PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 348275-0 1978 Effects of the spoT and relA mutation on the synthesis and accumulation of ppGpp and RNA during glucose starvation. Glucose 96-103 RELA proto-oncogene, NF-kB subunit Homo sapiens 24-28 34129225-0 2021 Metformin reverses the effects of high glucose on human dermal fibroblasts of aged skin via downregulating RELA/p65 expression. Glucose 39-46 RELA proto-oncogene, NF-kB subunit Homo sapiens 107-111 34129225-0 2021 Metformin reverses the effects of high glucose on human dermal fibroblasts of aged skin via downregulating RELA/p65 expression. Glucose 39-46 RELA proto-oncogene, NF-kB subunit Homo sapiens 112-115 34129225-8 2021 The expression of COL3A1 and RELA/p65 were upregulated (P < 0.01 for COL3A1), and percentage of late apoptotic cells increased significantly by HG without metformin (P < 0.001) while it decreased in two concentrations of metformin dramatically compared with 5.5 mM glucose (P < 0.01 for expressions and < 0.001 for apoptosis). Glucose 265-272 RELA proto-oncogene, NF-kB subunit Homo sapiens 29-33 34129225-8 2021 The expression of COL3A1 and RELA/p65 were upregulated (P < 0.01 for COL3A1), and percentage of late apoptotic cells increased significantly by HG without metformin (P < 0.001) while it decreased in two concentrations of metformin dramatically compared with 5.5 mM glucose (P < 0.01 for expressions and < 0.001 for apoptosis). Glucose 265-272 RELA proto-oncogene, NF-kB subunit Homo sapiens 34-37 35607953-4 2022 Our results indicated that high glucose increases monocyte/endothelial adhesion, vascular cell adhesion molecule-1 (VCAM-1) expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Glucose 32-39 RELA proto-oncogene, NF-kB subunit Homo sapiens 139-142 33028948-6 2020 Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Glucose 39-46 RELA proto-oncogene, NF-kB subunit Homo sapiens 133-136 187574-1 1977 The presence of a relA mutant allele affects the kinetics of cyclic adenosine 3",5"-monophosphate accumulation during downshift from glucose to succinate. Glucose 133-140 RELA proto-oncogene, NF-kB subunit Homo sapiens 18-22 31447391-4 2019 Here, we show that, under low glucose, GDH1 is phosphorylated at serine (S) 384 and interacts with RelA and IKKbeta. Glucose 30-37 RELA proto-oncogene, NF-kB subunit Homo sapiens 99-103 31544029-0 2019 SUMOylation and deacetylation affect NF-kappaB p65 activity induced by high glucose in human lens epithelial cells. Glucose 76-83 RELA proto-oncogene, NF-kB subunit Homo sapiens 47-50 31544029-1 2019 AIM: To explore the effects of IkappaBalpha SUMOylation and NF-kappaB p65 deacetylation on NF-kappaB p65 activity induced by high glucose in cultured human lens epithelial cells (HLECs). Glucose 130-137 RELA proto-oncogene, NF-kB subunit Homo sapiens 101-104 31544029-11 2019 SUMO1 or SIRT1 overexpression and MG132 or RSV treatment affected the nuclear expression and activity of IkappaBalpha and NF-kappaB p65 under high glucose condition. Glucose 147-154 RELA proto-oncogene, NF-kB subunit Homo sapiens 122-135 31544029-12 2019 CONCLUSION: IkappaBalpha SUMOylation and NF-kappaB p65 deacetylation affect NF-kappaB p65 activity in cultured HLECs under high glucose, and presumably play a significant role in controlling diabetic cataract. Glucose 128-135 RELA proto-oncogene, NF-kB subunit Homo sapiens 86-89 31544029-10 2019 IkappaBalpha nuclear expression was attenuated and NF-kappaB p65 was opposite under high glucose, while IkappaBalpha and NF-kappaB p65 location was transferred to the nucleus. Glucose 89-96 RELA proto-oncogene, NF-kB subunit Homo sapiens 61-64 29717634-6 2018 In the present study, we found that activated Notch1 enhanced nuclear p65 levels, resulting in an increase in glucose metabolism through the upregulation of glycolytic factors, including GLUT3. Glucose 110-117 RELA proto-oncogene, NF-kB subunit Homo sapiens 70-73 31167690-12 2019 Compared with the blank group, the protein levels of NF-kappaBp65, p-IkappaBalpha, IKKalpha, MCP-1 