PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24116164-8 2013 In conclusion, UII increased ROS production by NADPH oxidase, leading to the inhibition of signaling pathways involving glucose transport, such as AKT/PKC/ERK. Glucose 120-127 mitogen-activated protein kinase 1 Mus musculus 155-158 23942551-10 2013 These data indicate a role for Src in a high glucose-Src-TACE-heparin-binding epidermal growth factor-EGFR-MAPK-signaling pathway to collagen accumulation. Glucose 45-52 mitogen-activated protein kinase 1 Mus musculus 107-111 23530005-0 2013 Extracellular signal-regulated kinase in the ventromedial hypothalamus mediates leptin-induced glucose uptake in red-type skeletal muscle. Glucose 95-102 mitogen-activated protein kinase 1 Mus musculus 0-37 23954796-3 2013 High glucose/fatty acid toxicity, inflammation, and oxidative stress, all of which are associated with insulin resistance, can activate ERK. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 136-139 23530005-4 2013 Given that leptin requires 6 h to increase muscle glucose uptake, the transient activation of the MEK-ERK pathway in the VMH by leptin may play a role in the induction of synaptic plasticity in the VMH, resulting in the enhancement of MCR signaling in the nucleus and leading to an increase in insulin sensitivity in red-type muscle. Glucose 50-57 mitogen-activated protein kinase 1 Mus musculus 102-105 23530005-2 2013 We now show that signaling by extracellular signal-regulated kinase (ERK) and its upstream kinase MEK in the ventromedial hypothalamus (VMH) mediates the leptin-induced increase in glucose utilization as well as its insulin sensitivity in the whole body and in red-type skeletal muscle of mice through activation of the melanocortin receptor (MCR) in the VMH. Glucose 181-188 mitogen-activated protein kinase 1 Mus musculus 30-67 23530005-2 2013 We now show that signaling by extracellular signal-regulated kinase (ERK) and its upstream kinase MEK in the ventromedial hypothalamus (VMH) mediates the leptin-induced increase in glucose utilization as well as its insulin sensitivity in the whole body and in red-type skeletal muscle of mice through activation of the melanocortin receptor (MCR) in the VMH. Glucose 181-188 mitogen-activated protein kinase 1 Mus musculus 69-72 21678423-8 2012 In an in vitro culture system, high glucose and insulin significantly altered TNF-alpha, IL-6, and NO production and arginase activity of macrophages, which was reversed by the treatment with AKT and ERK inhibitors. Glucose 36-43 mitogen-activated protein kinase 1 Mus musculus 200-203 23531619-10 2013 Elevated SHP-1 expression induced by high glucose levels was directly associated with insulin receptor-beta in vitro and in vivo to prevent insulin-stimulated Akt and ERK phosphorylation. Glucose 42-49 mitogen-activated protein kinase 1 Mus musculus 167-170 23936866-11 2013 Both ERK/MAPK and TGF- beta /smad signaling pathways seem to play a role in the development of kidney fibrosis accelerated by blood glucose fluctuation. Glucose 132-139 mitogen-activated protein kinase 1 Mus musculus 5-8 23349910-9 2013 MMC stimulated with 30 mM D-glucose showed increased PKC and ERK mediated fibronectin and collagen type III synthesis. Glucose 26-35 mitogen-activated protein kinase 1 Mus musculus 61-64 23349910-11 2013 Sulodexide showed a dose-dependent inhibition of 30 mM D-glucose-induced PKC-betaII and ERK phosphorylation, but had no effect on PKC-alpha or PKC-betaI phosphorylation. Glucose 55-64 mitogen-activated protein kinase 1 Mus musculus 88-91 23379999-14 2013 The exposure of RGC-5 cells to high glucose activated ERK1/2 and JNK MAPK signaling blocking by GPR91 shRNA (P < 0.01). Glucose 36-43 mitogen-activated protein kinase 1 Mus musculus 69-73 23379999-15 2013 These results indicate that GPR91 