PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22532027-10 2012 In addition, overexpression of c-Src as well as treatment with ATO could stimulate EGFR-Y845/ERK phosphorylation, p21 expression, and cellular arrest/apoptosis, which could be attenuated by pretreatment with apocynin or knockdown of p67(phox). Arsenic Trioxide 63-66 mitogen-activated protein kinase 1 Homo sapiens 93-96 22532027-3 2012 Previously, we demonstrated in keratinocytes that arsenic trioxide (ATO)-induced p21(WAF1/CIP1) (p21) expression leading to cellular cytotoxicity through the c-Src/EGFR/ERK pathway and generation of reactive oxygen species (ROS). Arsenic Trioxide 50-66 mitogen-activated protein kinase 1 Homo sapiens 169-172 21523454-9 2012 Some significant decreases in the viability of the cells exposed to ATO in the presence of MAPK inhibitors comparing with the cells exposed to ATO alone were observed; however, the effects likely resulted from a simple additive cytotoxicity of the drugs. Arsenic Trioxide 68-71 mitogen-activated protein kinase 1 Homo sapiens 91-95 22532027-3 2012 Previously, we demonstrated in keratinocytes that arsenic trioxide (ATO)-induced p21(WAF1/CIP1) (p21) expression leading to cellular cytotoxicity through the c-Src/EGFR/ERK pathway and generation of reactive oxygen species (ROS). Arsenic Trioxide 68-71 mitogen-activated protein kinase 1 Homo sapiens 169-172 21523454-9 2012 Some significant decreases in the viability of the cells exposed to ATO in the presence of MAPK inhibitors comparing with the cells exposed to ATO alone were observed; however, the effects likely resulted from a simple additive cytotoxicity of the drugs. Arsenic Trioxide 143-146 mitogen-activated protein kinase 1 Homo sapiens 91-95 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 1 Homo sapiens 50-53 20799280-0 2011 Arsenic trioxide induces apoptosis through JNK and ERK in human mesothelioma cells. Arsenic Trioxide 0-16 mitogen-activated protein kinase 1 Homo sapiens 51-54 21278055-10 2011 Furthermore, ATO-induced GSK-3beta(Ser9) phosphorylation was through the ERK pathway, but not the PI3K/Akt pathway. Arsenic Trioxide 13-16 mitogen-activated protein kinase 1 Homo sapiens 73-76 21278055-11 2011 We suggest that, taken together, ATO-induced ERK phosphorylation could inhibit GSK-3beta activity to dephosphorylate the C-terminus (Ser243) of c-Jun to increase p21 expression and resultant cell death. Arsenic Trioxide 33-36 mitogen-activated protein kinase 1 Homo sapiens 45-48 20799280-4 2011 As2O3 induced apoptosis of NCI-H2052 cells, which was accompanied by activation of c-Jun NH2-terminal kinase (JNK)1/2, extracellular signal-regulated kinase (ERK)1/2, and caspase-3. Arsenic Trioxide 0-5 mitogen-activated protein kinase 1 Homo sapiens 119-165 20129490-0 2010 Arsenic trioxide-mediated antiplatelet activity: pivotal role of the phospholipase C gamma 2-protein kinase C-p38 MAPK cascade. Arsenic Trioxide 0-16 mitogen-activated protein kinase 1 Homo sapiens 110-113 20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Arsenic Trioxide 0-3 mitogen-activated protein kinase 1 Homo sapiens 35-38 20129490-0 2010 Arsenic trioxide-mediated antiplatelet activity: pivotal role of the phospholipase C gamma 2-protein kinase C-p38 MAPK cascade. Arsenic Trioxide 0-16 mitogen-activated protein kinase 1 Homo sapiens 114-118 20129490-8 2010 Moreover, arsenic trioxide markedly inhibited p38 mitogen-activated protein kinase (MAPK) but not JNK1/2 or ERK2 phosphorylation in washed platelets. Arsenic Trioxide 10-26 mitogen-activated protein kinase 1 Homo sapiens 84-88 20129490-11 2010 The most important findings of this study suggest that the inhibitory effect of arsenic trioxide possibly involves inhibition of the PLC gamma 2-PKC-p38 MAPK cascade, thereby leading to inhibition of [Ca(+2)]i or free radical formation, and finally the inhibition of platelet aggregation. Arsenic Trioxide 80-96 mitogen-activated protein kinase 1 Homo sapiens 149-152 20129490-11 2010 The most important findings of this study suggest that the inhibitory effect of arsenic trioxide possibly involves inhibition of the PLC gamma 2-PKC-p38 MAPK cascade, thereby leading to inhibition of [Ca(+2)]i or free radical formation, and finally the inhibition of platelet aggregation. Arsenic Trioxide 80-96 mitogen-activated protein kinase 1 Homo sapiens 153-157 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 1 Homo sapiens 126-172 19428345-7 2009 Our study showed that esculetin, PD98059 (MEK/ERK inhibitor), and SP600125 (JNK inhibitor) similarly enhanced the As(2)O(3)-induced GSH depletion. Arsenic Trioxide 114-123 mitogen-activated protein kinase 1 Homo sapiens 46-49 19428345-14 2009 Based on these studies, esculetin enhances the As(2)O(3)-provoked apoptosis by modulating the MEK/ERK and JNK pathways and reducing intracellular GSH levels. Arsenic Trioxide 47-56 mitogen-activated protein kinase 1 Homo sapiens 98-101 17168655-8 2006 Our pre-clinical studies showed that ATO is capable to induce cell death in acute leukemia cells but the apoptotic function is limited since it can induce also a mechanism of cell defense by activating pro-survival molecules such as MEK-ERK, Bcl-xL, Bcl-2. Arsenic Trioxide 37-40 mitogen-activated protein kinase 1 Homo sapiens 237-240 19038232-8 2009 By contrast, N-acetyl-L-cysteine and p38-MAPK inhibitor attenuate the apoptosis-sensitizing (pro-apoptotic) action of genistein when combined with the antileukaemic agent arsenic trioxide. Arsenic Trioxide 171-187 mitogen-activated protein kinase 1 Homo sapiens 37-40 18728151-0 2008 Novel human neutrophil agonistic properties of arsenic trioxide: involvement of p38 mitogen-activated protein kinase and/or c-jun NH2-terminal MAPK but not extracellular signal-regulated kinases-1/2. Arsenic Trioxide 47-63 mitogen-activated protein kinase 1 Homo sapiens 80-83 18728151-4 2008 We found that ATO activates p38 and that, unlike H2O2, this response was not inhibited by exogenous catalase. Arsenic Trioxide 14-17 mitogen-activated protein kinase 1 Homo sapiens 28-31 18728151-5 2008 Also, we demonstrated that ATO-induced p38 activation occurs before H2O2 generation and without a calcium burst. Arsenic Trioxide 27-30 mitogen-activated protein kinase 1 Homo sapiens 39-42 18728151-8 2008 In contrast, the ability of ATO to enhance adhesion, migration, phagocytosis, release, and activity of gelatinase and degranulation of secretory, specific, and gelatinase, but not azurophilic granules, is dependent upon activation of p38 and/or JNK. Arsenic Trioxide 28-31 mitogen-activated protein kinase 1 Homo sapiens 234-237 17168655-9 2006 By combining ATO with specific MEK inhibitors, we demonstrated that the block of MEK-ERK phosphorylation, the induction of Bad de-phosphorylation, and activation of p53AIP1 apoptotic pathway interrupt the pro-survival mechanisms of ATO and kill the leukemic cells by apoptotic synergism. Arsenic Trioxide 13-16 mitogen-activated protein kinase 1 Homo sapiens 85-88 15961274-4 2006 Using reporter assay, RT-PCR and Western blotting, we show that c-Src activation might be a prerequisite for As2O3-induced EGFR/Ras/Raf/ERK signaling. Arsenic Trioxide 109-114 mitogen-activated protein kinase 1 Homo sapiens 136-139 16972261-0 2006 Pharmacologic inhibitors of extracellular signal-regulated kinase (ERKs) and c-Jun NH(2)-terminal kinase (JNK) decrease glutathione content and sensitize human promonocytic leukemia cells to arsenic trioxide-induced apoptosis. Arsenic Trioxide 191-207 mitogen-activated protein kinase 1 Homo sapiens 67-71 15961274-0 2006 As2O3-induced c-Src/EGFR/ERK signaling is via Sp1 binding sites to stimulate p21WAF1/CIP1 expression in human epidermoid carcinoma A431 cells. Arsenic Trioxide 0-5 mitogen-activated protein kinase 1 Homo sapiens 25-28 15961274-7 2006 Taken together, we conclude that the Sp1 binding sites are required for As2O3-induced p21 gene transcription through c-Src/EGFR/Ras/Raf/ERK pathway. Arsenic Trioxide 72-77 mitogen-activated protein kinase 1 Homo sapiens 136-139 14610070-10 2004 It is concluded that TPA increases the apoptotic action of As(2)O(3), an effect mediated by ERK activation and GSH depletion. Arsenic Trioxide 59-68 mitogen-activated protein kinase 1 Homo sapiens 92-95 16445569-6 2005 It was found that As2O3 activates the prosurvival mitogen-activated protein kinase kinase (MEK)/ERK pathway