PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28803777-3 2017 We found that p53 transcriptionally represses paraoxonase 2 (PON2), which regulates GLUT1-mediated glucose transport via stomatin. Glucose 99-106 tumor protein p53 Homo sapiens 14-17 28131915-0 2017 ROCK1/p53/NOXA signaling mediates cardiomyocyte apoptosis in response to high glucose in vitro and vivo. Glucose 78-85 tumor protein p53 Homo sapiens 6-9 28149884-7 2016 So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress. Glucose 63-70 tumor protein p53 Homo sapiens 11-14 28104581-0 2017 High glucose stimulates proliferation and inhibits apoptosis of non-small-cell lung cancer cells by JNK-mediated downregulation of p53 pathway. Glucose 5-12 tumor protein p53 Homo sapiens 131-134 28230866-0 2017 Oridonin induces autophagy via inhibition of glucose metabolism in p53-mutated colorectal cancer cells. Glucose 45-52 tumor protein p53 Homo sapiens 67-70 27446805-9 2016 The interplay between the IGF1 and p53 pathways is also of major relevance in terms of metabolic regulation, including glucose transport and glycolysis. Glucose 119-126 tumor protein p53 Homo sapiens 35-38 27582538-8 2016 Applying metabolic inhibitors in the presence and absence of D-glucose and L-glutamine in cell culture experiments resulted in higher glycolytic and mitochondrial activity in TP53 mutant breast cancer cell lines. Glucose 61-70 tumor protein p53 Homo sapiens 175-179 27109893-10 2016 Pre-mature senescence induced due to limited glucose availability was found to be regulated by nuclear translocated p53 which, in turn, induced p21, pAkt and pERK. Glucose 45-52 tumor protein p53 Homo sapiens 116-119 27789249-0 2016 Ang-(1-7) inhibited mitochondrial fission in high-glucose-induced podocytes by upregulation of miR-30a and downregulation of Drp1 and p53. Glucose 50-57 tumor protein p53 Homo sapiens 134-137 27499152-1 2016 PURPOSE: p53, widely known as a tumor-suppressing gene, has recently been reported to regulate glucose metabolism in human cancers through the synthesis of cytochrome c oxidase 2 (SCO2), cytochrome c oxidase complex (COX), and TP53-induced glycolysis and apoptosis regulator (TIGAR). Glucose 95-102 tumor protein p53 Homo sapiens 9-12 26342198-9 2015 Furthermore, blockage of the beta1-integrin/FAK/PI3K/AKT/mTOR pathway by siRNA or specific chemical inhibitors, or rescue of p53 activation can partially reverse the switch of glucose metabolism and inhibit the migration of Twist-overexpressing MCF10A cells and Twist-positive breast cancer cells. Glucose 176-183 tumor protein p53 Homo sapiens 125-128 27221738-2 2016 We investigated role of microRNAs in regulating p53-p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis. Glucose 72-79 tumor protein p53 Homo sapiens 48-51 26924930-6 2016 Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Glucose 38-45 tumor protein p53 Homo sapiens 26-29 26764206-6 2016 Extending our observation of p53 inhibition on proximal tubule glucose tracer uptake, we demonstrated by intravital MPM that pharmacological inhibition of p53 diminishes mitochondrial potential difference. Glucose 63-70 tumor protein p53 Homo sapiens 29-32 26764206-6 2016 Extending our observation of p53 inhibition on proximal tubule glucose tracer uptake, we demonstrated by intravital MPM that pharmacological inhibition of p53 diminishes mitochondrial potential difference. Glucose 63-70 tumor protein p53 Homo sapiens 155-158 26629991-11 2015 In conclusion, short-term high glucose stimulation could induce sustained endothelial senescence via SIRT1/p300/p53/p21 pathway. Glucose 31-38 tumor protein p53 Homo sapiens 112-115 26342198-10 2015 Thus, our data suggest that Twist promotes reprogramming of glucose metabolism in MCF10A-Twist cells and Twist-positive breast cancer cells via activation of the beta1-integrin/FAK/PI3K/AKT/mTOR pathway and inhibition of the p53 pathway. Glucose 60-67 tumor protein p53 Homo sapiens 225-228 25221641-0 2014 PTEN deficiency and mutant p53 confer glucose-addiction to thyroid cancer cells: impact of glucose depletion on cell proliferation, cell survival, autophagy and cell migration. Glucose 38-45 tumor protein p53 Homo