PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20889557-0 2010 High expression of sphingosine 1-phosphate receptors, S1P1 and S1P3, sphingosine kinase 1, and extracellular signal-regulated kinase-1/2 is associated with development of tamoxifen resistance in estrogen receptor-positive breast cancer patients. Tamoxifen 171-180 mitogen-activated protein kinase 3 Homo sapiens 95-136 16740736-6 2006 The MAPK/ERK kinase inhibitor PD98059 blocked tamoxifen-resistant growth. Tamoxifen 46-55 mitogen-activated protein kinase 3 Homo sapiens 4-8 19544110-0 2009 Activated PKCalpha/ERK1/2 signaling inhibits tamoxifen-induced apoptosis in C6 cells. Tamoxifen 45-54 mitogen-activated protein kinase 3 Homo sapiens 19-25 19544110-3 2009 In this study, we provided the evidence that PKCalpha-ERK1/2 signaling pathway plays a negative role in TAM-induced C6 cell apoptosis, and a combined utilization of TAM with inhibitors of PKCalpha or ERK1/2 could enhance the effectiveness of TAM on inhibiting tumor growth. Tamoxifen 104-107 mitogen-activated protein kinase 3 Homo sapiens 54-60 16740736-3 2006 Gene expression profiling was used to identify mitogen-activated protein kinase (MAPK) phosphatase 3 (MKP3) whose expression was correlated with response to the antiestrogen tamoxifen in both patients and in vitro-derived cell line models. Tamoxifen 174-183 mitogen-activated protein kinase 3 Homo sapiens 81-85 19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tamoxifen 49-58 mitogen-activated protein kinase 3 Homo sapiens 111-117 19115248-6 2009 We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition. Tamoxifen 42-51 mitogen-activated protein kinase 3 Homo sapiens 223-227 17363451-6 2007 We observed that 5 mum Tam rapidly induced sustained activation of ERK1/2 in ER-positive breast cancer cell lines (MCF-7 and T47D) and that PD98059 (inhibitor of ERK activation) was able to protect MCF-7 cells against Tam-induced death. Tamoxifen 23-26 mitogen-activated protein kinase 3 Homo sapiens 67-73 17363451-6 2007 We observed that 5 mum Tam rapidly induced sustained activation of ERK1/2 in ER-positive breast cancer cell lines (MCF-7 and T47D) and that PD98059 (inhibitor of ERK activation) was able to protect MCF-7 cells against Tam-induced death. Tamoxifen 23-26 mitogen-activated protein kinase 3 Homo sapiens 67-70 17363451-8 2007 In addition, inhibition of epidermal growth factor receptor (EGFR) opposed both Tam-induced ERK1/2 phosphorylation and cell death, which suggests that EGFR-associated mechanisms are involved in Tam-induced death. Tamoxifen 80-83 mitogen-activated protein kinase 3 Homo sapiens 92-98 17363451-8 2007 In addition, inhibition of epidermal growth factor receptor (EGFR) opposed both Tam-induced ERK1/2 phosphorylation and cell death, which suggests that EGFR-associated mechanisms are involved in Tam-induced death. Tamoxifen 194-197 mitogen-activated protein kinase 3 Homo sapiens 92-98 16740736-6 2006 The MAPK/ERK kinase inhibitor PD98059 blocked tamoxifen-resistant growth. Tamoxifen 46-55 mitogen-activated protein kinase 3 Homo sapiens 9-12 16740736-8 2006 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells. Tamoxifen 97-106 mitogen-activated protein kinase 3 Homo sapiens 203-209 16740736-8 2006 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells. Tamoxifen 97-106 mitogen-activated protein kinase 3 Homo sapiens 210-214 12060612-1 2002 PURPOSE: The purpose of this study is to address the hypothesis that activatedmitogen-activated protein kinase (MAPK; extracellular