PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24356899-6 2014 Moreover, after EGCG treatment, TrkA signaling was activated by increasing the phosphorylation of TrkA following the increased phosphorylation of c-Raf, ERK1/2, and cAMP response element-binding protein (CREB), simultaneously the p75NTR signaling was significantly inhibited by decreasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression, so that the Abeta deposits and neuronal apoptosis in the hippocampus were inhibited. epigallocatechin gallate 16-20 mitogen-activated protein kinase 3 Mus musculus 153-159 19838780-3 2010 EGCG inhibited the production of TNF-alpha and MIP-2, and attenuated phosphorylation levels of ERK1/2 and JNK, but not p38 in RAW264.7 cells stimulated with LPS. epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 95-101 19838780-4 2010 Also, EGCG attenuated the production of TNF-alpha and MIP-2, and the phosphorylation of ERK1/2 and JNK in the lungs of mice administered with LPS intratracheally. epigallocatechin gallate 6-10 mitogen-activated protein kinase 3 Mus musculus 88-94 19838780-6 2010 Our results showed that EGCG attenuated LPS-induced lung injury by suppression of the MIP-2 and TNF-alpha production, and ERK1/2 and JNK activation in macrophage stimulated with LPS. epigallocatechin gallate 24-28 mitogen-activated protein kinase 3 Mus musculus 122-128 22570747-7 2012 LPS-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by EGCG. epigallocatechin gallate 69-73 mitogen-activated protein kinase 3 Mus musculus 31-37 22253518-6 2012 The nude mouse xenograft assay showed that EGCG and the combinations of curcumin, EGCG and lovastatin suppressed esophageal cancer cell growth and reduced the expression of Ki67, phosphorylated Erk1/2 and COX-2. epigallocatechin gallate 43-47 mitogen-activated protein kinase 3 Mus musculus 194-200 22253518-6 2012 The nude mouse xenograft assay showed that EGCG and the combinations of curcumin, EGCG and lovastatin suppressed esophageal cancer cell growth and reduced the expression of Ki67, phosphorylated Erk1/2 and COX-2. epigallocatechin gallate 82-86 mitogen-activated protein kinase 3 Mus musculus 194-200 22253518-10 2012 CONCLUSION: The combinations of curcumin, EGCG and lovastatin were able to suppress esophageal cancer cell growth in vitro and in nude mouse xenografts, these drugs also inhibited phosphorylated Erk1/2, c-Jun and COX-2 expression. epigallocatechin gallate 42-46 mitogen-activated protein kinase 3 Mus musculus 195-201 17569628-7 2007 Furthermore, the activities of Ras, Raf-1 and ERK1/2 were inhibited, whereas the activities of MEKK1, JNK1/2 and p38 MAP kinases were induced by EGCG. epigallocatechin gallate 145-149 mitogen-activated protein kinase 3 Mus musculus 46-52 18500674-5 2008 EGCG attenuated the FGF-2-induced phosphorylation of p44/p42 MAP kinase and p38 MAP kinase. epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 53-56 18500674-6 2008 These results strongly suggest that EGCG inhibits the FGF-2-stimulated synthesis of IL-6 at least partly via suppression of the p44/p42 MAP kinase pathway and the p38 MAP kinase pathway in osteoblasts. epigallocatechin gallate 36-40 mitogen-activated protein kinase 3 Mus musculus 128-131 17705241-9 2007 In the VP, EGCG significantly reduced cell proliferation, induced apoptosis, and decreased androgen receptor (AR), insulin-like growth factor-1 (IGF-1), IGF-1 receptor (IGF-1R), phospho-extracellular signal-regulated kinases 1 and 2 (phospho-ERKs 1 and 2), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). epigallocatechin gallate 11-15 mitogen-activated protein kinase 3 Mus musculus 186-232 17705241-9 2007 In the VP, EGCG significantly reduced cell proliferation, induced apoptosis, and decreased androgen receptor (AR), insulin-like growth factor-1 (IGF-1), IGF-1 receptor (IGF-1R), phospho-extracellular signal-regulated kinases 1 and 2 (phospho-ERKs 1 and 2), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). epigallocatechin gallate 11-15 mitogen-activated protein kinase 3 Mus musculus 242-254 17949962-0 2007 (-)-epigallocatechin gallate inhibits prostaglandin D2-stimulated HSP27 induction via suppression of the p44/p42 MAP kinase pathway in osteoblasts. epigallocatechin gallate 0-28 mitogen-activated protein kinase 3 Mus musculus 105-108 17949962-5 2007 On the contrary, EGCG markedly suppressed the PGD2-induced phosphorylation of p44/p42 MAP kinase and MEK1/2. epigallocatechin gallate 17-21 mitogen-activated protein kinase 3 Mus musculus 78-81 15340218-7 2004 EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 84-88 17350626-0 2007 (-)-Epigallocatechin gallate suppresses endothelin-1-induced interleukin-6 synthesis in osteoblasts: inhibition of p44/p42 MAP kinase activation. epigallocatechin gallate 0-28 mitogen-activated protein kinase 3 Mus musculus 115-118 17350626-6 2007 On the other hand, EGCG suppressed the phosphorylation of p44/p42 MAP kinase induced by ET-1. epigallocatechin gallate 19-23 mitogen-activated protein kinase 3 Mus musculus 58-61 17350626-7 2007 Both the IL-6 synthesis and the phosphorylation of p44/p42 MAP kinase stimulated