sapiens 27-30 26211519-3 2015 This in combination with the glucose oxidation at the carbon nanotube/Meldola"s blue/glucose dehydrogenase bioanode can result in a current/or power decrease of BFC in the presence of wild-type p53. Glucose 29-36 tumor protein p53 Homo sapiens 194-197 25483438-12 2015 This attenuated high-glucose-induced ROS generation, ER stress signaling, and p53 expression. Glucose 21-28 tumor protein p53 Homo sapiens 78-81 25463242-7 2015 Data revealed that high glucose, FFA, and hypoxia down-regulated hCdc14A expression remarkably, and also affected the expression of other cell cycle-related proteins such as cyclin B, cyclin D, cyclin E, and p53. Glucose 24-31 tumor protein p53 Homo sapiens 208-211 25064493-0 2014 Indoleamine 2,3-dioxygenase increases p53 levels in alloreactive human T cells, and both indoleamine 2,3-dioxygenase and p53 suppress glucose uptake, glycolysis and proliferation. Glucose 134-141 tumor protein p53 Homo sapiens 121-124 25071015-9 2014 In the early setting, data suggested longer disease free survival in p53 negative patients in the lowest glucose category (p=0.053). Glucose 105-112 tumor protein p53 Homo sapiens 69-72 26113084-7 2015 [18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors. Glucose 55-62 tumor protein p53 Homo sapiens 80-84 26113084-7 2015 [18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors. Glucose 55-62 tumor protein p53 Homo sapiens 95-99 26113084-7 2015 [18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors. Glucose 55-62 tumor protein p53 Homo sapiens 95-99 25704813-4 2015 Here, we show that in oncogenic-Ras-expressing cells, p53 promotes oxidative phosphorylation (OXPHOS) and cell survival upon glucose starvation. Glucose 125-132 tumor protein p53 Homo sapiens 54-57 25071015-0 2014 p53 status as effect modifier of the association between pre-treatment fasting glucose and breast cancer outcomes in non diabetic, HER2 positive patients treated with trastuzumab. Glucose 79-86 tumor protein p53 Homo sapiens 0-3 25260780-0 2014 High glucose dephosphorylates serine 46 and inhibits p53 apoptotic activity. Glucose 5-12 tumor protein p53 Homo sapiens 53-56 25260780-5 2014 However, whether high glucose might modify p53Ser46 phosphorylation has never been addressed. Glucose 22-29 tumor protein p53 Homo sapiens 43-46 25260780-7 2014 Analyses of p53 posttranslational modifications showed that drug-induced p53Ser46 phosphorylation was reduced by high glucose. Glucose 118-125 tumor protein p53 Homo sapiens 12-15 25260780-7 2014 Analyses of p53 posttranslational modifications showed that drug-induced p53Ser46 phosphorylation was reduced by high glucose. Glucose 118-125 tumor protein p53 Homo sapiens 73-76 25260780-8 2014 Such reduction depended by high glucose-induced calyculin A-sensitive phosphatase(s), able to specifically target p53Ser46 phosphorylation. Glucose 32-39 tumor protein p53 Homo sapiens 114-117 25260780-10 2014 In agreement, a constitutively phosphorylated Ser46D p53 mutant was resistant to high glucose. Glucose 86-93 tumor protein p53 Homo sapiens 53-56 25260780-13 2014 CONCLUSIONS: These data indicate that high glucose specifically inhibited Ser46 phosphorylation thus reducing p53 apoptotic activity. Glucose 43-50 tumor protein p53 Homo sapiens 110-113 25221641-8 2014 Genetic silencing of either wild-type PTEN or p53 in WRO cells resulted in increased uptake of glucose, whereas the ectopic expression of PTEN in FTC133 cells resulted in diminished glucose uptake. Glucose 95-102 tumor protein p53 Homo sapiens 46-49 25221641-11 2014 We propose that concurrent PTEN deficiency and mutant p53 leads to a glucose-addiction state that renders the cancer cell more sensitive to glucose restriction. Glucose 69-76 tumor protein p53 Homo sapiens 54-57 24576095-1 2014 TIGAR [TP53 (tumour protein 53)-induced glycolysis and apoptosis regulator] protein is known for its ability to inhibit glycolysis, shifting glucose consumption towards the pentose phosphate pathway to promote antioxidant protection of cancer cells. Glucose 141-148 tumor protein p53 Homo sapiens 7-11 25009184-1 2014 In mammalian cells, tumor suppressor p53 plays critical roles