signal-regulated kinases 1 and 2) has a role in breast tumorigenesis, breast cancer progression, and the development of tamoxifen resistance. Tamoxifen 252-261 mitogen-activated protein kinase 3 Homo sapiens 118-164 16603346-0 2006 Activated ERK1/2 and phosphorylated oestrogen receptor alpha are associated with improved breast cancer survival in women treated with tamoxifen. Tamoxifen 135-144 mitogen-activated protein kinase 3 Homo sapiens 10-16 16603346-1 2006 The aim of this study was to investigate the expression of activated (phosphorylated) ERK1/2, oestrogen receptor alpha phosphorylated at S118 (ERalphaS118), and HER2 in primary breast cancer, and to make correlations with the outcome of tamoxifen therapy. Tamoxifen 237-246 mitogen-activated protein kinase 3 Homo sapiens 86-118 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 276-279 mitogen-activated protein kinase 3 Homo sapiens 39-43 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 276-279 mitogen-activated protein kinase 3 Homo sapiens 87-91 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 276-279 mitogen-activated protein kinase 3 Homo sapiens 93-104 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 315-324 mitogen-activated protein kinase 3 Homo sapiens 39-43 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 315-324 mitogen-activated protein kinase 3 Homo sapiens 87-91 16455819-6 2006 In contrast, transfection of activated MAPK kinase, an immediate upstream activator of MAPK (ERK 1 and 2) into MCF-7 cells leads to phosphorylation of Ser118 in the AF-1 domain of ERalpha, inhibition of ER-amplified in breast cancer 1 (ER:AIB1) interaction in the presence of Tam, and maintenance of sensitivity to tamoxifen. Tamoxifen 315-324 mitogen-activated protein kinase 3 Homo sapiens 93-104 16455819-8 2006 However, maximum sensitivity to tamoxifen was observed when both AKT and MAPK were inhibited. Tamoxifen 32-41 mitogen-activated protein kinase 3 Homo sapiens 73-77 15173068-9 2004 CONCLUSION: The results presented here show for the first time that ER redistribution to the cytoplasm and its interaction with HER2 are important downstream effects of HER2 overexpression, that ERK1/2 is important for ER cytoplasmic localization, and that subcellular localization of ER may play a mechanistic role in determining the responsiveness of breast cancer cells to tamoxifen. Tamoxifen 376-385 mitogen-activated protein kinase 3 Homo sapiens 195-201 14531500-0 2003 Oestrogen receptor-mediated modulation of the EGFR/MAPK pathway in tamoxifen-resistant MCF-7 cells. Tamoxifen 67-76 mitogen-activated protein kinase 3 Homo sapiens 51-55 16261397-1 2006 We have previously demonstrated that oestrogen receptor alpha (ERalpha) modulates epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK) signalling efficiency in a tamoxifen-resistant MCF-7 breast cancer cell line (Tam-R). Tamoxifen 189-198 mitogen-activated protein kinase 3 Homo sapiens 156-160 15806151-8 2005 Finally, patients with oestrogen receptor positive and ERK1/2 phosphorylated tumours also had an impaired tamoxifen response. Tamoxifen 106-115 mitogen-activated protein kinase 3 Homo sapiens 55-61 15502196-3 2005 They are based on cell-specific expression of the chimeric Cre recombinase Cre-ERT2, whose activity is induced by antiestrogens such as Tamoxifen (Tam), and which is obtained by fusing the Cre recombinase with a mutated ligand binding domain of the human estrogen receptor ERalpha. Tamoxifen 136-145 mitogen-activated protein kinase 3 Homo sapiens 79-83 15502196-3 