PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31332165-10 2019 In addition, MHY1485, an activator of mTOR, reduced Hcy-induced increase in LC3 and Beclin 1 protein levels, meanwhile ERK and PI3K activators (TPA, curcumin for ERK and IGF-1 for PI3K, respectively) enhanced Hcy-triggered mTOR inhibition in OGD/R NSCs. Homocysteine 52-55 mitogen-activated protein kinase 1 Homo sapiens 162-165 31332165-11 2019 Our findings suggest that Hcy may cause excessive autophagy by downregulation of both PI3K-AKT- and ERK- dependent mTOR signaling, thereby facilitates the toxicity of Hcy on NSCs in ischemic brains. Homocysteine 26-29 mitogen-activated protein kinase 1 Homo sapiens 86-103 31332165-11 2019 Our findings suggest that Hcy may cause excessive autophagy by downregulation of both PI3K-AKT- and ERK- dependent mTOR signaling, thereby facilitates the toxicity of Hcy on NSCs in ischemic brains. Homocysteine 167-170 mitogen-activated protein kinase 1 Homo sapiens 86-103 28543279-8 2017 These results suggest that homocysteine-NMDAR-mediated ERK MAPK phosphorylation leads to a decrease in surface expression of GluA2-AMPAR subunit resulting in Ca2+ influx through the GluA2-lacking Ca2+ -permeable AMPARs and p38 MAPK phosphorylation. Homocysteine 27-39 mitogen-activated protein kinase 1 Homo sapiens 55-58 28543279-8 2017 These results suggest that homocysteine-NMDAR-mediated ERK MAPK phosphorylation leads to a decrease in surface expression of GluA2-AMPAR subunit resulting in Ca2+ influx through the GluA2-lacking Ca2+ -permeable AMPARs and p38 MAPK phosphorylation. Homocysteine 27-39 mitogen-activated protein kinase 1 Homo sapiens 59-63 28543279-8 2017 These results suggest that homocysteine-NMDAR-mediated ERK MAPK phosphorylation leads to a decrease in surface expression of GluA2-AMPAR subunit resulting in Ca2+ influx through the GluA2-lacking Ca2+ -permeable AMPARs and p38 MAPK phosphorylation. Homocysteine 27-39 mitogen-activated protein kinase 1 Homo sapiens 223-226 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 150-187 20857402-5 2011 Furthermore, treatment with extracellular signal-related kinase (ERK) inhibitor (PD98059) and dominant negative Ras (RasN17) abolished homocysteine-induced cyclin A expression; and treatment with phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin) attenuated the homocysteine-induced cyclin D1 expression. Homocysteine 135-147 mitogen-activated protein kinase 1 Homo sapiens 28-63 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 189-192 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 198-201 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 229-232 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 272-275 28543279-2 2017 The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. Homocysteine 40-52 mitogen-activated protein kinase 1 Homo sapiens 202-206 28543279-6 2017 Inhibition of NMDAR activation with D-AP5 or ERK MAPK phosphorylation with PD98059 attenuates homocysteine-induced decrease in surface expression of GluA2-AMPAR subunit. Homocysteine 94-106 mitogen-activated protein kinase 1 Homo sapiens 45-48 28543279-6 2017 Inhibition of NMDAR activation with D-AP5 or ERK MAPK phosphorylation with PD98059 attenuates homocysteine-induced decrease in surface expression of GluA2-AMPAR subunit. Homocysteine 94-106 mitogen-activated protein kinase 1 Homo sapiens 49-53 23209759-9 2012 Increased homocysteine by levodopa led to increased apoptosis of NPCs through the NMDA receptor-dependent the extracellular signal-regulated kinase (ERK) signaling pathways. Homocysteine 10-22 mitogen-activated protein kinase 1 Homo sapiens 110-147 23209759-9 2012 Increased homocysteine by levodopa led to increased apoptosis of NPCs through the NMDA receptor-dependent the extracellular signal-regulated kinase (ERK) signaling pathways. Homocysteine 10-22 mitogen-activated protein kinase 1 Homo sapiens 149-152 23209759-12 2012 Our present study demonstrated that increased homocysteine by levodopa has a detrimental effect on neurogenesis through NMDA receptor-mediated ERK signaling pathway. Homocysteine 46-58 mitogen-activated protein kinase 1 Homo sapiens 143-146 23176034-2 2013 We recently established a role for NMDA receptor-mediated activation of extracellular signal-regulated kinase (ERK)-MAPK in homocysteine-induced neuronal cell death. Homocysteine 124-136 mitogen-activated protein kinase 1 Homo sapiens 72-109 23176034-2 2013 We recently established a role for NMDA