in the regulation of glucose metabolism, including glycolysis and oxidative phosphorylation, but whether and how p53 also regulates gluconeogenesis is less clear. Glucose 83-90 tumor protein p53 Homo sapiens 37-40 24668897-7 2014 Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle. Glucose 180-187 tumor protein p53 Homo sapiens 112-116 24668897-7 2014 Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle. Glucose 245-252 tumor protein p53 Homo sapiens 112-116 23999197-9 2014 While the glucose-intolerant GLP-1R KO mice showed decreased mesenteric p53 (-45.4%, P=0.017), high glucose led to decreased p53 in pre-adipocytes (-27%, P<0.0001). Glucose 10-17 tumor protein p53 Homo sapiens 72-75 23999197-9 2014 While the glucose-intolerant GLP-1R KO mice showed decreased mesenteric p53 (-45.4%, P=0.017), high glucose led to decreased p53 in pre-adipocytes (-27%, P<0.0001). Glucose 100-107 tumor protein p53 Homo sapiens 125-128 24275138-2 2014 Others subsequently indicated that mutant p53 tumor cells undergo p53 degradation and cell death under aerobic glucose-free conditions. Glucose 111-118 tumor protein p53 Homo sapiens 66-69 24556689-7 2014 The activities of both forkhead box O (FOXO1) and p53 were required for upregulation of bim RNA expression in high glucose. Glucose 115-122 tumor protein p53 Homo sapiens 50-53 24556689-9 2014 High glucose coupled with oxidative stress resulted in upregulation of miR28-5p, which directly inhibited expression of the p53 deacetylase sirtuin 3, resulting in increased levels of acetylated p53. Glucose 5-12 tumor protein p53 Homo sapiens 124-127 24556689-9 2014 High glucose coupled with oxidative stress resulted in upregulation of miR28-5p, which directly inhibited expression of the p53 deacetylase sirtuin 3, resulting in increased levels of acetylated p53. Glucose 5-12 tumor protein p53 Homo sapiens 195-198 24275138-2 2014 Others subsequently indicated that mutant p53 tumor cells undergo p53 degradation and cell death under aerobic glucose-free conditions. Glucose 111-118 tumor protein p53 Homo sapiens 42-45 23796712-0 2013 p53 regulates glucose metabolism by miR-34a. Glucose 14-21 tumor protein p53 Homo sapiens 0-3 24275138-4 2014 p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (<=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia. Glucose 36-43 tumor protein p53 Homo sapiens 0-3 24275138-4 2014 p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (<=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia. Glucose 198-205 tumor protein p53 Homo sapiens 0-3 23796712-3 2013 p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism. Glucose 61-68 tumor protein p53 Homo sapiens 0-3 23796712-8 2013 The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism. Glucose 86-93 tumor protein p53 Homo sapiens 25-28 23129176-0 2013 Notch pathway is involved in high glucose-induced apoptosis in podocytes via Bcl-2 and p53 pathways. Glucose 34-41 tumor protein p53 Homo sapiens 87-90 23799024-4 2013 In the present study, we revealed that high glucose could induce GDF15 expression and secretion in cultured human umbilical vein endothelial cells in a ROS- and p53-dependent manner. Glucose 44-51 tumor protein p53 Homo sapiens 161-164 23612020-0 2013 Two p53-related metabolic regulators, TIGAR and SCO2, contribute to oroxylin A-mediated glucose metabolism in human hepatoma HepG2 cells. Glucose 88-95 tumor protein p53 Homo sapiens 4-7 23129176-2 2013 Here we demonstrated that high glucose (HG) upregulated Notch pathway in podocytes accompanied with the alteration of Bcl-2 and p53 pathways, subsequently leading to podocytes apoptosis. Glucose 31-38 tumor protein p53 Homo sapiens 128-131 23808158-7 2013 Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53. Glucose 35-42 tumor protein p53 Homo sapiens 82-85 24280180-0 2013 p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production. Glucose 82-89 tumor protein p53 Homo sapiens 0-3 23466706-4 2013 We have recently shown that macroautophagy (autophagy) provides a route for p53 mutant degradation during restriction of glucose. Glucose 121-128 tumor protein p53 Homo sapiens 76-79 24280180-4 2013 A gene expression microarray screen