2005 They are based on cell-specific expression of the chimeric Cre recombinase Cre-ERT2, whose activity is induced by antiestrogens such as Tamoxifen (Tam), and which is obtained by fusing the Cre recombinase with a mutated ligand binding domain of the human estrogen receptor ERalpha. Tamoxifen 136-139 mitogen-activated protein kinase 3 Homo sapiens 79-83 35054486-7 2022 Moreover, we demonstrated that IL-8 could activate both AKT and ERK1/2 via CXCR1 to confer tamoxifen resistance. Tamoxifen 91-100 mitogen-activated protein kinase 3 Homo sapiens 64-70 11773440-9 2002 Moreover, GPR30-dependent, cAMP-mediated attenuation of EGF-induced Erk-1/-2 activity was achieved by ER antagonists such as tamoxifen or ICI 182, 780; yet not by 17alpha-E2 or progesterone. Tamoxifen 125-134 mitogen-activated protein kinase 3 Homo sapiens 68-76 9372245-5 1997 Pretreatment of the cells with PKC inhibitors, CGP 41251 or tamoxifen, inhibited tyrosine phosphorylation of Erk1 and Erk2 MAP kinases induced by low concentrations of SP or TPA and significantly attenuated phosphorylation at high concentrations of SP or TPA. Tamoxifen 60-69 mitogen-activated protein kinase 3 Homo sapiens 109-113 33081566-1 2020 AIM: In this study, we explored the ability of TAMs to affect the malignant phenotype of human hepatoma Huh-7 cells through the Gli2/IGF-II/ERK1/2 pathway. Tamoxifen 47-51 mitogen-activated protein kinase 3 Homo sapiens 140-146 31592660-5 2019 Without tamoxifen to drive nuclear localization of ERT2-CreN-nMag, the typically high background of the photoactivation system was significantly suppressed. Tamoxifen 8-17 mitogen-activated protein kinase 3 Homo sapiens 51-55 33081566-12 2020 CONCLUSION: The TGF-beta1 secreted by TAMs promotes the migration, invasion and EMT of human hepatoma Huh-7 cells through the Gli2/IGF-II/ERK1/2 pathway. Tamoxifen 38-42 mitogen-activated protein kinase 3 Homo sapiens 138-144 32021441-0 2020 ERalpha36 as a Potential Therapeutic Target for Tamoxifen-Resistant Breast Cancer Cell Line Through EGFR/ERK Signaling Pathway. Tamoxifen 48-57 mitogen-activated protein kinase 3 Homo sapiens 105-108 29589904-3 2018 We show that when an analogue-sensitive ZAP70 allele is fused to the engineered ligand binding domain of the estrogen receptor, ERT2, its activity can be upregulated to an extent by a metabolite of an FDA-approved tamoxifen, 4-hydroxy-tamoxifen, and downregulated by an ATP analogue, 3-MB-PP1. Tamoxifen 214-223 mitogen-activated protein kinase 3 Homo sapiens 128-132 29945962-9 2018 Tamoxifen resistance mediated by the loss of miR-135a was shown to be partially dependent on the activation of the ERK1/2 and AKT pathways by miR-135a-targeted genes. Tamoxifen 0-9 mitogen-activated protein kinase 3 Homo sapiens 115-121 28855706-3 2017 Our data showed profound changes in skeletal shape, size and structure when Bmpr1a was deleted using Aggrecan-Cre ERT2 in early cartilage cells with a one-time tamoxifen injection. Tamoxifen 160-169 mitogen-activated protein kinase 3 Homo sapiens 114-118 28026072-4 2017 To activate KLF1 at defined time points during later stages of the differentiation process and to avoid transgene silencing that is commonly observed in differentiating pluripotent stem cells, we targeted a tamoxifen-inducible KLF1-ERT2 expression cassette into the AAVS1 locus. Tamoxifen 207-216 mitogen-activated protein kinase 3 Homo sapiens 232-236 28423577-0 2017 The cyclin-like protein, SPY1, regulates the ERalpha and ERK1/2 pathways promoting tamoxifen resistance. Tamoxifen 