in MCF-7 cells, which, conversely, may compromise the efficacy of As2O3. Arsenic Trioxide 18-23 mitogen-activated protein kinase 1 Homo sapiens 96-99 16445569-6 2005 It was found that As2O3 activates the prosurvival mitogen-activated protein kinase kinase (MEK)/ERK pathway in MCF-7 cells, which, conversely, may compromise the efficacy of As2O3. Arsenic Trioxide 174-179 mitogen-activated protein kinase 1 Homo sapiens 96-99 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 1 Homo sapiens 71-113 12754411-4 2003 When treated with micromolar concentrations of As(2)O(3), HepG2 cells became highly apoptotic paralleled with activation of caspase-3 and members of mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) and c-jun NH(2)-terminal kinase (JNK) but not p38 MAP kinase. Arsenic Trioxide 47-56 mitogen-activated protein kinase 1 Homo sapiens 201-238 12754411-4 2003 When treated with micromolar concentrations of As(2)O(3), HepG2 cells became highly apoptotic paralleled with activation of caspase-3 and members of mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) and c-jun NH(2)-terminal kinase (JNK) but not p38 MAP kinase. Arsenic Trioxide 47-56 mitogen-activated protein kinase 1 Homo sapiens 240-243 33858507-8 2021 Mechanistically, ATO mitigated venetoclax-induced upregulation of Mcl-1 by the inhibition of AKT and ERK, along with activation of GSK-3beta. Arsenic Trioxide 17-20 mitogen-activated protein kinase 1 Homo sapiens 101-104 11304686-0 2001 Apoptosis induced by arsenic trioxide in leukemia U937 cells is dependent on activation of p38, inactivation of ERK and the Ca2+-dependent production of superoxide. Arsenic Trioxide 21-37 mitogen-activated protein kinase 1 Homo sapiens 91-94 11304686-0 2001 Apoptosis induced by arsenic trioxide in leukemia U937 cells is dependent on activation of p38, inactivation of ERK and the Ca2+-dependent production of superoxide. Arsenic Trioxide 21-37 mitogen-activated protein kinase 1 Homo sapiens 112-115 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 1 Homo sapiens 100-104 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 1 Homo sapiens 108-111 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 1 Homo sapiens 171-174 34560123-10 2021 Moreover, both inositol-requiring enzyme 1alpha (IRE1alpha) RNase and kinase inhibitor KIRA6 and IRE1alpha kinase inhibitor APY29 completely inhibited As2O3-induced GRP78 protein expression and phosphorylation of JNK, ERK and p38 MAPK. Arsenic Trioxide 151-156 mitogen-activated protein kinase 1 Homo sapiens 218-221 12296996-0 2002 Arsenic trioxide induces apoptosis in chronic myelogenous leukemia K562 cells: possible involvement of p38 MAP kinase. Arsenic Trioxide 0-16 mitogen-activated protein kinase 1 Homo sapiens 103-106 32683294-10 2020 These results indicate that As2O3 inhibits occludin expression in vivo and in vitro at least partially via the ROS/ERK/ELK1/MLCK and ROS/p38 MAPK signaling pathways. Arsenic Trioxide 28-33 mitogen-activated protein kinase 1 Homo sapiens 115-118 24392034-0 2013 Arsenic trioxide overcomes rapamycin-induced feedback activation of AKT and ERK signaling to enhance the anti-tumor effects in breast cancer. Arsenic Trioxide 0-16 mitogen-activated protein kinase 1 Homo sapiens 76-79 25506699-10 2014 Apoptosis generation by etomoxir plus 2-deoxy-D-glucose was further increased by co-incubation with ATO, which is apparently explained by the capacity of ATO to attenuate Akt and ERK activation. Arsenic Trioxide 100-103 mitogen-activated protein kinase 1 Homo sapiens 179-182 25506699-10 2014 Apoptosis generation by etomoxir plus 2-deoxy-D-glucose was further increased by co-incubation with ATO, which is apparently explained by the capacity of ATO to attenuate Akt and ERK activation. Arsenic Trioxide 154-157 mitogen-activated protein kinase 1 Homo sapiens 179-182 24788596-5 2014 Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1alpha/MRP1 pathway and ERK. Arsenic Trioxide 118-123 mitogen-activated protein kinase 1 Homo sapiens 179-182 24307199-8 2014 Finally, 3-BrP was seen to cooperate with antitumor agents like arsenic trioxide and curcumin in causing cell death, a response apparently mediated by