receptor-mediated activation of extracellular signal-regulated kinase (ERK)-MAPK in homocysteine-induced neuronal cell death. Homocysteine 124-136 mitogen-activated protein kinase 1 Homo sapiens 111-114 23176034-2 2013 We recently established a role for NMDA receptor-mediated activation of extracellular signal-regulated kinase (ERK)-MAPK in homocysteine-induced neuronal cell death. Homocysteine 124-136 mitogen-activated protein kinase 1 Homo sapiens 116-120 23176034-3 2013 In this study, we examined the involvement of the stress-induced MAPK, p38 in homocysteine-induced neuronal cell death, and further explored the relationship between the two MAPKs, ERK and p38, in triggering cell death. Homocysteine 78-90 mitogen-activated protein kinase 1 Homo sapiens 71-74 23176034-4 2013 Homocysteine-mediated NMDA receptor stimulation and subsequent Ca(2+) influx led to a biphasic activation of p38 MAPK characterized by an initial rapid, but transient activation followed by a delayed and more prolonged response. Homocysteine 0-12 mitogen-activated protein kinase 1 Homo sapiens 110-113 23176034-5 2013 Selective inhibition of the delayed p38 MAPK activity was sufficient to attenuate homocysteine-induced neuronal cell death. Homocysteine 82-94 mitogen-activated protein kinase 1 Homo sapiens 36-39 23176034-5 2013 Selective inhibition of the delayed p38 MAPK activity was sufficient to attenuate homocysteine-induced neuronal cell death. Homocysteine 82-94 mitogen-activated protein kinase 1 Homo sapiens 40-44 20857402-5 2011 Furthermore, treatment with extracellular signal-related kinase (ERK) inhibitor (PD98059) and dominant negative Ras (RasN17) abolished homocysteine-induced cyclin A expression; and treatment with phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin) attenuated the homocysteine-induced cyclin D1 expression. Homocysteine 135-147 mitogen-activated protein kinase 1 Homo sapiens 65-68 20857402-5 2011 Furthermore, treatment with extracellular signal-related kinase (ERK) inhibitor (PD98059) and dominant negative Ras (RasN17) abolished homocysteine-induced cyclin A expression; and treatment with phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin) attenuated the homocysteine-induced cyclin D1 expression. Homocysteine 332-344 mitogen-activated protein kinase 1 Homo sapiens 28-63 20857402-5 2011 Furthermore, treatment with extracellular signal-related kinase (ERK) inhibitor (PD98059) and dominant negative Ras (RasN17) abolished homocysteine-induced cyclin A expression; and treatment with phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin) attenuated the homocysteine-induced cyclin D1 expression. Homocysteine 332-344 mitogen-activated protein kinase 1 Homo sapiens 65-68 20857402-6 2011 Homocysteine also induced transient phosphorylation of ERK, Akt, and p70 ribosomal S6 kinase (p70S6K). Homocysteine 0-12 mitogen-activated protein kinase 1 Homo sapiens 55-58 20857402-8 2011 In conclusion, homocysteine-induced differential activation of Ras/ERK and PI3K/Akt/p70S6K signaling pathways and consequent expression of cyclins A and D1 are dependent on beta1 integrin. Homocysteine 15-27 mitogen-activated protein kinase 1 Homo sapiens 67-70 15253728-17 2004 Erk activity in response to Hcy was insensitive to n-acetylcysteine and catalase, indicating oxidative stress did not play a role. Homocysteine 28-31 mitogen-activated protein kinase 1 Homo sapiens 0-3 19850060-0 2010 Potent homocysteine-induced ERK phosphorylation in cultured neurons depends on self-sensitization via system Xc(-). Homocysteine 7-19 mitogen-activated protein kinase 1 Homo sapiens 28-31 19745163-5 2009 METHODS AND RESULTS: Homocysteine stimulation induced dose- and time-dependent SDF-1 expression and phosphorylation of mitogen-activated protein kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Homocysteine 21-33 mitogen-activated protein kinase 1 Homo sapiens 153-190 19745163-5 2009 METHODS AND RESULTS: Homocysteine stimulation induced dose- and time-dependent SDF-1 expression and phosphorylation of mitogen-activated protein kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Homocysteine 21-33 mitogen-activated protein kinase 1 Homo sapiens 192-195 19745163-5 2009 METHODS AND RESULTS: Homocysteine stimulation induced dose- and time-dependent SDF-1 expression and phosphorylation of mitogen-activated protein kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Homocysteine 21-33 mitogen-activated protein kinase 1 Homo sapiens 