PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32936424-7 2021 A total of 33 upregulated and 52 downregulated genes associated with HCC progression and ferroptosis were obtained, and these genes were significantly involved in the negative regulation of ERK1 and ERK2 cascades; the NAD biosynthetic process; alanine, aspartate, and glutamate metabolism; and other pathways. Glutamic Acid 268-277 mitogen-activated protein kinase 1 Homo sapiens 199-203 32936424-12 2021 These genes played roles in HCC progression and ferroptosis via the negative regulation of the ERK1 and ERK2 cascades; the NAD biosynthetic process; and alanine, aspartate, and glutamate metabolism. Glutamic Acid 177-186 mitogen-activated protein kinase 1 Homo sapiens 104-108 32850814-6 2020 Subsequent immunoprecipitation analysis, including different MAPK1 mutants, revealed that VB1 directly interacted with the residues, glutamic acid 58 (E58) and arginine 65 (R65) of MAPK1, leading to the partial reversal of UVA-induced senescence in HEK293T cells. Glutamic Acid 133-146 mitogen-activated protein kinase 1 Homo sapiens 181-186 32708308-3 2020 Here, we report that these two bioactive tripeptides, phenylalanine-lysine-aspartic acid and phenylalanine-lysine-glutamic acid (FKD and FKE, respectively), inhibit ERK and cJun activation following human macrophage exposure to LPS. Glutamic Acid 114-127 mitogen-activated protein kinase 1 Homo sapiens 165-168 32407964-2 2020 During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted morphine-induced CTA and decreased plasma CORT levels; moreover, c-Fos and p-ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA. Glutamic Acid 43-52 mitogen-activated protein kinase 1 Homo sapiens 168-171 31018661-4 2019 This involves the transcriptional modulator CITED2 (Atypical chemokine receptor 3 CBP/p300-interacting transactivator with glutamic acid (E)/aspartic acid (D)-rich tail) and downstream activation of CXCL12 (chemokine [C-X-C motif] ligand-12) signaling through the CXCR7 (C-X-C chemokine receptor type 7) receptor and ERK1/2 (extracellular signal-regulated kinases 1/2). Glutamic Acid 123-136 mitogen-activated protein kinase 1 Homo sapiens 325-367 31073373-11 2019 Glioma cells were found to secrete glutamate in the extracellular space and to respond to receptor stimulation by activating downstream ERK. Glutamic Acid 35-44 mitogen-activated protein kinase 1 Homo sapiens 136-139 29466703-11 2018 Furthermore, we showed that sAPPalpha enhances ERK and CREB1 phosphorylation upon glutamate stimulation at DIV7, but not DIV4 or DIV14. Glutamic Acid 82-91 mitogen-activated protein kinase 1 Homo sapiens 47-50 29301251-5 2018 Transcriptional changes in activated microglia, mediated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NFkappaB) and extracellular signal-regulated kinase (ERK) signaling pathways, results in release of various pro-inflammatory mediators, including cytokines, chemokines, caspases and glutamate. Glutamic Acid 311-320 mitogen-activated protein kinase 1 Homo sapiens 143-180 29301251-5 2018 Transcriptional changes in activated microglia, mediated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NFkappaB) and extracellular signal-regulated kinase (ERK) signaling pathways, results in release of various pro-inflammatory mediators, including cytokines, chemokines, caspases and glutamate. Glutamic Acid 311-320 mitogen-activated protein kinase 1 Homo sapiens 182-185 28919534-0 2017 Glutamate-induced rapid induction of Arc/Arg3.1 requires NMDA receptor-mediated phosphorylation of ERK and CREB. Glutamic Acid 0-9 mitogen-activated protein kinase 1 Homo sapiens 99-102 28919534-9 2017 