modulates the high glucose-induced VEGF release of RGC-5 cells, possibly by inhibiting ERK1/2 and JNK MAPK signaling. Glucose 53-60 mitogen-activated protein kinase 1 Mus musculus 136-140 23123403-6 2012 In culture, 1,25-dihydroxyvitamin D suppressed high-glucose-induced apoptosis of podocytes by blocking p38- and ERK-mediated proapoptotic pathways. Glucose 52-59 mitogen-activated protein kinase 1 Mus musculus 112-115 22133746-4 2012 Application of the synthetic inhibitors of protein kinases revealed the involvement of Ca(2+)/calmodulin-dependent protein kinase (CaMK) II and extracellular signal-regulated protein kinase (ERK) in glucose- and thapsigargin-induced CSE expression. Glucose 199-206 mitogen-activated protein kinase 1 Mus musculus 144-189 22133746-4 2012 Application of the synthetic inhibitors of protein kinases revealed the involvement of Ca(2+)/calmodulin-dependent protein kinase (CaMK) II and extracellular signal-regulated protein kinase (ERK) in glucose- and thapsigargin-induced CSE expression. Glucose 199-206 mitogen-activated protein kinase 1 Mus musculus 191-194 21998735-5 2011 Chronic (48 h, 0.4 mM) palmitate treatment blunted glucose/AA-induced activation of CaMKII and ERK and caused a concomitant reduction (~75%) in GSIS/AASIS and autocrine-dependent activation of PKB. Glucose 51-58 mitogen-activated protein kinase 1 Mus musculus 95-98 21567393-3 2012 Using isolated retinal endothelial cells, the effect of regulation of H-Ras downstream signaling cascade, Raf-1, MEK, and ERK, was investigated on glucose-induced activation of MMP9. Glucose 147-154 mitogen-activated protein kinase 1 Mus musculus 122-125 21567393-5 2012 Regulation of Raf-1/MEK/ERK by their specific siRNAs and pharmacologic inhibitors prevented glucose-induced activation of MMP9 in retinal endothelial cells. Glucose 92-99 mitogen-activated protein kinase 1 Mus musculus 24-27 20929976-8 2011 In sharp contrast, in glucose-fed ob/ob mice, the Gck recruitment patterns of active MEK/Erk, IR, and Pol II were asynchronous. Glucose 22-29 mitogen-activated protein kinase 1 Mus musculus 89-92 21270272-10 2011 CONCLUSIONS: ERK-mediated suppression of Nrf2 activity leads to the oxidative stress-induced insulin resistance in adult cardiomyocytes and downregulated glucose utilization in the diabetic heart. Glucose 154-161 mitogen-activated protein kinase 1 Mus musculus 13-16 19887597-1 2010 Activators of 5"-AMP-activated protein kinase (AMPK) 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), metformin, and exercise activate atypical protein kinase C (aPKC) and ERK and stimulate glucose transport in muscle by uncertain mechanisms. Glucose 205-212 mitogen-activated protein kinase 1 Mus musculus 187-190 21085672-5 2010 We therefore investigated the role of mitogen-activated protein kinase (MAPK) signaling in the regulation of mouse T cell glucose metabolism. Glucose 122-129 mitogen-activated protein kinase 1 Mus musculus 72-76 21085672-6 2010 T cell stimulation strongly induces glucose uptake and glycolysis, both of which are severely impaired by inhibition of extracellular signal-regulated kinase (ERK), whereas p38 inhibition had a much smaller effect. Glucose 36-43 mitogen-activated protein kinase 1 Mus musculus 120-157 21085672-6 2010 T cell stimulation strongly induces glucose uptake and glycolysis, both of which are severely impaired by inhibition of extracellular signal-regulated kinase (ERK), whereas p38 inhibition had a much smaller effect. Glucose 36-43 mitogen-activated protein kinase 1 Mus musculus 159-162 21085672-8 2010 Thus, the ERK signaling pathway cooperates with PI3K to induce glucose utilization in activated T cells, with hexokinase serving as a potential point for coordinated regulation. Glucose 63-70 mitogen-activated protein kinase 1 Mus musculus 10-13 19887597-0 2010 