followed by constraint-based modeling (CBM) predicting metabolic changes imposed by the transcriptomic changes suggested a role for p53 in enhancing gluconeogenesis (de novo synthesis of glucose). Glucose 223-230 tumor protein p53 Homo sapiens 168-171 24280180-7 2013 CONCLUSIONS: These findings portray p53 as a novel regulator of glucose production. Glucose 64-71 tumor protein p53 Homo sapiens 36-39 24280180-8 2013 By facilitating glucose export, p53 may prevent it from being shunted to pro-cancerous pathways such as glycolysis and the PPP. Glucose 16-23 tumor protein p53 Homo sapiens 32-35 22926048-3 2013 HEDS is rapidly detoxified in normal glucose but triggered a p53-independent metabolic stress in glucose depleted state that caused loss of NADPH, protein and non-protein thiol homeostasis and Ku function, and enhanced sensitivity of both p53 wild type and mutant cells to radiation induced oxidative stress. Glucose 97-104 tumor protein p53 Homo sapiens 61-64 23151455-0 2012 Dietary downregulation of mutant p53 levels via glucose restriction: mechanisms and implications for tumor therapy. Glucose 48-55 tumor protein p53 Homo sapiens 33-36 22750268-3 2012 In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells. Glucose 155-162 tumor protein p53 Homo sapiens 313-316 23151455-3 2012 We report here that glucose restriction (GR) induces p53 mutant deacetylation, routing it for degradation via autophagy. Glucose 20-27 tumor protein p53 Homo sapiens 53-56 23151455-5 2012 Furthermore, we found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems. Glucose 88-95 tumor protein p53 Homo sapiens 110-113 23151455-6 2012 These findings indicate that the stability of mutant forms of p53 is influenced by the levels of glucose and by dietetic habits. Glucose 97-104 tumor protein p53 Homo sapiens 62-65 22378745-0 2012 A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells. Glucose 112-119 tumor protein p53 Homo sapiens 82-85 21671008-0 2011 Insulin receptor signaling activated by penta-O-galloyl-alpha-D: -glucopyranose induces p53 and apoptosis in cancer cells. Glucose 66-79 tumor protein p53 Homo sapiens 88-91 22442140-1 2012 Focus on "A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells". Glucose 122-129 tumor protein p53 Homo sapiens 92-95 22301190-2 2012 Moreover, p53 regulates glucose metabolism and its mutation results in the metabolic switch to the Warburg effect found in cancer cells. Glucose 24-31 tumor protein p53 Homo sapiens 10-13 22248668-0 2011 Regulation of glucose metabolism by p53: emerging new roles for the tumor suppressor. Glucose 14-21 tumor protein p53 Homo sapiens 36-39 22184616-9 2012 Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability. Glucose 227-234 tumor protein p53 Homo sapiens 53-56 22184616-9 2012 Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability. Glucose 227-234 tumor protein p53 Homo sapiens 108-111 21832879-0 2011 Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion. Glucose 111-118 tumor protein p53 Homo sapiens 54-57 21832879-4 2011 Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation. Glucose 111-118 tumor protein p53 Homo sapiens 7-10 21832879-6 2011 Metabolic utilization and survival under glucose depletion was increased by pyruvate in mutant p53 (R175H) cells. Glucose 41-48 tumor protein p53 Homo sapiens 95-98 21832879-7 2011 Our results show for the first time that melanoma cells harbouring a p53 (R175H) mutation increase: a) survival under glucose depletion, counteracted by NADPH-oxidase modulators like DPI; b) resistance to DPI when supplemented with exogenous pyruvate. Glucose 118-125 tumor protein p53 Homo sapiens 69-72 20404548-5 2010 The involvement of GAMT in both genotoxic and metabolic stressinduced apoptosis, as well as the requirement of p53-dependent upregulation of GAMT in glucose starvation-mediated fatty acid oxidation (FAO), demonstrate a further role of p53 in coordinating stress response with changes in cellular metabolism. Glucose 149-156 tumor protein p53 Homo sapiens 111-114 21357660-8 2011 Physiological concentrations of insulin also reversed high glucose-induced increases in p53 and vascular cell adhesion molecule-1 