In addition, the phosphorylation of ERK and CREB, two downstream factors of NMDAR signaling, markedly increased after glutamate exposure. Glutamic Acid 118-127 mitogen-activated protein kinase 1 Homo sapiens 36-39 28919534-10 2017 Blocking ERK and CREB activation via selective inhibitors partially prevented the glutamate-induced elevation of Arc/Arg3.1 protein levels. Glutamic Acid 82-91 mitogen-activated protein kinase 1 Homo sapiens 9-12 27941812-5 2016 Moreover, glutamate-induced ERK activation stimulates the expression of HSP70 and VRK3 at the transcriptional level. Glutamic Acid 10-19 mitogen-activated protein kinase 1 Homo sapiens 28-31 27941812-8 2016 The importance of nuclear localization of HSP70 in the negative regulation of glutamate-induced ERK activation was further confirmed in VRK3-deficient neurons. Glutamic Acid 78-87 mitogen-activated protein kinase 1 Homo sapiens 96-99 28598073-6 2016 The hBMSCs were identified by flow cytometry.Compared with control group, significant increases of ALP mRNA, OCN mRNA and Runx2mRNA levels, as well as phosphorylation of ERK, P38 and JNK were observed in Glu A, B, C groups.Compared with Glu B group, ALP, OCN and Runx2 mRNA levels, and phosphorylation of ERK, P38 and JNK were decreased in Glu B+FGF-21 group .Compared with Glu B+FGF-21 group, ALP and Runx2 mRNA levels, and phosphorylation of ERK, JNK and P38 were decreased in Glu B +FGF-21 +MAPK blocker groups. Glutamic Acid 204-207 mitogen-activated protein kinase 1 Homo sapiens 305-308 28598073-6 2016 The hBMSCs were identified by flow cytometry.Compared with control group, significant increases of ALP mRNA, OCN mRNA and Runx2mRNA levels, as well as phosphorylation of ERK, P38 and JNK were observed in Glu A, B, C groups.Compared with Glu B group, ALP, OCN and Runx2 mRNA levels, and phosphorylation of ERK, P38 and JNK were decreased in Glu B+FGF-21 group .Compared with Glu B+FGF-21 group, ALP and Runx2 mRNA levels, and phosphorylation of ERK, JNK and P38 were decreased in Glu B +FGF-21 +MAPK blocker groups. Glutamic Acid 204-207 mitogen-activated protein kinase 1 Homo sapiens 310-313 28598073-6 2016 The hBMSCs were identified by flow cytometry.Compared with control group, significant increases of ALP mRNA, OCN mRNA and Runx2mRNA levels, as well as phosphorylation of ERK, P38 and JNK were observed in Glu A, B, C groups.Compared with Glu B group, ALP, OCN and Runx2 mRNA levels, and phosphorylation of ERK, P38 and JNK were decreased in Glu B+FGF-21 group .Compared with Glu B+FGF-21 group, ALP and Runx2 mRNA levels, and phosphorylation of ERK, JNK and P38 were decreased in Glu B +FGF-21 +MAPK blocker groups. Glutamic Acid 204-207 mitogen-activated protein kinase 1 Homo sapiens 305-308 28598073-6 2016 The hBMSCs were identified by flow cytometry.Compared with control group, significant increases of ALP mRNA, OCN mRNA and Runx2mRNA levels, as well as phosphorylation of ERK, P38 and JNK were observed in Glu A, B, C groups.Compared with Glu B group, ALP, OCN and Runx2 mRNA levels, and phosphorylation of ERK, P38 and JNK were decreased in Glu B+FGF-21 group .Compared with Glu B+FGF-21 group, ALP and Runx2 mRNA levels, and phosphorylation of ERK, JNK and P38 were decreased in Glu B +FGF-21 +MAPK blocker groups. Glutamic Acid 204-207 mitogen-activated protein kinase 1 Homo sapiens 310-313 28598073-6 2016 The hBMSCs were identified by flow cytometry.Compared with control group, significant increases of ALP mRNA, OCN mRNA and Runx2mRNA levels, as well as phosphorylation of ERK, P38 and JNK were observed in Glu A, B, C groups.Compared with Glu B group, ALP, OCN and Runx2 mRNA levels, and phosphorylation