AICAR and metformin, but not exercise, increase muscle glucose transport through AMPK-, ERK-, and PDK1-dependent activation of atypical PKC. Glucose 55-62 mitogen-activated protein kinase 1 Mus musculus 88-91 20056832-9 2010 Autocrine insulin signaling partly accounted for the effects of glucose on ERK phosphorylation. Glucose 64-71 mitogen-activated protein kinase 1 Mus musculus 75-78 19907708-8 2009 Furthermore, when applied to mouse models of insulin-deficient diabetes, both type 1 and type 2, hepatic activation of ERK signaling increased pancreatic beta cell mass and normalized blood glucose. Glucose 190-197 mitogen-activated protein kinase 1 Mus musculus 119-122 18701453-5 2008 Incubation with selective kinase inhibitors showed that high glucose- and high insulin-induced laminin beta1 synthesis and phosphorylation of GSK3beta were dependent on PI 3-kinase, Erk, and mTOR. Glucose 61-68 mitogen-activated protein kinase 1 Mus musculus 182-185 19500499-9 2009 CONCLUSION: Losartan can inhibit high glucose-induced CTGF expression in mouse mesangial cells, and the mechanisms maybe involve the interruption of ERK1/2 MAPK pathway. Glucose 38-45 mitogen-activated protein kinase 1 Mus musculus 156-160 18783846-6 2009 Moreover, diacylgycerol-dependent protein kinase C isoenzymes and activation of extracellular signal-regulated protein kinase (ERK) are required for glucose-, tolbutamide- and KCl-induced Egr-1 expression. Glucose 149-156 mitogen-activated protein kinase 1 Mus musculus 80-125 18783846-6 2009 Moreover, diacylgycerol-dependent protein kinase C isoenzymes and activation of extracellular signal-regulated protein kinase (ERK) are required for glucose-, tolbutamide- and KCl-induced Egr-1 expression. Glucose 149-156 mitogen-activated protein kinase 1 Mus musculus 127-130 19500499-0 2009 [Losartan inhibits high glucose-induced CTGF expression via ERK1/2 MAPK pathways in mouse mesangial cells]. Glucose 24-31 mitogen-activated protein kinase 1 Mus musculus 67-71 19500499-7 2009 The protein expression of phosphor-ERK1/2 and CTGF were increased in high glucose group comparing with low glucose group(P<0.01), and reduced in losartan group and ERK inhibitors group comparing with high glucose group(P<0.05). Glucose 74-81 mitogen-activated protein kinase 1 Mus musculus 35-38 19500499-7 2009 The protein expression of phosphor-ERK1/2 and CTGF were increased in high glucose group comparing with low glucose group(P<0.01), and reduced in losartan group and ERK inhibitors group comparing with high glucose group(P<0.05). Glucose 107-114 mitogen-activated protein kinase 1 Mus musculus 35-38 19500499-7 2009 The protein expression of phosphor-ERK1/2 and CTGF were increased in high glucose group comparing with low glucose group(P<0.01), and reduced in losartan group and ERK inhibitors group comparing with high glucose group(P<0.05). Glucose 107-114 mitogen-activated protein kinase 1 Mus musculus 35-38 18701453-6 2008 High glucose and high insulin augmented activation of Akt, Erk, and p70S6 kinase. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 59-62 11095645-8 2000 Overexpression of MAPK phosphatase CL 100 prevented TGF-beta1 promoter activation by high glucose, confirming the involvement of the MEK-ERK pathway in response to high glucose. Glucose 90-97 mitogen-activated protein kinase 1 Mus musculus 18-22 18310510-0 2008 Resveratrol inhibits high glucose-induced PI3K/Akt/ERK-dependent interleukin-17 expression in primary mouse cardiac fibroblasts. Glucose 26-33 mitogen-activated protein kinase 1 Mus musculus 51-54 17440593-4 2007 The activation of MAPKS signaling pathway (ERK, p38 and JNK) by high glucose was also examined. Glucose 69-76 mitogen-activated protein kinase 1 Mus musculus 43-46 15498890-5 2005 Blocking activation of ERK1/2 using MEK1/2, the MAPK kinase inhibitor