and ICAM-1 increased in the high glucose group, while the protein levels above decreased in the PDTC group compared with the high glucose group. Glucose 132-139 RELA proto-oncogene, NF-kB subunit Homo sapiens 53-65 31167690-13 2019 Compared with the blank group, the proportion of positive cells of NF-kappaBp65 and alpha-SMA increased and the proportion of positive cells of E-cadherin decreased in the high glucose group. Glucose 177-184 RELA proto-oncogene, NF-kB subunit Homo sapiens 67-79 30706373-6 2019 Additionally, Western blot results showed that down-regulation of miR-377 restrained high glucose and hypoxia-induced protein expressions of p-IkappaBalpha, nuclear P65 and p-P65. Glucose 90-97 RELA proto-oncogene, NF-kB subunit Homo sapiens 165-168 30706373-6 2019 Additionally, Western blot results showed that down-regulation of miR-377 restrained high glucose and hypoxia-induced protein expressions of p-IkappaBalpha, nuclear P65 and p-P65. Glucose 90-97 RELA proto-oncogene, NF-kB subunit Homo sapiens 175-178 30906223-7 2019 The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1beta (IL-1beta), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR. Glucose 29-36 RELA proto-oncogene, NF-kB subunit Homo sapiens 192-195 29853786-0 2018 Characterization of Site-Specific Phosphorylation of NF-kappaB p65 in Retinal Cells in Response to High Glucose and Cytokine Polarization. Glucose 104-111 RELA proto-oncogene, NF-kB subunit Homo sapiens 63-66 29853786-5 2018 Since dysregulation of NF-kappaB has been linked to chronic inflammation, the current study examines site-specific p65 phosphorylation in retinal cells exposed to high glucose and investigates the effects of cytokine polarization. Glucose 168-175 RELA proto-oncogene, NF-kB subunit Homo sapiens 115-118 29853786-6 2018 Methods: Phosphorylation of NF-kappaB p65 sites was examined in human primary retinal endothelial cells (HREC) and MIO-M1 Muller cells after exposure to high glucose (HG) and pro- or anti-inflammatory cytokines. Glucose 158-165 RELA proto-oncogene, NF-kB subunit Homo sapiens 38-41 28976943-9 2017 High glucose-induced secretion of IL-8, TNF-alpha, ICAM-1, and VCAM-1 was reduced, and translocation of the p65 subunit of NF-kappaB to the endothelial cell nucleus was inhibited by EOFAZ. Glucose 5-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 108-132 29373048-7 2018 RESULTS: Compared with control group, the expression of p-TAK1, TAB1, NF-kappaB p65 were significantly higher in high glucose group (P < 0.05). Glucose 118-125 RELA proto-oncogene, NF-kB subunit Homo sapiens 70-83 28976943-11 2017 EOFAZ reduced high glucose-induced p65/DNA binding to inhibit NF-kappaB activation. Glucose 19-26 RELA proto-oncogene, NF-kB subunit Homo sapiens 35-38 23423566-8 2013 LSD1 siRNA ameliorated the glucose-induced decrease in H3K9me2 and increase in p65 at the MMP-9 promoter, and prevented MMP-9 activation, mitochondrial damage, and cell apoptosis. Glucose 27-34 RELA proto-oncogene, NF-kB subunit Homo sapiens 79-82 25616369-3 2015 The results of such a study revealed for the first time that NFkB induced miR-2909 RNomics is crucial for the regulation of RelA translocation within human PBMCs exposed to high glucose thereby enabling these epigenetically programmed cells to tailor immune response involving genes coding for CCL5; IFN-gamma and IL-17. Glucose 178-185 RELA proto-oncogene, NF-kB subunit Homo sapiens 124-128 24477458-8 2014 Moreover, downregulation of p65/RelA or HIF-1alpha expression in these cells restored normal glucose uptake, lactate production, mitochondrial respiration and glycolytic protein expression. Glucose 93-100 RELA proto-oncogene, NF-kB subunit Homo sapiens 28-31 24477458-8 2014 Moreover, downregulation of p65/RelA or HIF-1alpha expression in these cells restored normal glucose uptake, lactate production, mitochondrial respiration and glycolytic protein expression. Glucose 93-100 RELA proto-oncogene, NF-kB subunit Homo sapiens 32-36 24035224-5 2014 