of ERK, P38 and JNK were decreased in Glu B+FGF-21 group .Compared with Glu B+FGF-21 group, ALP and Runx2 mRNA levels, and phosphorylation of ERK, JNK and P38 were decreased in Glu B +FGF-21 +MAPK blocker groups. Glutamic Acid 204-207 mitogen-activated protein kinase 1 Homo sapiens 494-498 26286528-4 2015 Docking followed by inhibitor verification using the pNPP assay identified a series of polysulfonated aromatic inhibitors that occupy the DUSP5 active site in the region that is likely occupied by the dual-phosphorylated ERK2 substrate tripeptide (pThr-Glu-pTyr). Glutamic Acid 253-256 mitogen-activated protein kinase 1 Homo sapiens 221-225 26190261-6 2015 ERK2 activation during metabolic stress contributes to changes in TCA cycle and amino acid metabolism, and cell death, which is suppressed by glutamate and alpha-ketoglutarate supplementation. Glutamic Acid 142-151 mitogen-activated protein kinase 1 Homo sapiens 0-4 25661849-0 2015 Topiramate protects against glutamate excitotoxicity via activating BDNF/TrkB-dependent ERK pathway in rodent hippocampal neurons. Glutamic Acid 28-37 mitogen-activated protein kinase 1 Homo sapiens 88-91 24773940-1 2014 The Ras-Raf-mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)-ERK cascade is important in the intra-cellular transduction of neurotransmitters, such as dopamine and glutamate. Glutamic Acid 205-214 mitogen-activated protein kinase 1 Homo sapiens 84-87 24773940-1 2014 The Ras-Raf-mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)-ERK cascade is important in the intra-cellular transduction of neurotransmitters, such as dopamine and glutamate. Glutamic Acid 205-214 mitogen-activated protein kinase 1 Homo sapiens 102-105 24554693-5 2014 On the other side, post-receptor effectors such as protein kinase B (Akt), glycogen synthase kinase-3 (GSK-3) and the extracellular signal-regulated kinase (Erk), which are implicated in both molecular abnormalities and treatment of BD, may interact with PSD proteins, and participate in the interplay of the dopamine-glutamate signalling pathway. Glutamic Acid 318-327 mitogen-activated protein kinase 1 Homo sapiens 118-155 24554693-5 2014 On the other side, post-receptor effectors such as protein kinase B (Akt), glycogen synthase kinase-3 (GSK-3) and the extracellular signal-regulated kinase (Erk), which are implicated in both molecular abnormalities and treatment of BD, may interact with PSD proteins, and participate in the interplay of the dopamine-glutamate signalling pathway. Glutamic Acid 318-327 mitogen-activated protein kinase 1 Homo sapiens 157-160 24735639-11 2014 FGF-2 enhances microglial migration and phagocytosis of neuronal debris, and is neuroprotective against glutamate toxicity through FGFR3-extracellular signal-regulated kinase (ERK) signaling pathway, which is directly controlled by Wnt signaling in microglia. Glutamic Acid 104-113 mitogen-activated protein kinase 1 Homo sapiens 131-174 24735639-11 2014 FGF-2 enhances microglial migration and phagocytosis of neuronal debris, and is neuroprotective against glutamate toxicity through FGFR3-extracellular signal-regulated kinase (ERK) signaling pathway, which is directly controlled by Wnt signaling in microglia. Glutamic Acid 104-113 mitogen-activated protein kinase 1 Homo sapiens 176-179 24071517-8 2014 It could be concluded that TMP inhibited Glu/Ins-stimulated HSC activation and ECM production by inhibiting InsR-mediated PI3K/AKT and ERK pathways. Glutamic Acid 41-44 mitogen-activated protein kinase 1 Homo sapiens 135-138 24409148-0 2014 Convergence of dopamine and glutamate signaling onto striatal ERK activation in response to drugs of