83-92 mitogen-activated protein kinase 3 Homo sapiens 57-63 26487496-9 2015 Constitutive and Tam-induced phosphorylation of EGFR and ERK1/2 was blocked by the AR antagonist Enzalutamide, suggesting that AR-mediated EGFR activation was a mechanism of resistance in these cells. Tamoxifen 17-20 mitogen-activated protein kinase 3 Homo sapiens 57-63 26096876-0 2015 Tamoxifen Inhibits TGF-beta-Mediated Activation of Myofibroblasts by Blocking Non-Smad Signaling Through ERK1/2. Tamoxifen 0-9 mitogen-activated protein kinase 3 Homo sapiens 105-111 26096876-4 2015 Our data indicate that tamoxifen does not interfere with canonical Smad signaling downstream of TGF-beta but rather blocks non-Smad signaling through ERK1/2 MAP-kinase and the AP-1 transcription factor FRA2. Tamoxifen 23-32 mitogen-activated protein kinase 3 Homo sapiens 150-156 27378269-6 2016 RESULTS: We discovered emerging vulnerabilities towards specific drugs, such as ERK1/2-, proteasome- and BCL-family inhibitors as the cells became tamoxifen-resistant. Tamoxifen 147-156 mitogen-activated protein kinase 3 Homo sapiens 80-86 24874276-6 2014 Treatment with 17beta-estradiol (E2), the GPER-specific agonist G-1 and tamoxifen (TAM) led to rapid activation of p-ERK1/2, but not p-Akt. Tamoxifen 72-81 mitogen-activated protein kinase 3 Homo sapiens 117-123 26909308-3 2015 METHODS: We used lentiviral mediated gene transfer to stably integrate a tamoxifen inducible form of CRE (CRE-ERT2) into the recently developed conditionally immortalized EndoC betaH2 line. Tamoxifen 73-82 mitogen-activated protein kinase 3 Homo sapiens 110-114 25846733-9 2015 This study suggested that long-term endocrine therapy facilitates leptin and ObRb overexpression in breast cancer cells, which attenuates the inhibitory effect of tamoxifen by activating both the ERK1/2 and STAT3 signaling pathways and upregulating CCND1 gene expression. Tamoxifen 163-172 mitogen-activated protein kinase 3 Homo sapiens 196-202 25727020-5 2015 omega-3FFA and tamoxifen significantly increased Erk1/2 and Akt phosphorylation levels in a dose and time dependent manner. Tamoxifen 15-24 mitogen-activated protein kinase 3 Homo sapiens 49-55 25727020-6 2015 Compared to omega-3FFA alone, the combination of tamoxifen with omega-3FFA significantly increased Erk1/2 and Akt phosphorylation levels. Tamoxifen 49-58 mitogen-activated protein kinase 3 Homo sapiens 99-105 25727020-7 2015 Because Erk1/2 and Akt activation has been linked to tamoxifen-related anti-estrogen resistance in breast cancer patients, these results indicate that omega-3FFA may interfere with the effects of tamoxifen in the prevention of breast cancer risk. Tamoxifen 53-62 mitogen-activated protein kinase 3 Homo sapiens 8-14 24874276-6 2014 Treatment with 17beta-estradiol (E2), the GPER-specific agonist G-1 and tamoxifen (TAM) led to rapid activation of p-ERK1/2, but not p-Akt. Tamoxifen 83-86 mitogen-activated protein kinase 3 Homo sapiens 117-123 24447434-9 2014 RESULTS: Interactions were identified between tamoxifen and p-AKT(Thr308), p-mTOR, p-p70S6K and p-ERK1/2. Tamoxifen 46-55 mitogen-activated protein kinase 3 Homo sapiens 98-104 25085753-9 2014 In tamoxifen-treated cases, ERK1/2 expression was an independent prognostic marker of longer survival. Tamoxifen 3-12 mitogen-activated protein kinase 3 Homo sapiens 28-34 25085753-11 2014 Importantly, positivity of ERK1/2 is independently associated with better outcome in tamoxifen-treated cases. Tamoxifen 85-94 mitogen-activated protein kinase 3 Homo sapiens 27-33 