PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31377057-0 2019 Inhibition of the ERK1/2-mTORC1 axis ameliorates proteinuria and the fibrogenic action of transforming growth factor-beta in Adriamycin-induced glomerulosclerosis. Doxorubicin 125-135 mitogen-activated protein kinase 3 Mus musculus 18-24 31958563-4 2020 Moreover, the adriamycin-induced enhancement of phosphor-p65, phosphor-p38, phosphor-ERK1/2 and phosphor-JNK in the kidney of AKI mice were significantly suppressed by LJP61A. Doxorubicin 14-24 mitogen-activated protein kinase 3 Mus musculus 85-91 15833803-10 2005 However, levels of phosphorylated erbB2, Akt, and ERK-1/2 were significantly decreased in NRG-1(+/-)-Dox compared with WT-Dox mice. Doxorubicin 101-104 mitogen-activated protein kinase 3 Mus musculus 50-57 14557375-10 2003 Wild-type mouse embryo fibroblasts (MEFs) treated with doxorubicin showed increased phospho-p44/42-MAPK levels, but MEFs from MKP-1 heterozygous and homozygous knockout mice had blunted p44/42 activation. Doxorubicin 55-66 mitogen-activated protein kinase 3 Mus musculus 92-95 14557375-10 2003 Wild-type mouse embryo fibroblasts (MEFs) treated with doxorubicin showed increased phospho-p44/42-MAPK levels, but MEFs from MKP-1 heterozygous and homozygous knockout mice had blunted p44/42 activation. Doxorubicin 55-66 mitogen-activated protein kinase 3 Mus musculus 186-189 31377057-3 2019 Adriamycin administration elicited early activation of TGF-beta-ERK1/2-mTORC1 in podocytes, which persisted at later stages of albuminuria and glomerulosclerosis. Doxorubicin 0-10 mitogen-activated protein kinase 3 Mus musculus 64-70 31611788-0 2019 DiOHF Protects Against Doxorubicin-Induced Cardiotoxicity Through ERK1 Signaling Pathway. Doxorubicin 23-34 mitogen-activated protein kinase 3 Mus musculus 66-70 31611788-7 2019 The DOX-induced cardiotoxicity was accompanied by ERK1/2 activation and abolished by the silence of ERK1, rather than ERK2. Doxorubicin 4-7 mitogen-activated protein kinase 3 Mus musculus 50-56 31611788-7 2019 The DOX-induced cardiotoxicity was accompanied by ERK1/2 activation and abolished by the silence of ERK1, rather than ERK2. Doxorubicin 4-7 mitogen-activated protein kinase 3 Mus musculus 50-54 31611788-10 2019 Conclusion: DiOHF suppresses and reverses the DOX-induced cardiotoxicity by inhibiting ROS release, stabilizing mitochondrial function and reducing apoptosis through activation of the ERK1 signaling. Doxorubicin 46-49 mitogen-activated protein kinase 3 Mus musculus 184-188 30734460-7 2019 In addition, DOX downregulated survival proteins (p-Akt, Bcl-2) with concomitant upregulation in Erk (1/2), Bax and cleaved caspase-3 expressions. Doxorubicin 13-16 mitogen-activated protein kinase 3 Mus musculus 97-105 27323684-8 2016 Mechanistically, CHIP directly promotes ubiquitin-mediated degradation of p53 and SHP-1, which results in activation of ERK1/2 and STAT3 pathways thereby ameliorating DOX-induced cardiac toxicity. Doxorubicin 167-170 mitogen-activated protein kinase 3 Mus musculus 120-126 24024564-7 2013 TFD plus doxorubicin treatment further upregulated cardiac expression of NF-kappaB p65, p-p38, and p-ERK1/2 (P < 0.05). Doxorubicin 9-20 mitogen-activated protein kinase 3 Mus musculus 101-107 26980746-4 2016 By reducing the metabolic flux through the mevalonate pathway, NZ lowered the activity of Ras/ERK1/2/HIF-1alpha axis and the expression of P-glycoprotein, decreased the glycolysis and the mitochondrial respiratory chain, induced a cytochrome c/caspase 9/caspase 3-dependent apoptosis, thus restoring the direct cytotoxic effects of doxorubicin on tumor cell. Doxorubicin 332-343 