abuse. Glutamic Acid 28-37 mitogen-activated protein kinase 1 Homo sapiens 62-65 24409148-6 2014 ERK activation by drugs of abuse behaves as a key integrator of D1R and glutamate NMDAR signaling. Glutamic Acid 72-81 mitogen-activated protein kinase 1 Homo sapiens 0-3 24206109-0 2014 Stimulating ERK/PI3K/NFkappaB signaling pathways upon activation of mGluR2/3 restores OGD-induced impairment in glutamate clearance in astrocytes. Glutamic Acid 112-121 mitogen-activated protein kinase 1 Homo sapiens 12-15 24206109-9 2014 These results suggest that application of mGluR2/3 agonists after OGD insult can effectively reverse the OGD-reduced expression of GLAST proteins and restore clearance of extracellular glutamate by serially activating ERK/PI3K/NFkappaB signaling pathways in cultured astrocytes. Glutamic Acid 185-194 mitogen-activated protein kinase 1 Homo sapiens 218-221 23713463-7 2013 The modulation of glutamate uptake by GUO also involved MAPK/ERK activation. Glutamic Acid 18-27 mitogen-activated protein kinase 1 Homo sapiens 61-64 22575735-2 2012 We have also reported that exogenous TK administration can suppress glutamate- or acidosis-induced neurotoxicity through the extracellular signal-regulated kinase1/2 (ERK1/2) pathway. Glutamic Acid 68-77 mitogen-activated protein kinase 1 Homo sapiens 125-165 22260695-1 2012 Many stimuli mediate activation and nuclear translocation of ERK (extracellular-signal-regulated kinase) by phosphorylation on the TEY (Thr-Glu-Tyr) motif. Glutamic Acid 140-143 mitogen-activated protein kinase 1 Homo sapiens 61-64 22260695-1 2012 Many stimuli mediate activation and nuclear translocation of ERK (extracellular-signal-regulated kinase) by phosphorylation on the TEY (Thr-Glu-Tyr) motif. Glutamic Acid 140-143 mitogen-activated protein kinase 1 Homo sapiens 66-103 22334892-8 2012 Mutant Htt also hinders glutamate uptake from the synaptic cleft by down-regulating ERK-dependent expression of glutamate transporters, leaving cells vulnerable to excitotoxicity. Glutamic Acid 24-33 mitogen-activated protein kinase 1 Homo sapiens 84-87 22351066-6 2012 For example, the cAMP pathway is mostly regulated by dopamine D1 receptors in striatonigral neurons, whereas the ERK pathway detects a combination of glutamate and dopamine signals and is essential for long-lasting modifications. Glutamic Acid 150-159 mitogen-activated protein kinase 1 Homo sapiens 113-116 21820214-3 2011 Here we show that extracellular PGRN stimulates phosphorylation/activation of the neuronal MEK/extracellular regulated kinase (ERK)/p90 ribosomal S6 kinase (p90RSK) and phosphatidylinositol-3 kinase (PI3K)/Akt cell survival pathways and rescues cortical neurons from cell death induced by glutamate or oxidative stress. Glutamic Acid 289-298 mitogen-activated protein kinase 1 Homo sapiens 91-125 21820214-3 2011 Here we show that extracellular PGRN stimulates phosphorylation/activation of the neuronal MEK/extracellular regulated kinase (ERK)/p90 ribosomal S6 kinase (p90RSK) and phosphatidylinositol-3 kinase (PI3K)/Akt cell survival pathways and rescues cortical neurons from cell death induced by glutamate or oxidative stress. Glutamic Acid 289-298 mitogen-activated protein kinase 1 Homo sapiens 127-130 21820214-4 2011 Pharmacological inhibition of MEK/ERK/p90RSK signaling blocks the PGRN-induced phosphorylation and neuroprotection against glutamate toxicity while inhibition of either MEK/ERK/p90RSK or PI3K/Akt blocks PGRN protection against neurotoxin MPP(+). Glutamic Acid 123-132 mitogen-activated protein kinase 1 Homo sapiens 34-37 21798274-6 2011 These two different ERK-mediated pathways were involved in the