	
16283431-0	2006	Opposite effect of ERK1/2 and JNK on p53-independent p21WAF1/CIP1 activation involved in the arsenic trioxide-induced human epidermoid carcinoma A431 cellular cytotoxicity.	Arsenic Trioxide	93-109	mitogen-activated protein kinase 3	Homo sapiens	19-25	
20799280-8	2011	Moreover, JNK1 siRNA, but not JNK2 siRNA, abrogated As2O3-induced ERK1/2 phosphorylation.	Arsenic Trioxide	52-57	mitogen-activated protein kinase 3	Homo sapiens	66-72	
20799280-9	2011	JNK2 siRNA together with PD98059, a specific MAPK/ERK kinase inhibitor, suppressed As2O3-induced apoptosis more significantly than JNK2 siRNA alone.	Arsenic Trioxide	83-88	mitogen-activated protein kinase 3	Homo sapiens	45-49	
20799280-10	2011	These results indicated that As2O3 induces apoptosis of NCI-H2052 cells mainly through JNK1/2 activation, and that ERK1/2 is involved in As2O3-induced apoptosis when JNK1/2 are inactivated.	Arsenic Trioxide	137-142	mitogen-activated protein kinase 3	Homo sapiens	115-121	
20164150-0	2010	The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide.	Arsenic Trioxide	133-149	mitogen-activated protein kinase 3	Homo sapiens	23-27	
19242099-0	2009	Combination treatment with arsenic trioxide and irradiation enhances autophagic effects in U118-MG cells through increased mitotic arrest and regulation of PI3K/Akt and ERK1/2 signaling pathways.	Arsenic Trioxide	27-43	mitogen-activated protein kinase 3	Homo sapiens	169-175	
19060284-5	2009	At a low concentration, the ATO-induced differentiation of retinoblastoma cells was evaluated by neurofilament expression and extracellular signal-regulated kinase (ERK)1/2 activation, which was confirmed by the inhibition of ERK1/2.	Arsenic Trioxide	28-31	mitogen-activated protein kinase 3	Homo sapiens	226-232	
19060284-9	2009	At a low dose (<or= 1 microM), ATO induced the differentiation of retinoblastoma cells through ERK1/2 activation, whereas ROS generation by a high dose (>or= 2 microM) of ATO induced apoptosis in retinoblastoma cells.	Arsenic Trioxide	34-37	mitogen-activated protein kinase 3	Homo sapiens	98-104	
19088370-3	2008	Treatment with As(2)O(3) resulted in rapid phosphorylation of the p42/p44 MAPK which could be abolished by addition of the MAPK inhibitor, U0126.	Arsenic Trioxide	15-24	mitogen-activated protein kinase 3	Homo sapiens	70-78	
18210215-2	2008	Previously, we had demonstrated that opposing effects of ERK1/2 and JNK on p21 expression in response to arsenic trioxide (As(2)O(3)) are mediated through the Sp1 responsive elements of the p21 promoter in A431 cells.	Arsenic Trioxide	105-121	mitogen-activated protein kinase 3	Homo sapiens	57-63	
23253724-13	2012	CONCLUSIONS: As2O3, as a main component of arsenolite, can inhibit the production of MMPs by HSFb and THP-1 cells in an inflammatory state through inhibiting the release of inflammatory factors and the activation of the MAPK cascade pathway.	Arsenic Trioxide	13-18	mitogen-activated protein kinase 3	Homo sapiens	220-224	
23253724-13	2012	CONCLUSIONS: As2O3, as a main component of arsenolite, can inhibit the production of MMPs by HSFb and THP-1 cells in an inflammatory state through inhibiting the release of inflammatory factors and the activation of the MAPK cascade pathway.	Arsenic Trioxide	43-53	mitogen-activated protein kinase 3	Homo sapiens	220-224	
20862710-6	2010	Low-dose ATO produced reactive oxygen species (ROS), and activated the p38 MAPK, Akt, and ERK1/2 pathways at different time points within 60 min.	Arsenic Trioxide	9-12	mitogen-activated protein kinase 3	Homo sapiens	90-96	