233-236 18777088-2 2009 We recently reported homocysteine (Hcy)-induced ERK-phosphorylation was suppressed by pertussis toxin (PTX), which suggested the involvement of GPCRs in initiating signal transduction. Homocysteine 21-33 mitogen-activated protein kinase 1 Homo sapiens 48-51 18777088-2 2009 We recently reported homocysteine (Hcy)-induced ERK-phosphorylation was suppressed by pertussis toxin (PTX), which suggested the involvement of GPCRs in initiating signal transduction. Homocysteine 35-38 mitogen-activated protein kinase 1 Homo sapiens 48-51 17900592-5 2008 Homocysteine-induced expression of ET-1 mRNA, ERK, pERK and c-jun/AP-1 protein was measured using RT-PCR and Western blot analysis, respectively. Homocysteine 0-12 mitogen-activated protein kinase 1 Homo sapiens 46-49 17255340-7 2007 PKCepsilon and active ERK were mutually associated and co-localized with mitochondria in HCs. Homocysteine 89-92 mitogen-activated protein kinase 1 Homo sapiens 22-25 15253728-6 2004 Previous work has shown Hcy- mediated induction of Erk mitogen-activated protein kinase (MAPK) in vascular smooth muscle cells (VSMCs). Homocysteine 24-27 mitogen-activated protein kinase 1 Homo sapiens 51-54 15253728-8 2004 Consequently, we studied the effect of Hcy on mesangial cell Erk signaling. Homocysteine 39-42 mitogen-activated protein kinase 1 Homo sapiens 61-64 19508427-5 2009 The study also shows that homocysteine-dependent NMDA receptor stimulation and resultant Ca2+ influx leads to rapid and sustained phosphorylation of ERK-MAP kinase. Homocysteine 26-38 mitogen-activated protein kinase 1 Homo sapiens 149-152 19508427-6 2009 Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. Homocysteine 45-57 mitogen-activated protein kinase 1 Homo sapiens 14-17 19508427-6 2009 Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. Homocysteine 45-57 mitogen-activated protein kinase 1 Homo sapiens 128-131 19508427-6 2009 Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. Homocysteine 198-210 mitogen-activated protein kinase 1 Homo sapiens 14-17 19508427-6 2009 Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. Homocysteine 198-210 mitogen-activated protein kinase 1 Homo sapiens 128-131 19508427-7 2009 The findings also show that cAMP response-element binding protein (CREB), a pro-survival transcription factor and a downstream target of ERK, is only transiently activated following homocysteine exposure. Homocysteine 182-194 mitogen-activated protein kinase 1 Homo sapiens 137-140 19508427-8 2009 The sustained activation of ERK but a transient activation of CREB together suggest that exposure to homocysteine initiates a feedback loop that shuts off CREB signaling without affecting ERK phosphorylation and thereby facilitates homocysteine-mediated neurotoxicity. Homocysteine 101-113 mitogen-activated protein kinase 1 Homo sapiens 28-31 19508427-8 2009 The sustained activation of ERK but a transient activation of CREB together suggest that exposure to homocysteine initiates a feedback loop that shuts off CREB signaling without affecting ERK phosphorylation and thereby facilitates homocysteine-mediated neurotoxicity. Homocysteine 101-113 mitogen-activated protein kinase 1 Homo sapiens 188-191 19308943-0 2009 Activation of GABA-A receptor ameliorates homocysteine-induced MMP-9 activation by ERK pathway. Homocysteine 42-54 mitogen-activated protein kinase 1 Homo sapiens 83-86 19308943-5 2009 We hypothesized that Hcy causes cerebrovascular remodeling by increasing redox stress and MMP-9 activity via the extracellular signal-regulated kinase (ERK) signaling pathway and by inhibition of GABA-A receptors, thus behaving as an inhibitory neurotransmitter. Homocysteine 21-24 mitogen-activated protein kinase 1 Homo sapiens 113-150 19308943-5 2009 We hypothesized that Hcy causes cerebrovascular remodeling by increasing redox stress and MMP-9 activity via the extracellular signal-regulated kinase (ERK) signaling pathway and by inhibition of GABA-A receptors, thus behaving as an inhibitory neurotransmitter. Homocysteine 21-24 mitogen-activated protein kinase 1 Homo sapiens 152-155 19308943-10 2009 In parallel, Hcy caused phosphorylation of ERK and selectively decreased levels of tissue inhibitors of metalloproteinase-4 (TIMP-4). Homocysteine 13-16 mitogen-activated protein kinase 1 Homo sapiens 43-46 19308943-13 2009 Furthermore muscimol attenuated Hcy-induced MMP-9 via ERK signaling pathway. Homocysteine 32-35 mitogen-activated protein