PD98059 or using small interfering RNA-mediated silencing of ERK1 and ERK2 expressions resulted in partial inhibition of glucose-induced insulin release, indicating that ERK1/2 pathway participates also in the regulation of insulin secretion. Glucose 191-198 mitogen-activated protein kinase 1 Mus musculus 140-144 12364324-2 2002 In this report, we show that treatment of the mouse pancreatic beta-cell line MIN6 with GLP1 leads to the glucose-dependent activation of Erk. Glucose 106-113 mitogen-activated protein kinase 1 Mus musculus 138-141 12364324-7 2002 In conclusion, our results indicate that, in the presence of stimulatory concentrations of glucose, GLP1 stimulates the activation of Erk through a mechanism dependent on MEK but independent of both Raf and Ras. Glucose 91-98 mitogen-activated protein kinase 1 Mus musculus 134-137 11095645-2 2000 Extracellular signal-regulated kinase (ERK), a member of the mitogen-activated protein kinase (MAPK) cascade, is activated in mesangial cells cultured in high glucose and in glomeruli of diabetic rats. Glucose 159-166 mitogen-activated protein kinase 1 Mus musculus 95-99 17198096-3 2007 In this study, we used Western blot analysis and propidium iodide stain to determine whether the activations of nPKCepsilon and ERKs were involved in oxygen-glucose deprivation (OGD)-induced neuroprotection via N-methyl-D-aspartate (NMDA) receptors. Glucose 157-164 mitogen-activated protein kinase 1 Mus musculus 128-132 16638805-10 2006 Taken together, these data demonstrate that F-actin reorganization prior to insulin secretion requires gelsolin and plays a role in the glucose-dependent MAPK signal transduction that regulates beta-cell insulin secretion. Glucose 136-143 mitogen-activated protein kinase 1 Mus musculus 154-158 11779150-0 2002 High glucose induced VEGF expression via PKC and ERK in glomerular podocytes. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 49-52 11779150-3 2002 High glucose induced up-regulation of VEGF mRNA and protein expression in podocytes via activation of PKC (PKC-alpha and -betaII isoforms) and ERK. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 107-146 11779150-7 2002 These observations suggested that high glucose-induced VEGF expression in podocytes was largely mediated through PKC and ERK pathways that may be involved in diabetic nephropathy. Glucose 39-46 mitogen-activated protein kinase 1 Mus musculus 121-124 11095645-8 2000 Overexpression of MAPK phosphatase CL 100 prevented TGF-beta1 promoter activation by high glucose, confirming the involvement of the MEK-ERK pathway in response to high glucose. Glucose 169-176 mitogen-activated protein kinase 1 Mus musculus 18-22 10229678-1 1999 Physiological concentrations of glucose that lead to Ca2+ entry and insulin secretion activate extracellular signal-regulated protein kinases (ERK1 and ERK2) in the MIN6 pancreatic beta-cell line. Glucose 32-39 mitogen-activated protein kinase 1 Mus musculus 152-156 10619403-0 1999 Leptin stimulates glucose uptake in C2C12 muscle cells by activation of ERK2. Glucose 18-25 mitogen-activated protein kinase 1 Mus musculus 72-76 10229678-6 1999 Thus the activation of ERKs in response to glucose depends on PKC and possibly on a tyrosine kinase/tyrosine phosphatase couple. Glucose 43-50 mitogen-activated protein kinase 1 Mus musculus 23-27 10229678-7 1999 To define the role of ERK activation by glucose we studied the regulation of transcription of the insulin gene. Glucose 40-47 mitogen-activated protein kinase 1 Mus musculus 22-25 10229678-8 1999 We found that this transcription is regulated in the MIN6 cells in the same range of glucose concentration as in primary islets, and that specific inhibition of mitogen-activated protein kinase kinase, the direct activator of ERK, impaired the response of the insulin gene