neuroprotective effects displayed by both P2Y(13) and P2X7 receptors against apoptosis induced by an excitotoxic concentration of glutamate, in a similar manner to the neurotrophin, BDNF. Glutamic Acid 193-202 mitogen-activated protein kinase 1 Homo sapiens 20-23 20560877-9 2010 The results indicate that leptin may act through Akt and ERK signaling pathways to protect neurons from GOSD insult; the protection was in part IL-1beta dependent and through which the glutamate release from GOSD neurons was inhibited. Glutamic Acid 185-194 mitogen-activated protein kinase 1 Homo sapiens 57-60 20202085-0 2010 Prolonged activation of ERK triggers glutamate-induced apoptosis of astrocytes: neuroprotective effect of FK506. Glutamic Acid 37-46 mitogen-activated protein kinase 1 Homo sapiens 24-27 20202085-4 2010 We demonstrated enhanced and mostly cytoplasmic activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) during glutamate-induced apoptosis of cultured astrocytes. Glutamic Acid 125-134 mitogen-activated protein kinase 1 Homo sapiens 62-108 20202085-5 2010 Treatment with UO126, inhibitor of MEK1, threo-beta-benzyloxyaspartic acid, glutamate transporter inhibitor, and FK506, a cytoprotective drug prevented ERK activation and glutamate-induced apoptosis. Glutamic Acid 76-85 mitogen-activated protein kinase 1 Homo sapiens 152-155 20202085-9 2010 The results demonstrate a pro-apoptotic role of sustained activation of ERK1/2 signaling in glutamate-induced death of astrocytes and the ability of FK506 to block both ERK activation and astrocytic cell death in vitro and in ischemic brains. Glutamic Acid 92-101 mitogen-activated protein kinase 1 Homo sapiens 72-75 19598250-8 2009 Furthermore, we found that the extracellular signal-regulated kinase 1/2 cascade (ERK1/2), particularly ERK1, and nuclear factor-kappaB (NF-kappaB) were involved in TK neuroprotection against glutamate-induced neurotoxicity. Glutamic Acid 192-201 mitogen-activated protein kinase 1 Homo sapiens 31-72 19416748-8 2009 We found that activation of ERK (p<0.05) and CREB (p<0.05) after 30s of glutamate stimulation or KCl depolarization was decreased in hippocampal slices from animals at 2, 8, or 12 weeks after TBI as compared to sham animals. Glutamic Acid 78-87 mitogen-activated protein kinase 1 Homo sapiens 28-31 19398002-0 2009 Endocytosis controls glutamate-induced nuclear accumulation of ERK. Glutamic Acid 21-30 mitogen-activated protein kinase 1 Homo sapiens 63-66 19398002-3 2009 In cultured neurons, we identified endocytosis as a prime event in glutamate-induced nuclear trafficking of ERK2. Glutamic Acid 67-76 mitogen-activated protein kinase 1 Homo sapiens 108-112 19398002-4 2009 We show that glutamate triggers a rapid recruitment of ERK2 to a protein complex comprising markers of the clathrin-dependent endocytotic and AMPA/glutamate receptor subtype. Glutamic Acid 13-22 mitogen-activated protein kinase 1 Homo sapiens 55-59 19398002-7 2009 Our data provide the first evidence that the endocytic pathway controls ERK nuclear translocation and ERK-dependent gene regulations induced by glutamate. Glutamic Acid 144-153 mitogen-activated protein kinase 1 Homo sapiens 72-75 19398002-7 2009 Our data provide the first evidence that the endocytic pathway controls ERK nuclear translocation and ERK-dependent gene regulations induced by glutamate. Glutamic Acid 144-153 mitogen-activated protein kinase 1 Homo sapiens 102-105 19012740-0 2009 Glutamate and nitric oxide modulate ERK and CREB phosphorylation in the avian retina: evidence for direct signaling from neurons to Muller glial cells. Glutamic Acid 0-9 mitogen-activated protein kinase 1 