Sauchinone inhibited the phosphorylation and degradation of IkappaB-alpha, as well as the nuclear translocation of nuclear factor kappa B (NF-kappaB) p65 caused by the stimulation of high glucose. Glucose 188-195 RELA proto-oncogene, NF-kB subunit Homo sapiens 150-153 24035224-7 2014 The effects of sauchinone on the high glucose-induced expression of VCAM-1 and ICAM-1 and nuclear translocation of NF-kappaB p65 were partially reversed by transfection of the cells with HO-1 siRNA. Glucose 38-45 RELA proto-oncogene, NF-kB subunit Homo sapiens 115-128 24124747-6 2013 And NF-kappaB p65 and phosphorylation of NF-kappaB p65 (P-NF-kappaBp65) in podocytes cultured in high glucose were detected at different timepoints. Glucose 102-109 RELA proto-oncogene, NF-kB subunit Homo sapiens 4-17 24124747-6 2013 And NF-kappaB p65 and phosphorylation of NF-kappaB p65 (P-NF-kappaBp65) in podocytes cultured in high glucose were detected at different timepoints. Glucose 102-109 RELA proto-oncogene, NF-kB subunit Homo sapiens 41-54 23755819-6 2013 RESULTS: (1) Podocytes with high glucose could activate the NF-kappaBp65 signaling pathway. Glucose 33-40 RELA proto-oncogene, NF-kB subunit Homo sapiens 60-72 23755819-9 2013 The up-regulated protein expression of p-NF-kappaBp65 induced with high glucose was significantly inhibited by PDTC and A771726 (both P < 0.05). Glucose 72-79 RELA proto-oncogene, NF-kB subunit Homo sapiens 41-53 23755819-11 2013 (2) High glucose-induced podocyte activated the NF-kappaBp65 signaling path. Glucose 9-16 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-60 23755819-14 2013 (3) Immunofluorescent assay of high glucose-induced podocyte cytoskeleton showed disorderly F-actin and a disappearance of tensile fiber after 72 h. CONCLUSION: Active leflunomide metabolite A771726 may protect podocytes through blocking the high glucose-induced signaling pathway of NF-kappaBp65. Glucose 36-43 RELA proto-oncogene, NF-kB subunit Homo sapiens 284-296 20599797-8 2010 Furthermore, Set7 knockdown prevents glucose-induced p65 expression. Glucose 37-44 RELA proto-oncogene, NF-kB subunit Homo sapiens 53-56 23026048-5 2012 Also, high glucose increased nuclear factor kappa B (NF-kappaB) p65 nuclear activity, tumor necrosis factor-alpha (TNF-alpha) and interleukin-lbeta (IL-1beta) levels. Glucose 11-18 RELA proto-oncogene, NF-kB subunit Homo sapiens 64-67 22659134-7 2012 High glucose increased nuclear translocation of p65 without serine phosphorylation of IkappaBalpha and without degradation of IkappaBalpha, but with an increase in tyrosine phosphorylation of IkappaBalpha that may account for the activation of NF-kappaB. Glucose 5-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-51 22659134-8 2012 Both Syk inhibitors and Syk-siRNA attenuated high glucose-induced IkappaBalpha tyrosine phosphorylation and p65 nuclear translocation. Glucose 50-57 RELA proto-oncogene, NF-kB subunit Homo sapiens 108-111 22045316-6 2012 Compared with placebo, DHEA administration raised levels of testosterone, androstenedione, and DHEA-S, increased the percent change in fasting and glucose-challenged activated NF-kappaB, p65, p105, TNFalpha, and IL-1beta RNA and p65 protein, and decreased the percent change in fasting and glucose-challenged IkappaB protein. Glucose 147-154 RELA proto-oncogene, NF-kB subunit Homo sapiens 229-232 18650365-6 2008 High glucose increased TLR expression, myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, and nuclear factor-kappaB (NF-kappaB) p65-dependent activation in THP-1 cells. Glucose 5-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 156-159 19208907-6 2009 Furthermore, glucose was shown to have other epigenetic effects, including the suppression of H3K9m2 and H3K9m3 methylation on the p65 promoter. Glucose 13-20 RELA proto-oncogene, NF-kB subunit Homo sapiens 131-134 20200188-9 2010 Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. Glucose 42-49 RELA proto-oncogene, NF-kB subunit Homo sapiens 185-188 18353872-4 2008 High glucose