to glucose. Glucose 85-92 mitogen-activated protein kinase 1 Mus musculus 226-229 10229678-8 1999 We found that this transcription is regulated in the MIN6 cells in the same range of glucose concentration as in primary islets, and that specific inhibition of mitogen-activated protein kinase kinase, the direct activator of ERK, impaired the response of the insulin gene to glucose. Glucose 276-283 mitogen-activated protein kinase 1 Mus musculus 226-229 34518608-9 2021 Ketamine treatment in depressive-like mice significantly increased the expression levels of p-ERK1/2 and GLUT3 in the prefrontal cortex (P < 0.01), whereas an ERK1/2 inhibitor significantly inhibited ketamine-induced increases (P < 0.01).Our present findings demonstrate that ketamine mitigated depressive-like behaviors in female mice by activating the ERK/GLUT3 signal pathway, which further increased glucose uptake in the prefrontal cortex. Glucose 404-411 mitogen-activated protein kinase 1 Mus musculus 354-357 9624138-2 1998 We report below that the response to glucose in the MIN6 cells includes an activation of the p42 and p44 mitogen-activated protein (MAP) kinases (ERK2 and ERK1). Glucose 37-44 mitogen-activated protein kinase 1 Mus musculus 146-150 34518608-0 2021 Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway. Glucose 74-81 mitogen-activated protein kinase 1 Mus musculus 106-109 35490780-5 2022 Mechanistically, the high glucose-induced phosphorylation of YB-1 at S102 is dependent on the upstream extracellular signal-regulated kinase (ERK)/Ras-mitogen-activated protein kinase (RSK) signaling pathway. Glucose 26-33 mitogen-activated protein kinase 1 Mus musculus 103-140 34341463-6 2021 Moreover, enhanced glucose uptake was observed in both preadipocytes and mature adipocytes, which is associated with upregulated phosphorylation of AKT and ERK but reduced p-JNK. Glucose 19-26 mitogen-activated protein kinase 1 Mus musculus 156-159 35490780-5 2022 Mechanistically, the high glucose-induced phosphorylation of YB-1 at S102 is dependent on the upstream extracellular signal-regulated kinase (ERK)/Ras-mitogen-activated protein kinase (RSK) signaling pathway. Glucose 26-33 mitogen-activated protein kinase 1 Mus musculus 142-145 29199516-6 2018 In conclusion, both ERK and Smad2 signal pathways are involved in the activation of macrophages induced by TGF-beta1 and high-ambient glucose, while there is no crosstalk shown in the process. Glucose 134-141 mitogen-activated protein kinase 1 Mus musculus 20-23 34015900-9 2021 MAPK-ERK inhibition strongly decreased the expression of insulin and S1P in glucose- or alloxan-treated RIN-5F cells. Glucose 76-83 mitogen-activated protein kinase 1 Mus musculus 5-8 29987888-11 2018 These results indicate that eucalyptol blocked glucose-induced AGE-RAGE axis and podocyte injury through disturbing RAGE-ERK-c-Myc signaling. Glucose 47-54 mitogen-activated protein kinase 1 Mus musculus 121-124 29018002-10 2018 These results indicate that glucose uptake by GLUT1 is required for RANKL and osteocalcin expressions in osteocytes, and that inhibition of glucose uptake decreases their expressions through AMPK, ERK1/2, and p38 MAPK pathways. Glucose 140-147 mitogen-activated protein kinase 1 Mus musculus 213-217 29160030-0 2018 Dihydromyricetin enhances glucose uptake by inhibition of MEK/ERK pathway and consequent down-regulation of phosphorylation of PPARgamma in 3T3-L1 cells. Glucose 26-33 mitogen-activated protein kinase 1 Mus musculus 62-65 29160030-11 2018 In conclusion, our findings indicate that DHM improves glucose uptake in adipocytes by inhibiting ERK-induced phosphorylation of PPARgamma at serine 273. Glucose 55-62 mitogen-activated protein kinase 1 Mus musculus 98-101 29199516-0 2018 The role of ERK and Smad2 signal pathways in the alternatively activated