PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30003929-0 2019 Ketamine-induced hypnosis and neuroplasticity in mice is associated with disrupted p-MEK/p-ERK sequential activation and sustained upregulation of survival p-FADD in brain cortex: Involvement of GABAA receptor. Ketamine 0-8 mitogen-activated protein kinase 1 Mus musculus 91-94 30003929-2 2019 The working hypothesis postulated that KET-induced sleep in mice results in dysregulation of mitogen-activated protein kinases (MAPK) MEK-ERK sequential phosphorylation and upregulation of survival p-FADD and other neuroplastic markers in brain. Ketamine 39-42 mitogen-activated protein kinase 1 Mus musculus 128-132 30003929-2 2019 The working hypothesis postulated that KET-induced sleep in mice results in dysregulation of mitogen-activated protein kinases (MAPK) MEK-ERK sequential phosphorylation and upregulation of survival p-FADD and other neuroplastic markers in brain. Ketamine 39-42 mitogen-activated protein kinase 1 Mus musculus 138-141 30003929-4 2019 During the time course of KET (150 mg/kg)-induced sleep (up to 50 min) p-MEK was increased (up to +79%) and p-ERK decreased (up to -46%) indicating disruption of MEK to ERK signal. Ketamine 26-29 mitogen-activated protein kinase 1 Mus musculus 169-172 30423425-1 2019 Midazolam and ketamine-induced anesthesia were recently shown to induce a disruption of MEK/ERK sequential phosphorylation with parallel upregulation of p-FADD in the mouse brain. Ketamine 14-22 mitogen-activated protein kinase 1 Mus musculus 92-95 28501494-0 2017 Focused microwave irradiation-assisted immunohistochemistry to study effects of ketamine on phospho-ERK expression in the mouse brain. Ketamine 80-88 mitogen-activated protein kinase 1 Mus musculus 100-103 28651788-5 2018 METHODS: The effects of mTOR inhibitors (rapamycin and AZD8055) and an ERK inhibitor (SL327) on the antidepressant effects of ketamine enantiomers in the chronic social defeat stress (CSDS) model (n = 7 or 8) and on those of ketamine enantiomers in these signaling pathways in mouse brain regions were examined. Ketamine 126-134 mitogen-activated protein kinase 1 Mus musculus 71-74 28501494-2 2017 Preclinical studies demonstrate that ketamine stimulates AMPA receptor transmission and activates BDNF/TrkB-Akt/ERK-mTOR signaling cascades, leading to a sustained increase in synaptic protein synthesis and strengthening of synaptic plasticity, a potential mechanism underlying the antidepressant effects. Ketamine 37-45 mitogen-activated protein kinase 1 Mus musculus 112-115 28501494-3 2017 The purpose of this study was to develop an immunohistochemistry (IHC) assay to map the distribution of extracellular signal-regulated kinase (ERK) phosphorylation in the mouse brain in response to systemic ketamine treatment. Ketamine 207-215 mitogen-activated protein kinase 1 Mus musculus 104-141 28501494-3 2017 The purpose of this study was to develop an immunohistochemistry (IHC) assay to map the distribution of extracellular signal-regulated kinase (ERK) phosphorylation in the mouse brain in response to systemic ketamine treatment. Ketamine 207-215 mitogen-activated protein kinase 1 Mus musculus 143-146 28501494-5 2017 A single dose of ketamine produced a robust, dose- and time-dependent increase in phospho-ERK immunoreactive (phospho-ERK-ir) neurons in the medial prefrontal cortex (mPFC) and the central nucleus of the amygdala. Ketamine 17-25 mitogen-activated protein kinase 1 Mus musculus 90-93 28501494-5 2017 A single dose of ketamine produced a robust, dose- and time-dependent increase in phospho-ERK immunoreactive (phospho-ERK-ir) neurons in the medial prefrontal cortex (mPFC) and the central nucleus of the amygdala. Ketamine 17-25 mitogen-activated protein kinase 1 Mus musculus 118-121 28501494-9 2017 In summary, we have established a sensitive and reliable focused microwave irradiation-assisted IHC assay, and defined the activation pattern of ERK, in response to systemic ketamine and Ro 25-6981 treatment, in brain regions that are potentially responsible for mediating the antidepressant effects. Ketamine 174-182 mitogen-activated protein kinase 1 Mus musculus 145-148 17826804-4 2007 At anesthetic doses that produced loss of righting reflex, isoflurane, propofol, and ketamine all reduced phosphorylation of the activating residue T183 of ERK2 (but not of ERK1); S897 of the NR1 NMDA receptor subunit; and S831 (but not S845) of the GluR1 AMPA receptor subunit in cerebral cortex. Ketamine 85-93 mitogen-activated protein kinase 1 Mus musculus 156-160 27074656-8 2016 We further demonstrate that diverse anesthetics (sevoflurane, urethane, ketamine) produce essentially similar phosphorylation changes on GSK3beta, p44/p42-MAPK, and MAP2 as observed with isoflurane. Ketamine 72-80 mitogen-activated protein kinase 1 Mus musculus 151-159 19293695-4 2009 (1) Do ketamine and propofol mimic ethanol in suppressing ERK phosphorylation? Ketamine 7-15 mitogen-activated protein kinase 1 Mus musculus 58-61 19293695-9 2009 RESULTS: Ketamine and propofol suppressed phosphorylated ERK, and lithium counteracted both the phosphorylated ERK suppressant action and neuroapoptotic action of these anesthetic drugs. Ketamine 9-17 mitogen-activated protein kinase 1 Mus musculus 57-60 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. Ketamine 0-8 mitogen-activated protein kinase 1 Mus musculus 354-357 34518608-0 2021 Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway. Ketamine 0-8 mitogen-activated protein kinase 1 Mus musculus 106-109 34518608-6 2021 Treatment with ketamine significantly increased glucose uptake, extracellular lactic-acid content, expression levels of GLUT3 and p-ERK in astrocytes and glucose uptake in the prefrontal cortex (P < 0.05), and the immobility time was significantly shortened in depressive-like mice (P < 0.01). Ketamine 15-23 mitogen-activated protein kinase 1 Mus musculus 132-135 34469122-4 2021 The expressions of neuroplasticity signaling molecules of pCREB/BDNF/PSD95/Synapsin1 were upregulated at 2 h, and ERK signaling was upregulated for 3 days in the hippocampus after a single administration of Oc or ketamine. Ketamine 213-221 mitogen-activated protein kinase 1 Mus musculus 114-117 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. Ketamine 200-208 mitogen-activated protein kinase 1 Mus musculus 354-357 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. Ketamine 276-284 mitogen-activated protein kinase 1 Mus musculus 354-357 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Ketamine 6-14 mitogen-activated protein kinase 1 Mus musculus 156-193 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Ketamine 6-14 mitogen-activated protein kinase 1 Mus musculus 195-198