PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32824997-8 2020 Piceatannol was proposed to bind with VEGF, thus attenuating VEGF in activating VEGF receptor and blocking VEGF-mediated downstream signaling, including expressions of phosphorylated eNOS, Erk and Akt. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 189-192 17250586-7 2007 The ZAP-70 inhibitor piceatannol reduced CXCR3-mediated tyrosine phosphorylation of ZAP-70, LAT, PLCgamma1 and mitogen-activated protein kinase Erk and it reduced CXCL10-mediated chemotaxis of both CXCR3-transfected Jurkat T cells and normal T cells expressing CXCR3. 3,3',4,5'-tetrahydroxystilbene 21-32 mitogen-activated protein kinase 1 Homo sapiens 144-147 15240695-5 2004 TNF-induced Syk activation was abolished by piceatannol (Syk-selective inhibitor), which led to the suppression of TNF-induced activation of c- JNK, p38 MAPK, and p44/p42 MAPK. 3,3',4,5'-tetrahydroxystilbene 44-55 mitogen-activated protein kinase 1 Homo sapiens 149-152 15240695-5 2004 TNF-induced Syk activation was abolished by piceatannol (Syk-selective inhibitor), which led to the suppression of TNF-induced activation of c- JNK, p38 MAPK, and p44/p42 MAPK. 3,3',4,5'-tetrahydroxystilbene 44-55 mitogen-activated protein kinase 1 Homo sapiens 167-175 19996316-5 2010 Specifically, we identified the extracellular signal-regulated kinase (ERK) signaling pathway as a mediator of signals from FcgammaR activation to cyclin D1 expression, because cyclin D1 expression associated with FcgammaR cross-linking was attenuated by specific inhibitors of the ERK1/2 signaling pathway, PD98059 and U0126 and the spleen tyrosine kinase (Syk) inhibitor, Piceatannol. 3,3',4,5'-tetrahydroxystilbene 374-385 mitogen-activated protein kinase 1 Homo sapiens 32-69 19996316-5 2010 Specifically, we identified the extracellular signal-regulated kinase (ERK) signaling pathway as a mediator of signals from FcgammaR activation to cyclin D1 expression, because cyclin D1 expression associated with FcgammaR cross-linking was attenuated by specific inhibitors of the ERK1/2 signaling pathway, PD98059 and U0126 and the spleen tyrosine kinase (Syk) inhibitor, Piceatannol. 3,3',4,5'-tetrahydroxystilbene 374-385 mitogen-activated protein kinase 1 Homo sapiens 71-74 19796718-6 2010 Most importantly, the induction of Cxcl5, Cxcl12 and Tnfsf11 in osteoblasts by PC-3-conditioned medium was abrogated by the Stat3/5 inhibitor piceatannol, whereas the selective blockade of Stat1 and Erk activation had no effect. 3,3',4,5'-tetrahydroxystilbene 142-153 mitogen-activated protein kinase 1 Homo sapiens 199-202 14982949-3 2004 We found that Src inhibitor PP2 and Syk inhibitor piceatannol inhibited phagocytosis, macrophage-inflammatory protein-1alpha (MIP-1alpha) release, as well as phosphorylation of extracellular-regulated kinase (ERK) and Akt, consistent with Src/Syk involvement early in FcgammaR signaling. 3,3',4,5'-tetrahydroxystilbene 50-61 mitogen-activated protein kinase 1 Homo sapiens 177-207 14982949-3 2004 We found that Src inhibitor PP2 and Syk inhibitor piceatannol inhibited phagocytosis, macrophage-inflammatory protein-1alpha (MIP-1alpha) release, as well as phosphorylation of extracellular-regulated kinase (ERK) and Akt, consistent with Src/Syk involvement early in FcgammaR signaling. 3,3',4,5'-tetrahydroxystilbene 50-61 mitogen-activated protein kinase 1 Homo sapiens 209-212 11907067-6 2002 Inhibition of Syk function by kinase-deficient Syk or piceatannol blocked target cell-induced PI3K, Rac1, PAK1, mitogen-activated protein/ERK kinase, and ERK activation, perforin movement, as well as NK cytotoxicity, indicating that Syk is upstream of all these signaling events. 3,3',4,5'-tetrahydroxystilbene 54-65 mitogen-activated protein kinase 1 Homo sapiens 138-141 11907067-6 2002 Inhibition of Syk function by kinase-deficient Syk or piceatannol blocked target cell-induced PI3K, Rac1, PAK1, mitogen-activated protein/ERK kinase, and ERK activation, perforin movement, as well as NK cytotoxicity, indicating that Syk is upstream of all these signaling events. 3,3',4,5'-tetrahydroxystilbene 54-65 mitogen-activated protein kinase 1 Homo sapiens 154-157 10528214-3 1999 While ERK activation is rapid and transient, peaking at 10 min, the JNK1 activation is delayed and more sustained reaching a maximum at 2 h. ERK activation was blocked by CP 118556, indicating it is regulated by a Src-like kinase, while JNK1 was inhibited by piceatannol, revealing an upstream regulation by Syk. 3,3',4,5'-tetrahydroxystilbene 259-270 mitogen-activated protein kinase 1 Homo sapiens 141-144 22705645-6 2012 Piceatannol treatment induced p38 MAPK phosphorylation but inactivation of Akt and ERK. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 34-38 32914125-6 2020 Moreover, piceatannol significantly suppressed FA-induced oxidative stress and inhibited phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinases 1/2 (ERK1/2). 3,3',4,5'-tetrahydroxystilbene 10-21 mitogen-activated protein kinase 1 Homo sapiens 142-184 22705645-6 2012 Piceatannol treatment induced p38 MAPK phosphorylation but inactivation of Akt and ERK. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 83-86 19696164-5 2010 In contrast, 25 muM PIC inhibited deoxynucleotide triphosphate synthesis, activated Chk2 and p38-MAPK and this was accompanied by an attenuation of cancer cell growth. 3,3',4,5'-tetrahydroxystilbene 20-23 mitogen-activated protein kinase 1 Homo sapiens 93-96 21167276-0 2011 Piceatannol enhances TRAIL-induced apoptosis in human leukemia THP-1 cells through Sp1- and ERK-dependent DR5 up-regulation. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 92-95 21167276-8 2011 In conclusion, our results suggest that PIC sensitizes TRAIL-induced-apoptosis via Sp1- and ERK-dependent DR5 up-regulation. 3,3',4,5'-tetrahydroxystilbene 40-43 mitogen-activated protein kinase 1 Homo sapiens 92-95 20580678-2 2010 Piceatannol-induced apoptotic death of human leukemia U937 cells was characterized by increase in intracellular Ca(2+) concentration ([Ca(2+)]i), ERK inactivation, p38 MPAK activation, degradation of procaspase-8 and production of t-Bid. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 146-149 20580678-5 2010 Abolition of piceatannol-induced increase in [Ca(2+)]i abrogated p38 MAPK activation and up-regulation of Fas and FasL expression, but restored ERK activation and viability of piceatannol-treated cells. 3,3',4,5'-tetrahydroxystilbene 13-24 mitogen-activated protein kinase 1 Homo sapiens 144-147 20580678-7 2010 Piceatannol treatment repressed ERK-mediated c-Fos phosphorylation but evoked p38alpha MAPK-mediated c-Jun and ATF-2 phosphorylation. 3,3',4,5'-tetrahydroxystilbene 0-11 mitogen-activated protein kinase 1 Homo sapiens 32-35