macrophages induced by TGF-beta1 and high-ambient glucose. Glucose 123-130 mitogen-activated protein kinase 1 Mus musculus 12-15 29199516-1 2018 Macrophages can be alternatively activated by TGF-beta1 and high-ambient glucose, in which the role of Smad2 and the crosstalk between ERK and Smad2 pathways are not fully understood. Glucose 73-80 mitogen-activated protein kinase 1 Mus musculus 135-138 33906910-0 2021 MEK/ERK Signaling in beta Cells Bifunctionally Regulates beta-cell Mass and Glucose-stimulated Insulin-secretion Response to Maintain Glucose Homeostasis. Glucose 76-83 mitogen-activated protein kinase 1 Mus musculus 4-7 33906910-3 2021 In mice with abrogation of ERK signaling in pancreatic beta cells through deletion of Mek1 and Mek2, glucose intolerance aggravates under high-fat diet-fed conditions due to insufficient insulin production with lower beta-cell proliferation and reduced beta-cell mass, while in individual beta cells dampening of the number of insulin exocytosis events is observed, with the molecules involved in insulin exocytosis being less phosphorylated. Glucose 101-108 mitogen-activated protein kinase 1 Mus musculus 27-30 33906910-4 2021 These data reveal bifunctional roles for MEK/ERK signaling in beta cells for glucose homeostasis, i.e., in regulating beta-cell mass as well as in controlling insulin exocytosis in individual beta cells, thus providing not only a novel perspective for the understanding of diabetes pathophysiology but also a potential clue for new drug development for diabetes treatment. Glucose 77-84 mitogen-activated protein kinase 1 Mus musculus 45-48 32861799-12 2020 Besides the inhibition of c-jun/JNK, MCP-1 expression can be attenuated by inhibiting stat1 and ERK under high glucose condition after LPS stimulation. Glucose 111-118 mitogen-activated protein kinase 1 Mus musculus 96-99 32450527-9 2020 Inhibition of ERK by inhibitor (U0126) significantly blocked high glucose-induced calcification, which further confirmed the significance of MAPKs. Glucose 66-73 mitogen-activated protein kinase 1 Mus musculus 14-17 32161481-0 2020 High Glucose Downregulates Connexin 43 Expression and Its Gap Junction and Hemichannel Function in Osteocyte-like MLO-Y4 Cells Through Activation of the p38MAPK/ERK Signal Pathway. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 161-164 32161481-14 2020 Conclusion: High glucose dampened Cx43 gap junction and hemichannel function in MLO-Y4 cells by activating the p38MAPK/ERK pathway leading to subsequent mCx43 internalization. Glucose 17-24 mitogen-activated protein kinase 1 Mus musculus 119-122 31646578-0 2019 The effect of SOX9 on islet beta cells in high glucose environment through regulation of ERK/P38 signaling pathway. Glucose 47-54 mitogen-activated protein kinase 1 Mus musculus 89-92 31646578-4 2019 RESULTS: Under high glucose environment, SOX9 mRNA and protein expression were significantly increased, MIN6 cell proliferation was inhibited, apoptosis rate and secretion of TNF-alpha and IL-2 were increased, along with decreased insulin secretion, increased MPO content, decreased SOD activity and phosphorylation of ERK/P38, compared with control group (p < 0.05). Glucose 20-27 mitogen-activated protein kinase 1 Mus musculus 319-322 30111835-9 2018 Further biochemical analysis indicated mutual regulation between GLUT1 and the MEK/ERK cascade to relay potential communication between glucose uptake and mechanical stress response. Glucose 136-143 mitogen-activated protein kinase 1 Mus musculus 83-86 29662125-5 2018 Exogenous netrin-1 promoted the corneal epithelial wound healing in diabetic mice, and facilitated the proliferation and migration by reactivating the phosphorylation of ERK and EGFR in high-glucose treated corneal epithelial cells. Glucose 191-198 mitogen-activated protein kinase 