both the generation of oxidative stress induced by 3-BrP and the attenuation of Akt and ERK activation by curcumin. Arsenic Trioxide 64-80 mitogen-activated protein kinase 1 Homo sapiens 239-242 25758096-6 2015 In U937 cells, rapamycin alone increased the activity of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and the addition of ATO decreased the level of phosphorylated ERK, Ser473 phosphorylated Akt and anti-apoptotic Mcl-1 protein. Arsenic Trioxide 159-162 mitogen-activated protein kinase 1 Homo sapiens 134-137 25758096-6 2015 In U937 cells, rapamycin alone increased the activity of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and the addition of ATO decreased the level of phosphorylated ERK, Ser473 phosphorylated Akt and anti-apoptotic Mcl-1 protein. Arsenic Trioxide 159-162 mitogen-activated protein kinase 1 Homo sapiens 201-204 25983101-0 2015 ANXA1 silencing increases the sensitivity of cancer cells to low-concentration arsenic trioxide treatment by inhibiting ERK MAPK activation. Arsenic Trioxide 79-95 mitogen-activated protein kinase 1 Homo sapiens 120-123 25983101-0 2015 ANXA1 silencing increases the sensitivity of cancer cells to low-concentration arsenic trioxide treatment by inhibiting ERK MAPK activation. Arsenic Trioxide 79-95 mitogen-activated protein kinase 1 Homo sapiens 124-128 25983101-10 2015 Furthermore, overexpression of ANXA1 induced by ATO resulted in activation of extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases (MAPKs), rendering cancer cells resistant to the agent. Arsenic Trioxide 48-51 mitogen-activated protein kinase 1 Homo sapiens 78-115 25983101-10 2015 Furthermore, overexpression of ANXA1 induced by ATO resulted in activation of extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases (MAPKs), rendering cancer cells resistant to the agent. Arsenic Trioxide 48-51 mitogen-activated protein kinase 1 Homo sapiens 117-120 25983101-11 2015 In addition, PD98059, a specific ERK inhibitor, increased the sensitivity of cancer cells to a lower concentration of ATO treatment. Arsenic Trioxide 118-121 mitogen-activated protein kinase 1 Homo sapiens 33-36 25983101-12 2015 CONCLUSIONS: Taken together, these data indicate that overexpression of ANXA1 induced by low-concentration ATO makes cancer cells more resistant to the agent via activated ERK MAPKs. Arsenic Trioxide 107-110 mitogen-activated protein kinase 1 Homo sapiens 172-175 24392034-7 2013 Treatment with rapalog also results in activated ERK signaling, which is decreased with ATO co-treatment in all cell lines tested. Arsenic Trioxide 88-91 mitogen-activated protein kinase 1 Homo sapiens 49-52 22751450-7 2013 Both ERK and AKT inhibitors decreased Mcl-1 levels and enhanced ATO-induced apoptosis in HL-60 cells. Arsenic Trioxide 64-67 mitogen-activated protein kinase 1 Homo sapiens 5-8 24004656-0 2013 Importance of ERK activation in As2O3-induced differentiation and promyelocytic leukemia nuclear bodies formation in neuroblastoma cells. Arsenic Trioxide 32-37 mitogen-activated protein kinase 1 Homo sapiens 14-17 24004656-4 2013 As2O3 (2muM) induced neurite outgrowth in all cell lines, which was dependent on ERK activation but independent on MYCN status. Arsenic Trioxide 0-5 mitogen-activated protein kinase 1 Homo sapiens 81-84 24004656-6 2013 In parallel, As2O3 induced a rapid assembly of promyelocytic leukemia nuclear bodies (PML-NB) in an ERK-dependent manner. Arsenic Trioxide 13-18 mitogen-activated protein kinase 1 Homo sapiens 100-103 24004656-7 2013 In conclusion, mechanisms leading to neuroblastoma cell differentiation in response to As2O3 appear to involve the ERK pathway activation and PML-NB formation, which are observed in response to other differentiating molecules such as retinoic acid derivates. Arsenic Trioxide 87-92 mitogen-activated protein kinase 1 Homo sapiens 115-118 23178716-7 2013 Collectively, As2O3 mediates an initial rise in pY-Src(416) to regulate the PI3K/AKT pathway which increases SnoN and cell survival; these early events may counter the cell death response associated with increased pY-EGFR/MAPK activation. Arsenic Trioxide 14-19 mitogen-activated protein kinase 1 Homo sapiens 222-226