PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24906890-8 2014 Thus, our results indicate that mitochondrial H2O2 is a key culprit of age-associated cognitive impairment, and that a reduction of mitochondrial H2O2 could improve cognition by maintaining mitochondrial health and enhancing CREB signaling. Hydrogen Peroxide 146-150 cAMP responsive element binding protein 1 Mus musculus 225-229 31348437-8 2019 Consistently, inhibition of PKA-CREB decreased PACAP-promoted YAP expression in primary hepatocytes culture, and made them vulnerable to H2O2 stress in vitro. Hydrogen Peroxide 137-141 cAMP responsive element binding protein 1 Mus musculus 32-36 29753754-2 2018 In addition, administration of PEP-1-PEBP1 fusion protein ameliorated H2O2-induced phosphorylation of extracellular signal-regulated kinases (ERK1/2) and facilitated the phosphorylation of cyclic-AMP response element binding protein (CREB) in HT22 cells after exposure to H2O2. Hydrogen Peroxide 70-74 cAMP responsive element binding protein 1 Mus musculus 189-232 29753754-2 2018 In addition, administration of PEP-1-PEBP1 fusion protein ameliorated H2O2-induced phosphorylation of extracellular signal-regulated kinases (ERK1/2) and facilitated the phosphorylation of cyclic-AMP response element binding protein (CREB) in HT22 cells after exposure to H2O2. Hydrogen Peroxide 70-74 cAMP responsive element binding protein 1 Mus musculus 234-238 29753754-2 2018 In addition, administration of PEP-1-PEBP1 fusion protein ameliorated H2O2-induced phosphorylation of extracellular signal-regulated kinases (ERK1/2) and facilitated the phosphorylation of cyclic-AMP response element binding protein (CREB) in HT22 cells after exposure to H2O2. Hydrogen Peroxide 272-276 cAMP responsive element binding protein 1 Mus musculus 189-232 34751416-11 2022 The results indicated that PD protected neuronal cells from H2O2 by activating CREB/Ngb signaling in neuronal cells, indicating that PD has a neuroprotective effect against neurodegenerative diseases. Hydrogen Peroxide 60-64 cAMP responsive element binding protein 1 Mus musculus 79-83 29126931-6 2018 In addition, allylguaiacol inhibited H2O2-induced damage of HT22 with increasing production of brain-derived neurotrophic factor (BDNF), phosphorylation of phosphoinositide 3-kinase (PI3K), and cyclic AMP response element-binding protein (CREB). Hydrogen Peroxide 37-41 cAMP responsive element binding protein 1 Mus musculus 194-237 29126931-6 2018 In addition, allylguaiacol inhibited H2O2-induced damage of HT22 with increasing production of brain-derived neurotrophic factor (BDNF), phosphorylation of phosphoinositide 3-kinase (PI3K), and cyclic AMP response element-binding protein (CREB). Hydrogen Peroxide 37-41 cAMP responsive element binding protein 1 Mus musculus 239-243 28302174-6 2017 RESULTS: Treatment of Y1 cells with H2O2 greatly enhanced the phosphorylation of both p38 MAPK and CREB protein. Hydrogen Peroxide 36-40 cAMP responsive element binding protein 1 Mus musculus 99-103 27284348-8 2016 In addition, allicin was demonstrated to be able to significantly ameliorate the repressed phosphoinositide 3-kinase (PI3K)/AKT and cyclic adenosine monophosphate response element-binding protein (CREB)/extracellular-signal-regulated kinase (ERK) signaling pathways by H2O2, which may also be associated with the anti-oxidative stress effects of allicin. Hydrogen Peroxide 269-273 cAMP responsive element binding protein 1 Mus musculus 197-201 23523934-3 2013 Treatment with 1mM H2O2 increased the cellular melanin content; the expression of PAH, TYR, and MITF; and the phosphorylation of CREB in B16F10 and SK-Mel-2 cells. Hydrogen Peroxide 19-23 cAMP responsive element binding protein 1 Mus musculus 129-133 17074386-6 2007 In N2a cells in calcium-free media, 200 microM H2O2 stimulated ERK and CREB phosphorylation, while preincubation with thapsigargin prevented these