Homo sapiens 36-39 18022816-2 2008 In neurons, glutamate has been shown to activate the Ras/Raf/MEK/ERK cascade, which participates in the regulation of proliferation, differentiation, and survival processes. Glutamic Acid 12-21 mitogen-activated protein kinase 1 Homo sapiens 65-68 18022816-6 2008 Results demonstrate that glutamate stimulates RPE cell proliferation as well as ERK and CREB phosphorylation. Glutamic Acid 25-34 mitogen-activated protein kinase 1 Homo sapiens 80-83 18089844-12 2008 These results suggest that estrogens protect cells against glutamate-induced oxidative stress through an ER-independent mediated mechanism that serves to preserve phosphatase activity in the face of oxidative insults, resulting in attenuation of the persistent phosphorylation of ERK associated with neuronal death. Glutamic Acid 59-68 mitogen-activated protein kinase 1 Homo sapiens 280-283 18160653-5 2007 In this study we show that the excitatory neurotransmitter, glutamate, induces an ERK-dependent Elk-1 activation and nuclear relocalization. Glutamic Acid 60-69 mitogen-activated protein kinase 1 Homo sapiens 82-85 18160653-8 2007 This results in a differential regulation of glutamate-induced IEG regulation when compared with classical inhibitors of the ERK pathway. Glutamic Acid 45-54 mitogen-activated protein kinase 1 Homo sapiens 125-128 18031600-0 2007 Neuroprotection by sodium ferulate against glutamate-induced apoptosis is mediated by ERK and PI3 kinase pathways. Glutamic Acid 43-52 mitogen-activated protein kinase 1 Homo sapiens 86-89 18031600-10 2007 CONCLUSION: The results indicate that PI3K/Akt/p70S6K and the MEK/ERK signaling pathways play important roles in the protective effect of SF against glutamate toxicity in cortical neurons. Glutamic Acid 149-158 mitogen-activated protein kinase 1 Homo sapiens 66-69 19305741-3 2007 Their activity is controlled by phosphorylation on specific aminoacidic residues, which is induced by a variety of external cues, including growth-promoting factors.In the nervous system, ERK phosphorylation is induced by binding of neurotrophins to their specific tyrosine kinase receptors or by neuronal activity leading to glutamate release and binding to its ionotropic and metabotropic receptors. Glutamic Acid 326-335 mitogen-activated protein kinase 1 Homo sapiens 188-191 17897358-2 2007 The mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in mediating neuronal activation induced by dopamine, glutamate, and drugs of abuse. Glutamic Acid 133-142 mitogen-activated protein kinase 1 Homo sapiens 38-42 17085074-7 2007 We suggest that the ERK2 pathway acts as a logical AND gate, permissive for plasticity, in neurons on which dopamine-mediated reward signals and glutamate-mediated contextual information converge. Glutamic Acid 145-154 mitogen-activated protein kinase 1 Homo sapiens 20-24 17263796-6 2007 In contrast, similar levels of glutamate-induced ERK activation were observed in both loss-of-function mutants, but were further increased in galanin over-expressing animals. Glutamic Acid 31-40 mitogen-activated protein kinase 1 Homo sapiens 49-52 16151022-9 2005 Furthermore, the p38 MAPK signaling pathway may mediate Ang II-induced pressor response via enhancement of presynaptic release of glutamate to RVLM neurons. Glutamic Acid 130-139 mitogen-activated protein kinase 1 Homo sapiens 17-20 15905876-0 2005 Neuroprotection by BDNF against glutamate-induced apoptotic cell death is mediated by ERK and PI3-kinase pathways. Glutamic Acid 32-41 mitogen-activated protein kinase 1 Homo sapiens 86-89 15865443-2 2005 Previous studies have shown that p42(mapk/erk2) phosphorylates