PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29170390-4 2017 Stimulation with CD3/CD28, PMA/ionomycin, or latency reversing agents prostratin and SAHA, yielded increased phosphorylation of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells across two in vitro latency models. Ionomycin 31-40 mitogen-activated protein kinase 1 Homo sapiens 142-145 20432446-0 2010 Low-concentration heparin suppresses ionomycin-activated CAMK-II/EGF receptor- and ERK-mediated signaling in mesangial cells. Ionomycin 37-46 mitogen-activated protein kinase 1 Homo sapiens 83-86 28955885-5 2016 Ionomycin increased [Ca2+]i and activation of Ras ERK pathway, and MKP-1 induction, in the presence, but not in the absence, of LPS. Ionomycin 0-9 mitogen-activated protein kinase 1 Homo sapiens 52-55 22200849-6 2012 In addition, Jurkat T cells, transfected with various expression plasmids and/or stimulated with TPA, UV or ionomycin strongly induced the c-Jun N-terminal kinase (JNK) and p38, whereas the extracellular signal-regulated kinase (ERK)-1/2 kinase pathway was weekly activated. Ionomycin 108-117 mitogen-activated protein kinase 1 Homo sapiens 173-176 20432446-5 2010 Low-dose heparin suppresses the ionomycin-dependent phosphorylation of EGFR, c-Src, and Erk 1/2, but not of CaMK-II, whereas inhibition of activated CaMK-II reduces phosphorylation of EGFR, c-Src, and Erk. Ionomycin 32-41 mitogen-activated protein kinase 1 Homo sapiens 88-91 20045933-9 2010 Pre-incubation with matrine or ionomycin could also shorten extracellular signal-regulated kinase (ERK) and suppress c-Jun NH(2)-terminal kinase (JNK) expression on the anergic Jurkat cells when the cells were stimulated with anti-OKT-3 plus anti-CD28 antibodies. Ionomycin 31-40 mitogen-activated protein kinase 1 Homo sapiens 60-97 20045933-9 2010 Pre-incubation with matrine or ionomycin could also shorten extracellular signal-regulated kinase (ERK) and suppress c-Jun NH(2)-terminal kinase (JNK) expression on the anergic Jurkat cells when the cells were stimulated with anti-OKT-3 plus anti-CD28 antibodies. Ionomycin 31-40 mitogen-activated protein kinase 1 Homo sapiens 99-102 12447987-7 2003 Furthermore, ERK but not JNK phosphorylation was evidenced in both conditions, ionomycin and hypoxia. Ionomycin 79-88 mitogen-activated protein kinase 1 Homo sapiens 13-16 19766325-8 2009 Patients with HAM/TSP had a higher p38/ERK ratio (p<0.05) associated with a reduced response to mitogens (phytohaemagglutinin or PMA+ionomycin) (p<0.001) and higher sensitivity to dexamethasone (p<0.05). Ionomycin 136-145 mitogen-activated protein kinase 1 Homo sapiens 39-42 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. Ionomycin 147-156 mitogen-activated protein kinase 1 Homo sapiens 167-170 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. Ionomycin 147-156 mitogen-activated protein kinase 1 Homo sapiens 249-252 12447987-8 2003 PD98059, an inhibitor of the ERK pathway as well as a ERK1 dominant negative mutant also blocked HIF-1 activation by hypoxia and by ionomycin. Ionomycin 132-141 mitogen-activated protein kinase 1 Homo sapiens 29-32 11880263-2 2002 Previously, we demonstrated that ionomycin-, angiotensin II-, and thrombin-induced activation of extracellular signal-regulated kinase (ERK)1/2 in VSM cells was attenuated by pretreatment with KN-93, a selective inhibitor of the multifunctional Ca(2+)/calmodulin-dependent protein kinase (CaM kinase II). Ionomycin 33-42 mitogen-activated protein kinase 1 Homo sapiens 97-143 12485909-8 2002 PD98059, an inhibitor of the ERK pathway, but not