enhancements. Hydrogen Peroxide 47-51 cAMP responsive element binding protein 1 Mus musculus 71-75 18814142-4 2009 Exposure to adrenaline not only increased cAMP formation, phosphorylation of cAMP responsive element (CRE) binding protein (CREB) on serine133 and CRE reporter activity in a manner sensitive to propranolol, but also rendered C3H10T1/2 cells resistant to the cytotoxicity of hydrogen peroxide, but not of either 2,4-dinitirophenol or tunicamycin. Hydrogen Peroxide 274-291 cAMP responsive element binding protein 1 Mus musculus 124-128 17074386-0 2007 Calcium release by ryanodine receptors mediates hydrogen peroxide-induced activation of ERK and CREB phosphorylation in N2a cells and hippocampal neurons. Hydrogen Peroxide 48-65 cAMP responsive element binding protein 1 Mus musculus 96-100 17074386-7 2007 These combined results strongly suggest that H2O2 promotes ryanodine receptors redox modification; the resulting calcium release signals, by enhancing ERK activity, would increase CREB phosphorylation. Hydrogen Peroxide 45-49 cAMP responsive element binding protein 1 Mus musculus 180-184 17074386-3 2007 In mouse hippocampal slices, H2O2 (1 microM) also stimulated ERK and CREB phosphorylation. Hydrogen Peroxide 29-33 cAMP responsive element binding protein 1 Mus musculus 69-73 16164634-9 2005 Inhibition of ERK and CREB abrogates survival after 0.5 mmol/L H(2)O(2) treatment, while overexpression of CREB ameliorates necrotic death caused by 1 mmol/L H(2)O(2). Hydrogen Peroxide 158-166 cAMP responsive element binding protein 1 Mus musculus 107-111 17074386-5 2007 In N2a cells, the ERK kinase inhibitor U0126 suppressed ERK phosphorylation and abolished the stimulation of CREB phosphorylation produced by H2O2, suggesting that H2O2 enhanced CREB phosphorylation via ERK activation. Hydrogen Peroxide 142-146 cAMP responsive element binding protein 1 Mus musculus 109-113 17074386-5 2007 In N2a cells, the ERK kinase inhibitor U0126 suppressed ERK phosphorylation and abolished the stimulation of CREB phosphorylation produced by H2O2, suggesting that H2O2 enhanced CREB phosphorylation via ERK activation. Hydrogen Peroxide 142-146 cAMP responsive element binding protein 1 Mus musculus 178-182 17074386-5 2007 In N2a cells, the ERK kinase inhibitor U0126 suppressed ERK phosphorylation and abolished the stimulation of CREB phosphorylation produced by H2O2, suggesting that H2O2 enhanced CREB phosphorylation via ERK activation. Hydrogen Peroxide 164-168 cAMP responsive element binding protein 1 Mus musculus 109-113 17074386-5 2007 In N2a cells, the ERK kinase inhibitor U0126 suppressed ERK phosphorylation and abolished the stimulation of CREB phosphorylation produced by H2O2, suggesting that H2O2 enhanced CREB phosphorylation via ERK activation. Hydrogen Peroxide 164-168 cAMP responsive element binding protein 1 Mus musculus 178-182 16164634-11 2005 Binding of phosphorylated CREB to a CREB oligonucleotide was significantly increased after 0.5 mmol/L H(2)O(2) but decreased after 1 mmol/L H(2)O(2). Hydrogen Peroxide 102-110 cAMP responsive element binding protein 1 Mus musculus 26-30 16164634-11 2005 Binding of phosphorylated CREB to a CREB oligonucleotide was significantly increased after 0.5 mmol/L H(2)O(2) but decreased after 1 mmol/L H(2)O(2). Hydrogen Peroxide 102-110 cAMP responsive element binding protein 1 Mus musculus 36-40 16164634-12 2005 Similarly, CREB-mediated transcription was significantly increased after 0.5 mmol/L H(2)O(2) treatment, while 1 mmol/L H(2)O(2) inhibited it. Hydrogen Peroxide 84-92 cAMP responsive element binding protein 1 Mus musculus 11-15 16164634-13 2005 Interestingly, transcription from the CREB-driven bcl-2 promoter was unchanged after 0.5 mmol/L but decreased after 1 mmol/L H(2)O(2) treatment in agreement with Western blot studies. Hydrogen Peroxide 125-133 cAMP responsive element binding protein 1 Mus musculus 38-42