mitogen-activated protein kinase 3 Mus musculus 94-100 24326424-9 2014 Doxorubicin induced fibrosis (accumulated collagen deposition and increased CTGF), activated apoptosis (increased TUNEL index, apoptotic DNA fragmentation, and caspase-3 activity and decreased Bcl-2/Bax ratio), and suppressed phosphorylation status of prosurvival signals (ERK1/2 and Akt) in ventricular muscles. Doxorubicin 0-11 mitogen-activated protein kinase 3 Mus musculus 273-279 23322372-10 2013 Doxorubicin treatment also up-regulated cardiac expression of p-p38, p-ERK 1/2 and p-JNK, and ellagic acid at 0.5 and 1% suppressed p-p38 expression and at 1% down-regulated p-ERK 1/2 expression. Doxorubicin 0-11 mitogen-activated protein kinase 3 Mus musculus 71-78 23322372-10 2013 Doxorubicin treatment also up-regulated cardiac expression of p-p38, p-ERK 1/2 and p-JNK, and ellagic acid at 0.5 and 1% suppressed p-p38 expression and at 1% down-regulated p-ERK 1/2 expression. Doxorubicin 0-11 mitogen-activated protein kinase 3 Mus musculus 176-183 18256352-6 2008 In vitro, incubation of RAGE-expressing murine podocytes with adriamycin stimulated AGE formation, and treatment with RAGE ligands rapidly activated nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, via p44/p42 MAP kinase signaling, and upregulated pro-fibrotic growth factors. Doxorubicin 62-72 mitogen-activated protein kinase 3 Mus musculus 214-217 21738612-10 2011 Nrdp1 may be a key mediator in the development of cardiac dysfunction after DOX treatment and associated with inhibition of Akt, ERK1/2 and STAT3. Doxorubicin 76-79 mitogen-activated protein kinase 3 Mus musculus 129-135 21508279-11 2011 Doxorubicin treatment increased the expression of Bcl-2, an anti-apoptotic protein, but this upregulation was blocked by combined treatment with PD98059, suggesting a role for ERK1/2 in conferring drug resistance. Doxorubicin 0-11 mitogen-activated protein kinase 3 Mus musculus 176-182 21508279-15 2011 CONCLUSIONS: Inhibiting ERK1/2 signaling resulted in osteosarcoma cell death by upregulating pro-apoptotic genes and inhibiting the Bcl-2-mediated resistance to doxorubicin. Doxorubicin 161-172 mitogen-activated protein kinase 3 Mus musculus 24-30 16905201-7 2006 Taken together, our results clearly suggest that the differential regulation of the PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways are crucial in the context of DNA-damaging drug-induced apoptosis, and this has compelled us to propose that the sustained activation of ERK1/2 pathway may be generally involved in the apoptosis induced by anticancer DNA-damaging drugs, including doxorubicin and etoposide. Doxorubicin 381-392 mitogen-activated protein kinase 3 Mus musculus 94-100 17974986-9 2007 In vitro investigations confirmed the regulation of endothelin-1 by doxorubicin and indicated that the doxorubicin-mediated increase of endothelin-1 expression involves epidermal growth factor receptor signaling via the MEK1/2-ERK1/2 cascade, which was further confirmed by immunoblotting studies in the left ventricle of treated animals. Doxorubicin 103-114 mitogen-activated protein kinase 3 Mus musculus 227-233 16905201-7 2006 Taken together, our results clearly suggest that the differential regulation of the PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways are crucial in the context of DNA-damaging drug-induced apoptosis, and this has compelled us to propose that the sustained activation of ERK1/2 pathway may be generally involved in the apoptosis induced by anticancer DNA-damaging drugs, including doxorubicin and etoposide. Doxorubicin 381-392 mitogen-activated protein kinase 3 Mus musculus 271-277