increased nuclear translocation of p65 and also increased NF-kappaB DNA binding activity. Glucose 5-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-51 18167242-5 2007 Glucose dose- and time-dependently reduced the protein expression of IkappaBalpha in the PMCs and increased the p65 expression in the nucleus, and accelerated the PMCs to express MCP-1 mRNA and protein (P < 0.05 and P < 0.01). Glucose 0-7 RELA proto-oncogene, NF-kB subunit Homo sapiens 112-115 18353872-7 2008 High glucose increased the generation of ROS, whereas both alpha-lipoic acid and N-acetylcysteine scavenged the ROS and decreased high glucose-induced tyrosine phosphorylation of IkappaBalpha, nuclear translocation of p65, and NF-kappaB DNA binding activity. Glucose 135-142 RELA proto-oncogene, NF-kB subunit Homo sapiens 218-221 18353872-8 2008 Protein kinase C pseudosubstrate inhibited high glucose-induced ROS production, tyrosine phosphorylation of IkappaBalpha, and nuclear translocation of p65. Glucose 48-55 RELA proto-oncogene, NF-kB subunit Homo sapiens 151-154 18353872-9 2008 Both BAY 61-3606, a specific inhibitor of Syk protein-tyrosine kinase, and small interfering RNA directed against Syk inhibited high glucose-induced tyrosine phosphorylation of IkappaBalpha as well as p65 nuclear translocation. Glucose 133-140 RELA proto-oncogene, NF-kB subunit Homo sapiens 201-204 12419773-5 2003 The signaling cascade activated by glucose-induced oxidant stress included the heterodimeric redox-sensitive transcription factor NF-kappaB, which exhibited an upregulation in p65/c-Rel binding activity and suppressed binding activity of the p50 dimer. Glucose 35-42 RELA proto-oncogene, NF-kB subunit Homo sapiens 176-179 12086956-6 2002 Pericytes exposed to high glucose showed increased expression of Bax and of tumor necrosis factor-alpha, which were prevented by the NF-kappaB inhibitors and mimicked by transfection with the p65 subunit of NF-kappaB, and failed to increase the levels of the NF-kappaB-dependent inhibitors of apoptosis. Glucose 26-33 RELA proto-oncogene, NF-kB subunit Homo sapiens 192-216 9835032-2 1998 In the relA+ strain, Act production was inversely related to specific growth rate in continuous cultures limited by glucose, ammonium, or phosphate, while Red biosynthesis was optimal at 0.05 h-1 regardless of the specific nutrient limitation. Glucose 116-123 RELA proto-oncogene, NF-kB subunit Homo sapiens 7-11 9835032-3 1998 Production of Act and Red in the relA mutant was lower than that of the parental strain, particularly under conditions of glucose- and ammonium-limitation, indicating an important and general role for ppGpp in determining the onset of the antibiotic biosynthesis under conditions of nutrient limitation. Glucose 122-129 RELA proto-oncogene, NF-kB subunit Homo sapiens 33-37 33782381-7 2021 In vitro, high glucose increased endothelial inflammatory factor levels and p65 phosphorylation by augmenting PTP1B expression in human umbilical vein endothelial cells (HUVECs). Glucose 15-22 RELA proto-oncogene, NF-kB subunit Homo sapiens 76-79 33782381-9 2021 CREB overexpression and KMT5A overexpression both inhibited high glucose-induced PTP1B expression, p65 phosphorylation and endothelial inflammatory factor levels. Glucose 65-72 RELA proto-oncogene, NF-kB subunit Homo sapiens 99-102 34494136-14 2021 Analysis of mRNA expression in VICs confirmed these findings; glucose caused a 6.9-fold increase in expression of RELA (NF-kappaB p65 subunit), with the ROS and NF-kappaB inhibitor reducing the raised expression of RELA by 1.8- and 3.2-fold, respectively. Glucose 62-69 RELA proto-oncogene, NF-kB subunit Homo sapiens 114-118 34494136-14 2021 Analysis of mRNA expression in VICs confirmed these findings; glucose caused a 6.9-fold increase in expression of RELA (NF-kappaB p65 subunit), with the ROS and NF-kappaB inhibitor reducing the raised expression of RELA by 1.8- and 3.2-fold, respectively. Glucose 62-69 RELA proto-oncogene, NF-kB subunit Homo sapiens 120-133