Ser and Thr residues (T236, S240, S244, and S270) in the membrane proximal region of TNF-R1 and that mutation of these residues to Glu and Asp residues (TNF-R1.4D/E) mimics the effect of phosphorylation on receptor signaling and localization. Glutamic Acid 194-197 mitogen-activated protein kinase 1 Homo sapiens 42-46 15709155-3 2005 The aim of the present study was to investigate the role of various kinases and the extracellular signal-regulated kinase (ERK) pathway in the induction of the AR and associated phosphorylation of tyrosine (Tyr) residues and of the threonine-glutamic acid-tyrosine (Thr-Glu-Tyr) motif that occurs in 80 and 105 kDa proteins (p80/p105). Glutamic Acid 270-273 mitogen-activated protein kinase 1 Homo sapiens 84-121 15709155-3 2005 The aim of the present study was to investigate the role of various kinases and the extracellular signal-regulated kinase (ERK) pathway in the induction of the AR and associated phosphorylation of tyrosine (Tyr) residues and of the threonine-glutamic acid-tyrosine (Thr-Glu-Tyr) motif that occurs in 80 and 105 kDa proteins (p80/p105). Glutamic Acid 270-273 mitogen-activated protein kinase 1 Homo sapiens 123-126 15447667-6 2004 These results suggest that glutamate released from corticostriatal afferents modulates the ability of amphetamine to engage striatopallidal neurons through an ERK/MAPK signaling-dependent mechanism. Glutamic Acid 27-36 mitogen-activated protein kinase 1 Homo sapiens 159-162 15447667-6 2004 These results suggest that glutamate released from corticostriatal afferents modulates the ability of amphetamine to engage striatopallidal neurons through an ERK/MAPK signaling-dependent mechanism. Glutamic Acid 27-36 mitogen-activated protein kinase 1 Homo sapiens 163-167 14715649-4 2004 We have previously determined that glutamate-induced oxidative toxicity is accompanied by a robust increase in activation of the mitogen-activated protein kinase (MAPK) member extracellular-signal regulated kinase (ERK) and that this activation is essential for neuronal cell death. Glutamic Acid 35-44 mitogen-activated protein kinase 1 Homo sapiens 163-167 14715649-4 2004 We have previously determined that glutamate-induced oxidative toxicity is accompanied by a robust increase in activation of the mitogen-activated protein kinase (MAPK) member extracellular-signal regulated kinase (ERK) and that this activation is essential for neuronal cell death. Glutamic Acid 35-44 mitogen-activated protein kinase 1 Homo sapiens 176-213 14715649-4 2004 We have previously determined that glutamate-induced oxidative toxicity is accompanied by a robust increase in activation of the mitogen-activated protein kinase (MAPK) member extracellular-signal regulated kinase (ERK) and that this activation is essential for neuronal cell death. Glutamic Acid 35-44 mitogen-activated protein kinase 1 Homo sapiens 215-218 12754209-4 2003 Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation. Glutamic Acid 47-50 mitogen-activated protein kinase 1 Homo sapiens 179-183 11356868-7 2001 Inhibitor analysis as well as immunochemical characterization has indicated that the MEK (MAPK/ERK kinase)-ERK (extracellular signal-regulated kinase) cascade plays an indispensable role in glutamate-stimulated induction of Homer 1a mRNA. Glutamic Acid 190-199 mitogen-activated protein kinase 1 Homo sapiens 90-94 11356868-7 2001 Inhibitor analysis as well as immunochemical characterization has indicated that the MEK (MAPK/ERK kinase)-ERK (extracellular signal-regulated kinase) cascade plays an indispensable role in glutamate-stimulated induction of Homer 1a mRNA. Glutamic Acid 190-199 mitogen-activated