KN-93, an inhibitor of calmodulin kinases II and IV, also blocked HIF-1 activation by hypoxia and by ionomycin. Ionomycin 151-160 mitogen-activated protein kinase 1 Homo sapiens 29-32 11489986-8 2001 PMA and ionomycin restored proliferation and IL-2 production in AINR cells, indicating a signaling defect upstream of Ras and protein kinase C. Inhibitors of ERK (PD98059) and of p38 kinase (SB202190) blocked IL-2 mRNA expression and proliferation of both peptide-MHC/B7-1/ICAM-1-stimulated normal cells and PMA/ionomycin-stimulated AINR cells. Ionomycin 8-17 mitogen-activated protein kinase 1 Homo sapiens 158-161 11750912-8 2002 PD098,029 and U0126 showed a small dose-dependent inhibitory effect on ionomycin-induced glutamate release, at concentrations shown to inhibit ionomycin-stimulated ERK phosphorylation. Ionomycin 71-80 mitogen-activated protein kinase 1 Homo sapiens 164-167 11750912-8 2002 PD098,029 and U0126 showed a small dose-dependent inhibitory effect on ionomycin-induced glutamate release, at concentrations shown to inhibit ionomycin-stimulated ERK phosphorylation. Ionomycin 143-152 mitogen-activated protein kinase 1 Homo sapiens 164-167 11489986-8 2001 PMA and ionomycin restored proliferation and IL-2 production in AINR cells, indicating a signaling defect upstream of Ras and protein kinase C. Inhibitors of ERK (PD98059) and of p38 kinase (SB202190) blocked IL-2 mRNA expression and proliferation of both peptide-MHC/B7-1/ICAM-1-stimulated normal cells and PMA/ionomycin-stimulated AINR cells. Ionomycin 8-17 mitogen-activated protein kinase 1 Homo sapiens 179-182 11489986-8 2001 PMA and ionomycin restored proliferation and IL-2 production in AINR cells, indicating a signaling defect upstream of Ras and protein kinase C. Inhibitors of ERK (PD98059) and of p38 kinase (SB202190) blocked IL-2 mRNA expression and proliferation of both peptide-MHC/B7-1/ICAM-1-stimulated normal cells and PMA/ionomycin-stimulated AINR cells. Ionomycin 312-321 mitogen-activated protein kinase 1 Homo sapiens 179-182 11164895-11 2000 Treatment of Jurkat cells with the MEK inhibitor PD98059 blocked ionomycin-induced ERK activation, but not the shift in the mobility of p56(Lck). Ionomycin 65-74 mitogen-activated protein kinase 1 Homo sapiens 83-86 10373510-1 1999 The full-length versions of the Ras-specific exchange factors Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2), which are expressed in brain and a restricted number of other organs, possess an ionomycin-dependent activation of Erk mitogen-activated protein kinase activity in 293T cells (C. L. Farnsworth et al., Nature 376:524-527, 1995; N. P. Fam et al., Mol. Ionomycin 180-189 mitogen-activated protein kinase 1 Homo sapiens 214-217 10652349-5 2000 Moreover, we found that overexpression of JNK, ERK, or p38 is able to block ionomycin-induced NFATc nuclear translocation, whereas treatment of cells with both PD98059 and SB202190, which inhibit MAPK/SAPK signaling pathways, is sufficient to trigger NFATc nuclear localization. Ionomycin 76-85 mitogen-activated protein kinase 1 Homo sapiens 47-50 10652349-5 2000 Moreover, we found that overexpression of JNK, ERK, or p38 is able to block ionomycin-induced NFATc nuclear translocation, whereas treatment of cells with both PD98059 and SB202190, which inhibit MAPK/SAPK signaling pathways, is sufficient to trigger NFATc nuclear localization. Ionomycin 76-85 mitogen-activated protein kinase 1 Homo sapiens 196-200 10373510-12 1999 Both mutants were impaired in their ability to mediate ionomycin-dependent Erk activity in 293T cells. Ionomycin 