by 12-O-tetradecanoylphorbol 13-acetate (TPA), a direct activator of PKC, were markedly suppressed by EGCG. epigallocatechin gallate 183-187 mitogen-activated protein kinase 3 Mus musculus 51-54 17350626-9 2007 These results strongly suggest that EGCG inhibits ET-1-stimulated synthesis of IL-6 via suppression of p44/p42 MAP kinase pathway in osteoblasts, and the inhibitory effect is exerted at a point between PKC and Raf-1 in the ET-1 signaling cascade. epigallocatechin gallate 36-40 mitogen-activated protein kinase 3 Mus musculus 103-106 16288056-7 2005 administration of EGCG resulted in increased levels of E-cadherin and decreased levels of nuclear beta-catenin, c-Myc, phospho-Akt, and phospho-extracellular signal-regulated kinase 1/2 (ERK1/2) in small intestinal tumors. epigallocatechin gallate 18-22 mitogen-activated protein kinase 3 Mus musculus 187-193 15340218-9 2004 These results suggest that gallate-containing catechins, particularly EGCG, inhibits LPS-induced IL-12p40 production in murine macrophages by inhibiting p38 MAPK while enhancing p44/p42 ERK, leading to the inhibition of IkappaBalpha degradation and NF-kappaB activation. epigallocatechin gallate 70-74 mitogen-activated protein kinase 3 Mus musculus 178-181 15340218-7 2004 EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 180-183 15340218-7 2004 EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 225-228 15340218-7 2004 EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). epigallocatechin gallate 134-138 mitogen-activated protein kinase 3 Mus musculus 180-183 15340218-7 2004 EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). epigallocatechin gallate 134-138 mitogen-activated protein kinase 3 Mus musculus 225-228 14672711-5 2004 EGCG-pretreated DC inhibited LPS-induced MAPKs, such as ERK1/2, p38, JNK, and NF-kappaB p65 translocation. epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 56-62 34740634-0 2021 EGCG protects against myocardial I/RI by regulating lncRNA Gm4419-mediated epigenetic silencing of the DUSP5/ERK1/2 axis. epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 109-115 12771038-5 2003 Further, to delineate the inhibition of UVB-induced oxidative stress with cell signaling pathways, treatment of EGCG to mouse skin resulted in marked inhibition of a single UVB irradiation-induced phosphorylation of ERK1/2 (16-95%), JNK (46-100%) and p38 (100%) proteins of MAPK family in a time-dependent manner. epigallocatechin gallate 112-116 mitogen-activated protein kinase 3 Mus musculus 216-222 34740634-12 2021 CONCLUSIONS: In conclusion, our findings demonstrated that EGCG protected against myocardial I/RI by modulating Gm4419/DUSP5/ERK1/2-mediated autophagy. epigallocatechin gallate 59-63 mitogen-activated protein kinase 3 Mus musculus 125-131 35287352-15 2022 The anti-inflammatory and anti-apoptotic effects of EGCG occur not only through direct binding to six target proteins (IL-6,TNF-alpha, Caspase3, MAPK3, AKT1, and VEGFA) but also by reducing their expression. epigallocatechin gallate 52-56 mitogen-activated protein kinase 3 Mus musculus 145-150 35287352-11 2022 Molecular docking results suggest that EGCG has a high affinity for the crystal structure of six targets (IL-6 (interleukin-6), TNF (tumor necrosis factor), Caspase3, MAPK3 (Mitogen-activated protein kinase 3), AKT1, and VEGFA (vascular endothelial growth factor)), and the experimental verification result showed levated expression of these 6 hub targets in the LPS group, but there is an obvious decrease in expression in the LPS + EGCG group. epigallocatechin gallate 39-43 mitogen-activated protein kinase 3 Mus musculus 167-172 35287352-11 2022 Molecular docking results suggest that EGCG has a high affinity for the crystal structure of six targets (IL-6 (interleukin-6), TNF (tumor necrosis factor), Caspase3, MAPK3 (Mitogen-activated protein kinase 3), AKT1, and VEGFA (vascular endothelial growth factor)), and the experimental verification result showed levated expression of these 6 hub targets in the LPS group, but there is an obvious decrease in expression in the LPS + EGCG group. epigallocatechin gallate 39-43 mitogen-activated protein kinase 3 Mus musculus 174-208 35243817-10 2022 In addition, EGCG-induced apoptosis suppressed the expression of the phosphorylation protein kinase B and extracellular signal-regulated kinase 1/2 signaling proteins in tumors from xenografted mice. epigallocatechin gallate 13-17 mitogen-activated protein kinase 3 Mus musculus 106-147 27180749-10 2016 CONCLUSION: EGCG protects the kidney in diabetic db/db mice via anti-oxidative stress pathway, as well as inhibiting Erk1/2-P38MAPK pathway and improving PI3K-AKT signaling transduction pathway. epigallocatechin gallate 12-16 mitogen-activated protein kinase 3 Mus musculus 117-123 28849144-7 2017 EGCG by itself markedly induced the phosphorylation of p44/p42 MAP kinase for up to 10 min and the status decreased subsequently, whereas EGCG did not significantly affect the phosphorylation status of p38 MAPK or SAPK/JNK within 60 min. epigallocatechin gallate 0-4 mitogen-activated protein kinase 3 Mus musculus 55-58