24481325-6 2014 Tamoxifen (TAM) in addition to 17beta-estradiol (E2) and the GPER agonist G1 activated GPER, resulting in transient increases in cell index, intracellular calcium, and ERK1/2 phosphorylation. Tamoxifen 0-9 mitogen-activated protein kinase 3 Homo sapiens 168-174 24481325-6 2014 Tamoxifen (TAM) in addition to 17beta-estradiol (E2) and the GPER agonist G1 activated GPER, resulting in transient increases in cell index, intracellular calcium, and ERK1/2 phosphorylation. Tamoxifen 11-14 mitogen-activated protein kinase 3 Homo sapiens 168-174 24658355-8 2014 These data suggest that tamoxifen-induced death of these cells is not dependent upon JNK signaling, but rather that ERK is the major MAPK driving their proliferation. Tamoxifen 24-33 mitogen-activated protein kinase 3 Homo sapiens 133-137 23086641-10 2012 In MCF-7/TAM-R cells,the expression of phosphorylation of AKT and MAPK44/42 protein was not changed in Evn-50 or TAM alone group,but significantly inhibited in the combination group at 72 h. CONCLUSION: Evn-50 can inhibit cell growth and induce apoptosis in MCF-7 and MCF-7/TAM-R cells,it can reverse tamoxifen-resistance of MCF-7/TAM-R cells.The mechanisms may be related to the down-regulation of phosphorylated ERK1/2 in MAPK signal pathway and phosphorylated AKT in AKT signal pathway. Tamoxifen 9-12 mitogen-activated protein kinase 3 Homo sapiens 66-70 23843844-7 2013 In MCF-7, the inhibitory effect against tamoxifen was a result from the activation of the ERK1/2 and STAT3 signal transduction pathway. Tamoxifen 40-49 mitogen-activated protein kinase 3 Homo sapiens 90-96 23338782-0 2013 Dose-dependent effect of tamoxifen in tamoxifen-resistant breast cancer cells via stimulation by the ERK1/2 and AKT signaling pathways. Tamoxifen 25-34 mitogen-activated protein kinase 3 Homo sapiens 113-119 23338782-0 2013 Dose-dependent effect of tamoxifen in tamoxifen-resistant breast cancer cells via stimulation by the ERK1/2 and AKT signaling pathways. Tamoxifen 38-47 mitogen-activated protein kinase 3 Homo sapiens 113-119 23338782-6 2013 Low-dose Tam was found to act as an estrogen agonist via stimulation of the ERK1/2 signaling pathway, resulting in acquired resistance to Tam, whereas high-dose Tam inhibited TAM-R cell growth by blocking the activation of ERK1/2 and AKT. Tamoxifen 9-12 mitogen-activated protein kinase 3 Homo sapiens 88-94 23086641-10 2012 In MCF-7/TAM-R cells,the expression of phosphorylation of AKT and MAPK44/42 protein was not changed in Evn-50 or TAM alone group,but significantly inhibited in the combination group at 72 h. CONCLUSION: Evn-50 can inhibit cell growth and induce apoptosis in MCF-7 and MCF-7/TAM-R cells,it can reverse tamoxifen-resistance of MCF-7/TAM-R cells.The mechanisms may be related to the down-regulation of phosphorylated ERK1/2 in MAPK signal pathway and phosphorylated AKT in AKT signal pathway. Tamoxifen 113-116 mitogen-activated protein kinase 3 Homo sapiens 66-70 23086641-10 2012 In MCF-7/TAM-R cells,the expression of phosphorylation of AKT and MAPK44/42 protein was not changed in Evn-50 or TAM alone group,but significantly inhibited in the combination group at 72 h. CONCLUSION: Evn-50 can inhibit cell growth and induce apoptosis in MCF-7 and MCF-7/TAM-R cells,it can reverse tamoxifen-resistance of MCF-7/TAM-R cells.The mechanisms may be related to the down-regulation of phosphorylated ERK1/2 in MAPK signal pathway and phosphorylated AKT in AKT signal pathway. Tamoxifen 113-116 mitogen-activated protein kinase 3 Homo sapiens 