20862710-8	2010	Inhibiting the activation of Akt and ERK1/2, but not p38 MAPK, decreased the ATO-induced expression of cyclin D1 protein.	Arsenic Trioxide	77-80	mitogen-activated protein kinase 3	Homo sapiens	37-43	
20862710-9	2010	This study reports for the first time that p38 MAPK/Akt/ERK1/2 activation is required for the protein stabilization of CDC6 in addition to cyclin D1 in ATO-induced cell proliferation and cell cycle modulation from G1 to S phase.	Arsenic Trioxide	152-155	mitogen-activated protein kinase 3	Homo sapiens	56-62	
20074581-3	2010	Our previous study found that arsenic trioxide (ATO)-induced activation of p21(WAF1/CIP1) (p21) led to A431 cell death through the antagonistic effects of the signaling of ERK1/2 and JNK1.	Arsenic Trioxide	30-46	mitogen-activated protein kinase 3	Homo sapiens	172-178	
20074581-3	2010	Our previous study found that arsenic trioxide (ATO)-induced activation of p21(WAF1/CIP1) (p21) led to A431 cell death through the antagonistic effects of the signaling of ERK1/2 and JNK1.	Arsenic Trioxide	48-51	mitogen-activated protein kinase 3	Homo sapiens	172-178	
18822310-4	2008	Previously, we demonstrated the opposing effects of ERK1/2 and JNK on p21(WAF1/CIP1) (p21) expression in response to ATO in A431 cells.	Arsenic Trioxide	117-120	mitogen-activated protein kinase 3	Homo sapiens	52-58	
18822310-6	2008	Presently, we demonstrated that a high concentration of ATO sustains ERK1/2 phosphorylation, and increases c-Fos biosynthesis and stability, which enhances p21 gene expression.	Arsenic Trioxide	56-59	mitogen-activated protein kinase 3	Homo sapiens	69-75	
18822310-8	2008	In conclusion, a high concentration of ATO can sustain ERK1/2 activation to enhance c-Fos expression, then dimerize with dephosphorylated c-Jun (Ser(63/73)) and recruit p300/CBP to the Sp1 sites (-84/-64) to activate p21 gene expression in A431 cells.	Arsenic Trioxide	39-42	mitogen-activated protein kinase 3	Homo sapiens	55-61	
16283431-11	2006	Therefore, we conclude that in A431 cells the ERK1/2 and JNK pathways might differentially contribute to As2O3-induced p21 expression and then due to cellular cytotoxicity.	Arsenic Trioxide	105-110	mitogen-activated protein kinase 3	Homo sapiens	46-52	
15538402-2	2005	In this study, we report that acute promyelocytic leukemia (APL) cells exploit the Ras-MAPK activation pathway to phosphorylate at Ser112 and to inactivate the proapoptotic protein Bad, delaying arsenic trioxide (ATO)-induced apoptosis.	Arsenic Trioxide	195-211	mitogen-activated protein kinase 3	Homo sapiens	87-91	
15538402-2	2005	In this study, we report that acute promyelocytic leukemia (APL) cells exploit the Ras-MAPK activation pathway to phosphorylate at Ser112 and to inactivate the proapoptotic protein Bad, delaying arsenic trioxide (ATO)-induced apoptosis.	Arsenic Trioxide	213-216	mitogen-activated protein kinase 3	Homo sapiens	87-91	
15538402-3	2005	Both in APL cell line NB4 and in APL primary blasts, the inhibition of extracellular signal-regulated kinases 1/2 (ERK1/2) and Bad phosphorylation by MEK1 inhibitors enhanced apoptosis in ATO-treated cells.	Arsenic Trioxide	188-191	mitogen-activated protein kinase 3	Homo sapiens	115-121	
11304686-2	2001	Upon treatment of U937 cells with 50 microM of As2O3, complete inactivation of the kinases ERK1 and ERK2 was detected within 30 min.	Arsenic Trioxide	47-52	mitogen-activated protein kinase 3	Homo sapiens	91-95	
11304686-4	2001	Experiments with transfected cells that expressed constitutively activated MEK1 and a specific inhibitor of p38 also suggested that inactivation of ERKs and activation of p38 might be associated with the induction of apoptosis by As2O3.	Arsenic Trioxide	230-235	mitogen-activated protein kinase 3	Homo sapiens	148-152