1 Mus musculus 170-173 29018002-10 2018 These results indicate that glucose uptake by GLUT1 is required for RANKL and osteocalcin expressions in osteocytes, and that inhibition of glucose uptake decreases their expressions through AMPK, ERK1/2, and p38 MAPK pathways. Glucose 28-35 mitogen-activated protein kinase 1 Mus musculus 213-217 29204135-3 2017 We tested the hypothesis that ucOC per se stimulates muscle glucose uptake via extracellular signal-regulated kinase (ERK), adenosine monophosphate-activated protein kinase (AMPK), and/or the mechanistic target of rapamycin complex 2 (mTORC2)-protein kinase B (AKT)-AKT substrate of 160 kDa (AS160) signaling cascade. Glucose 60-67 mitogen-activated protein kinase 1 Mus musculus 79-116 29204135-3 2017 We tested the hypothesis that ucOC per se stimulates muscle glucose uptake via extracellular signal-regulated kinase (ERK), adenosine monophosphate-activated protein kinase (AMPK), and/or the mechanistic target of rapamycin complex 2 (mTORC2)-protein kinase B (AKT)-AKT substrate of 160 kDa (AS160) signaling cascade. Glucose 60-67 mitogen-activated protein kinase 1 Mus musculus 118-121 28992163-9 2017 Our study hence suggests the existence of a novel signaling cascade Pak1/MEK/ERK/Oct-1 for both insulin and curcumin in exerting their glucose-lowering effect via promoting hepatic ChREBP production, supports the recognition of beneficial functions of ChREBP, and brings us a new overview on dietary polyphenols. Glucose 135-142 mitogen-activated protein kinase 1 Mus musculus 77-80 28900165-4 2017 ERK inhibition restores FoxO1, gluconeogenic enzyme expression and glucose production. Glucose 67-74 mitogen-activated protein kinase 1 Mus musculus 0-3 25203596-0 2015 Role of MAPK signal pathways in differentiation process of M2 macrophages induced by high-ambient glucose and TGF-beta1. Glucose 98-105 mitogen-activated protein kinase 1 Mus musculus 8-12 24885625-8 2014 CONCLUSIONS: These results suggest that high glucose concentrations might prime dendritic cells for apoptosis induced by LPS in the intestinal tract through upregulating the expression of Bax and downregulating the expression of AKT, ERK and Bcl-2. Glucose 45-52 mitogen-activated protein kinase 1 Mus musculus 234-237 29129692-5 2018 High glucose administration induced elevation of PRMT1 expression in podocytes, accompanied with higher phosphorylation of ERK and cleaved caspase-3. Glucose 5-12 mitogen-activated protein kinase 1 Mus musculus 123-126 28721437-8 2017 RESULTS: Glucose induced rapid subplasmalemmal recruitment of ERK1 and ERK2. Glucose 9-16 mitogen-activated protein kinase 1 Mus musculus 71-75 28721437-10 2017 By contrast, ERK1 was required for glucose-induced full activation of several targets involved in beta cell survival; MSK1 and CREB were less active in Erk1 -/- mouse beta cells (p < 0.01) compared with Erk1 +/+ mouse beta cells, and their phosphorylation could only be restored when ERK1 was re-expressed and not when ERK2 was overexpressed. Glucose 35-42 mitogen-activated protein kinase 1 Mus musculus 322-326 27498780-10 2016 CONCLUSION: Linagliptin and liraglutide inhibit glucose- and Ang II-induced collagen formation in cardiac fibroblasts via activation of the ERK/NF-kappaB/pathway. Glucose 48-55 mitogen-activated protein kinase 1 Mus musculus 140-143 26769850-3 2016 In the current study, we showed that ionizing radiation-induced activation of the MEK-ERK-DAPK-p53 signaling axis is required for anoikis (anchorage-dependent apoptosis) of non-small cell lung cancer (NSCLC) cells in normal glucose media. Glucose 224-231 mitogen-activated protein kinase 1 Mus musculus 86-89 24874579-7 2014 NAP treatment reduced the phosphorylation levels of ERK and AKT in cells grown in high glucose. Glucose 87-94 mitogen-activated protein kinase 1 Mus musculus 52-55