66-70 23086641-10 2012 In MCF-7/TAM-R cells,the expression of phosphorylation of AKT and MAPK44/42 protein was not changed in Evn-50 or TAM alone group,but significantly inhibited in the combination group at 72 h. CONCLUSION: Evn-50 can inhibit cell growth and induce apoptosis in MCF-7 and MCF-7/TAM-R cells,it can reverse tamoxifen-resistance of MCF-7/TAM-R cells.The mechanisms may be related to the down-regulation of phosphorylated ERK1/2 in MAPK signal pathway and phosphorylated AKT in AKT signal pathway. Tamoxifen 301-310 mitogen-activated protein kinase 3 Homo sapiens 66-70 21256460-8 2011 Tamoxifen inhibited collagen-stimulated platelet activation accompanied by relative Ca(+2) mobilization, thromboxane A(2) (TxA(2)) formation, and phospholipase C (PLC)gamma2, protein kinase C (PKC), and mitogen-activated protein kinase (MAPK) phosphorylation (ie, p38 MAPK and extracellular signal-regulated kinase 1/2), but not hydroxyl radical (OH( )) formation. Tamoxifen 0-9 mitogen-activated protein kinase 3 Homo sapiens 237-241 22427054-1 2012 This study was designed to investigate the role of protein kinase C (PKC) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in tamoxifen (TAM)-induced apoptosis and drug resistance in human breast cancer cells. Tamoxifen 142-151 mitogen-activated protein kinase 3 Homo sapiens 121-127 22427054-1 2012 This study was designed to investigate the role of protein kinase C (PKC) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in tamoxifen (TAM)-induced apoptosis and drug resistance in human breast cancer cells. Tamoxifen 153-156 mitogen-activated protein kinase 3 Homo sapiens 121-127 22279179-6 2012 Furthermore, activation of p38 MAPK up-regulated the initial IL-12 production and the activation of ERK1/2 in tandem with GSH, found responsible for IFN-gamma production by TAMs. Tamoxifen 173-177 mitogen-activated protein kinase 3 Homo sapiens 100-106 21720253-1 2011 OBJECTIVE: The objectives of the study were to evaluate the role of mitogen-activated protein kinase (MAPK) signaling in normal, hyperplastic, and neoplastic endometrium in relation to estrogen receptor (ER) status and to investigate whether 17beta-estradiol (E2) and tamoxifen (TAM) mediate the proliferation and apoptosis of endometrial cancer cells through the MAPK pathway. Tamoxifen 268-277 mitogen-activated protein kinase 3 Homo sapiens 102-106 21175263-10 2011 ERK1/2 and AKT were activated during TAM-induced apoptosis. Tamoxifen 37-40 mitogen-activated protein kinase 3 Homo sapiens 0-6 21175263-11 2011 The ERK1/2 inhibitor PD98059, the PI3K/Akt inhibitor LY294002, and the c-Src inhibitor PP2 all enhanced TAM action. Tamoxifen 104-107 mitogen-activated protein kinase 3 Homo sapiens 4-10 21256460-8 2011 Tamoxifen inhibited collagen-stimulated platelet activation accompanied by relative Ca(+2) mobilization, thromboxane A(2) (TxA(2)) formation, and phospholipase C (PLC)gamma2, protein kinase C (PKC), and mitogen-activated protein kinase (MAPK) phosphorylation (ie, p38 MAPK and extracellular signal-regulated kinase 1/2), but not hydroxyl radical (OH( )) formation. Tamoxifen 0-9 mitogen-activated protein kinase 3 Homo sapiens 277-318 21256460-11 2011 In conclusion, this study demonstrates for the first time that tamoxifen possesses potent antiplatelet activity, the mechanism of which may be involved in the inhibition of the PLCgamma2-PKC-p38 MAPK-TxA(2) cascade, thereby leading to the inhibition of platelet activation. Tamoxifen 63-72 mitogen-activated protein kinase 3 Homo sapiens 195-199