55-64 mitogen-activated protein kinase 1 Homo sapiens 75-78 10373510-13 1999 In the absence of ionomycin, 293T cells expressing wild-type GRF1 contained much higher levels of Ras-GTP than control cells; the increase in Erk activity induced by ionomycin in the GRF1-expressing cells also induced a concomitant increase in Raf kinase activity, but without a further increase in the level Ras-GTP. Ionomycin 166-175 mitogen-activated protein kinase 1 Homo sapiens 142-145 9553058-2 1998 We have identified a distal IL-2 enhancer regulated by the Raf-MEK-ERK signaling pathway, which can be induced by TPA/ionomycin treatment. Ionomycin 118-127 mitogen-activated protein kinase 1 Homo sapiens 67-70 9553058-4 1998 TPA/ionomycin treatment of T cells stimulates both mitogen-activated ERK, as well as the stress-activated mitogen-activated protein kinase family members JNK/SAPK and p38. Ionomycin 4-13 mitogen-activated protein kinase 1 Homo sapiens 69-72 9553058-7 1998 Furthermore, the JNK/SAPK signaling pathway cooperates with the Raf-MEK-ERK cascade in TPA/ionomycin-induced DSE activity. Ionomycin 91-100 mitogen-activated protein kinase 1 Homo sapiens 72-75 9507015-10 1998 The focal adhesion dependence of IL-1-induced ERK activation and c-fos expression could be circumvented in cells plated on poly-L-lysine by simultaneous incubation with IL-1 and the calcium ionophore ionomycin. Ionomycin 200-209 mitogen-activated protein kinase 1 Homo sapiens 46-49 33182021-11 2020 NEAT1 expression in Jurkat cells was induced by PMA/ionomycin stimulation upon activation of the TCR-p38 pathway. Ionomycin 52-61 mitogen-activated protein kinase 1 Homo sapiens 101-104 9933633-5 1999 Here we show that extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38-mitogen-activated protein kinase (MAPK) pathways control the transcription and synthesis of TNF-alpha in A3.01 T cells that produce the cytokine upon T cell activation by costimulation with 12-O-tetradecanoylphorbol-13-acetate (TPA) and ionomycin. Ionomycin 339-348 mitogen-activated protein kinase 1 Homo sapiens 18-55 9736697-4 1998 Inhibition of Stat3 DNA-binding activity and tyrosine phosphorylation by PMA, ionomycin, and granulocyte/macrophage-colony-stimulating factor was reversed when activation of the extracellular signal-regulated kinase (ERK) group of MAPKs was blocked by using specific kinase inhibitors. Ionomycin 78-87 mitogen-activated protein kinase 1 Homo sapiens 178-215 9736697-4 1998 Inhibition of Stat3 DNA-binding activity and tyrosine phosphorylation by PMA, ionomycin, and granulocyte/macrophage-colony-stimulating factor was reversed when activation of the extracellular signal-regulated kinase (ERK) group of MAPKs was blocked by using specific kinase inhibitors. Ionomycin 78-87 mitogen-activated protein kinase 1 Homo sapiens 217-220 9674701-4 1998 Although both JNK and ERK activation by phorbol 12-myristate 13-acetate (PMA) plus ionomycin were suppressed by curcumin, the JNK pathway was more sensitive. Ionomycin 83-92 mitogen-activated protein kinase 1 Homo sapiens 22-25 8898934-7 1996 CA-MEK1 expression led to constitutive ERK activation, which acted synergystically with ionomycin treatment to stimulate cytokine production. Ionomycin 88-97 mitogen-activated protein kinase 1 Homo sapiens 39-42 33023539-5 2020 The expression of Egr2 and FasL, and the phosphorylation of AKT and ERK, after ionomycin and PMA co-stimulation, was detected, while the Ca2+ mobilization stimulated by K+ solution was determined. Ionomycin 79-88 mitogen-activated protein kinase 1 Homo sapiens 68-71