kinase 1 Homo sapiens 54-57 19308943-14 2009 These results suggest that Hcy competes with GABA-A receptors, inducing the oxidative stress transduction pathway and leading to ERK activation. Homocysteine 27-30 mitogen-activated protein kinase 1 Homo sapiens 129-132 17900592-10 2008 Collectively, our data indicated that alpha-ZAL may antagonize homocysteine-induced ET-1 gene induction, ROS accumulation, activation of ERK signaling pathway and AP-1 transcriptional factor, all of which may contribute to alpha-ZAL-induced beneficial effect on endothelial function. Homocysteine 63-75 mitogen-activated protein kinase 1 Homo sapiens 137-140 16251475-3 2006 In cultured MVECs, Hcy induced activation of ERK, which was blocked by PD-98059 and U0126 (MEK inhibitors). Homocysteine 19-22 mitogen-activated protein kinase 1 Homo sapiens 45-48 16251475-6 2006 Pretreatment of MVECs with genistein, BAPTA-AM, or thapsigargin abrogated Hcy-induced ERK activation, suggesting the involvement of the PTK pathway in Hcy-induced ERK activation, which was mediated by intracellular Ca(2+) pool depletion. Homocysteine 74-77 mitogen-activated protein kinase 1 Homo sapiens 86-89 16251475-6 2006 Pretreatment of MVECs with genistein, BAPTA-AM, or thapsigargin abrogated Hcy-induced ERK activation, suggesting the involvement of the PTK pathway in Hcy-induced ERK activation, which was mediated by intracellular Ca(2+) pool depletion. Homocysteine 74-77 mitogen-activated protein kinase 1 Homo sapiens 163-166 16251475-6 2006 Pretreatment of MVECs with genistein, BAPTA-AM, or thapsigargin abrogated Hcy-induced ERK activation, suggesting the involvement of the PTK pathway in Hcy-induced ERK activation, which was mediated by intracellular Ca(2+) pool depletion. Homocysteine 151-154 mitogen-activated protein kinase 1 Homo sapiens 86-89 16251475-6 2006 Pretreatment of MVECs with genistein, BAPTA-AM, or thapsigargin abrogated Hcy-induced ERK activation, suggesting the involvement of the PTK pathway in Hcy-induced ERK activation, which was mediated by intracellular Ca(2+) pool depletion. Homocysteine 151-154 mitogen-activated protein kinase 1 Homo sapiens 163-166 16251475-7 2006 ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation. Homocysteine 120-123 mitogen-activated protein kinase 1 Homo sapiens 0-3 16251475-7 2006 ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation. Homocysteine 120-123 mitogen-activated protein kinase 1 Homo sapiens 132-135 15671645-3 2004 We demonstrate a cell-based HCS assay to quantify the epidermal growth factor (EGF) receptor-specific activation of the MAPK ERK. Homocysteine 28-31 mitogen-activated protein kinase 1 Homo sapiens 125-128 15253728-18 2004 However, Hcy50 micromol/L induced a brief increase in intracellular mesangial cell calcium within 5 minutes, and the calcium ionophores A23187 and ionomycin increased Erk activity while chelation of intracellular calcium with BAPTA-AM abrogated the Erk response to Hcy. Homocysteine 9-12 mitogen-activated protein kinase 1 Homo sapiens 249-252 15253728-20 2004 Hcy- induced increases in thymidine incorporation and PCNA expression at 24 hours were Erk dependent. Homocysteine 0-3 mitogen-activated protein kinase 1 Homo sapiens 87-90 15019532-8 2004 We also show that Hcy increased intracellular H2O2 production by neutrophils, that Hcy enhanced the activation and phosphorylation of mitogen-activated protein kinases (MAPKs), specifically p38-MAPK and ERK1/2, and that the migration of neutrophils was increased by Hcy. Homocysteine 83-86 mitogen-activated protein kinase 1 Homo sapiens 190-193 12881478-8 2003 These data indicate that pathophysiological levels of Hcy can alter human monocyte function by upregulating MCP-1 and IL-8 expression and secretion via enhanced formation of intracellular ROS originated from NAD(P)H oxidase source via calmodulin or protein kinase C signaling pathways and that Hcy-induced ROS subsequently activates mitogen-activated protein kinase (p38 and ERK1/2) and nuclear factor-kappaB in a PPARgamma activator-sensitive manner. Homocysteine 54-57 mitogen-activated protein kinase 1 Homo sapiens 367-370 12700663-3 2003 We show that HCs contain phosphorylated/activated p38 MAPK, JNK and ERK1/ERK2 (ERK1/2). Homocysteine 13-16 mitogen-activated protein kinase 1 Homo sapiens 50-53 12700663-3 2003 We show that HCs contain phosphorylated/activated p38 MAPK, JNK and ERK1/ERK2 (ERK1/2). Homocysteine 13-16 mitogen-activated protein kinase 1 Homo sapiens 73-77