protein kinase 1 Homo sapiens 95-98 11356868-7 2001 Inhibitor analysis as well as immunochemical characterization has indicated that the MEK (MAPK/ERK kinase)-ERK (extracellular signal-regulated kinase) cascade plays an indispensable role in glutamate-stimulated induction of Homer 1a mRNA. Glutamic Acid 190-199 mitogen-activated protein kinase 1 Homo sapiens 107-110 10588362-0 1999 Glutamate-stimulated calcium activation of Ras/Erk pathway mediated by nitric oxide. Glutamic Acid 0-9 mitogen-activated protein kinase 1 Homo sapiens 47-50 10588362-2 1999 Calcium-dependent activation of Ras and extracellular signal-regulated kineses (Erks) may transmit the glutamate signal to the nucleus which is ultimately important for long-lasting neuronal responses. Glutamic Acid 103-112 mitogen-activated protein kinase 1 Homo sapiens 80-84 10349832-0 1999 Contrasting calcium dependencies of SAPK and ERK activations by glutamate in cultured striatal neurons. Glutamic Acid 64-73 mitogen-activated protein kinase 1 Homo sapiens 45-48 10349832-2 1999 However, SAPK and ERK can also be coordinately activated in neurons in response to glutamate stimulation of NMDA receptors. Glutamic Acid 83-92 mitogen-activated protein kinase 1 Homo sapiens 18-21 10349832-3 1999 To explore the mechanisms of these MAPK activations, we compared the ionic mechanisms mediating SAPK and ERK activations by glutamate. Glutamic Acid 124-133 mitogen-activated protein kinase 1 Homo sapiens 35-39 10349832-3 1999 To explore the mechanisms of these MAPK activations, we compared the ionic mechanisms mediating SAPK and ERK activations by glutamate. Glutamic Acid 124-133 mitogen-activated protein kinase 1 Homo sapiens 105-108 9572294-6 1998 H2O2 alone strongly enhanced the levels of immunodetectable activated mitogen-activated protein kinase (activated MAP kinases ERK1 and ERK2) in a Ca2+-dependent manner and this effect was additive with increases in the levels of activated MAP kinase evoked by glutamate. Glutamic Acid 260-269 mitogen-activated protein kinase 1 Homo sapiens 135-139 9314533-6 1997 However, transfection with MKK6 (Glu), which specifically activated p38, augmented cell size, induced NP and alpha-Ska promoter activities by up to 130-fold, and elicited sarcomeric organization in a manner similar to PE. Glutamic Acid 33-36 mitogen-activated protein kinase 1 Homo sapiens 68-71 9314533-7 1997 Moreover, all three growth features induced by MKK6 (Glu) or PE were blocked with the p38-specific inhibitor, SB 203580. Glutamic Acid 53-56 mitogen-activated protein kinase 1 Homo sapiens 86-89 9111004-5 1997 Conversion of L12 of p38 to an "ERK-like" structure was accomplished in several ways: (i) by replacing glycine with glutamate in the dual phosphorylation site, (ii) by placing a six-amino acid sequence present in L12 of ERK (but absent in p38) into p38, and (iii) by mutations of amino acid residues in loop 12. Glutamic Acid 116-125 mitogen-activated protein kinase 1 Homo sapiens 32-35 8757255-9 1996 Activation of the Elk-dependent pathway of transcription seems to require phosphorylation of Elk-1 by extracellular signal-regulated kinases (ERKs), providing evidence for a physiological function of ERKs in glutamate signaling in neurons. Glutamic Acid 208-217 mitogen-activated protein kinase 1 Homo sapiens 142-146 8757255-9 1996 Activation of the Elk-dependent pathway of transcription seems to require phosphorylation of Elk-1 by extracellular signal-regulated kinases (ERKs), providing evidence for a physiological function of ERKs in glutamate signaling in neurons. Glutamic Acid 208-217 mitogen-activated protein kinase 1 Homo sapiens 200-204