and decreases in senescence marker protein-30. Glucose 59-66 tumor protein p53 Homo sapiens 88-91 21336302-3 2011 The tumour suppressor p53 has now been reported to block a metabolic pathway (the pentose phosphate pathway) that diverts glucose away from bioenergetic into biosynthetic routes. Glucose 122-129 tumor protein p53 Homo sapiens 22-25 21336310-8 2011 Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose towards biosynthesis in tumour cells. Glucose 24-31 tumor protein p53 Homo sapiens 44-47 21336310-8 2011 Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose towards biosynthesis in tumour cells. Glucose 74-81 tumor protein p53 Homo sapiens 44-47 21500551-9 2011 Intra-cellular levels of gamma-H2AX and phosphorylated P53 protein were significantly increased in high glucose groups. Glucose 104-111 tumor protein p53 Homo sapiens 55-58 21500551-13 2011 ATM-P53 pathway, the key proteins related to DNA double strain damage repairing mechanisms, may play an important role in high glucose induced cellular senescence and atherosclerosis. Glucose 127-134 tumor protein p53 Homo sapiens 4-7 20590525-0 2010 p38(MAPK)/p53 signalling axis mediates neuronal apoptosis in response to tetrahydrobiopterin-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration. Glucose 122-129 tumor protein p53 Homo sapiens 10-13 21440619-6 2011 Furthermore, we found that interaction of PKCdelta and c-Abl played a crucial role in p53 accumulation in the nucleus, which was linked to the apoptosis of NPCs in response to high glucose. Glucose 181-188 tumor protein p53 Homo sapiens 86-89 21692052-11 2011 Exploration of 1 such cell line (HN30) suggested that the presence of wild-type p53 can partially protect tumor cells from glucose starvation. Glucose 123-130 tumor protein p53 Homo sapiens 80-83 21573174-0 2011 IFI16 induction by glucose restriction in human fibroblasts contributes to autophagy through activation of the ATM/AMPK/p53 pathway. Glucose 19-26 tumor protein p53 Homo sapiens 120-123 21573174-1 2011 BACKGROUND: Glucose restriction in cells increases the AMP/ATP ratio (energetic stress), which activates the AMPK/p53 pathway. Glucose 12-19 tumor protein p53 Homo sapiens 114-117 21573174-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: We found that glucose restriction or treatment of human diploid fibroblasts (HDFs) with the activators of the AMPK/p53 pathway induced the expression of IFI16 protein. Glucose 46-53 tumor protein p53 Homo sapiens 147-150 21573174-7 2011 Importantly, the knockdown of the IFI16 expression in HDFs inhibited the activation of the ATM/AMPK/p53 pathway in response to glucose restriction and also increased the survival of HDFs. Glucose 127-134 tumor protein p53 Homo sapiens 100-103 21287141-0 2011 Glucose oscillations, more than constant high glucose, induce p53 activation and a metabolic memory in human endothelial cells. Glucose 46-53 tumor protein p53 Homo sapiens 62-65 21287141-2 2011 Evaluation of the effects of exposure of HUVECs to oscillating high glucose on the induction of markers of oxidative stress and DNA damage (phospho-gamma-histone H2AX and PKCdelta) and onset of metabolic memory, and the possible role of the tumour suppressor transcriptional factor p53 is of pivotal interest. Glucose 68-75 tumor protein p53 Homo sapiens 282-285 21287141-4 2011 Transcriptional activity of p53 was also evaluated in the first 24 h after high glucose exposure. Glucose 80-87 tumor protein p53 Homo sapiens 28-31 21287141-8 2011 Transcriptional activity of p53 peaked 6 h after glucose exposure, showing a predicted oscillatory behaviour. Glucose 49-56 tumor protein p53 Homo sapiens 28-31 21287141-10 2011 Hyperactivation of p53 during glucose oscillation might be due to the absence of consistent feedback inhibition during each glucose spike and might account for the worse outcome of this condition. Glucose 30-37 tumor protein p53 Homo sapiens 19-22 20404548-5 2010 The involvement of GAMT in both genotoxic and metabolic stressinduced apoptosis, as well as the requirement of p53-dependent upregulation of GAMT in glucose starvation-mediated fatty acid oxidation (FAO), demonstrate a further role of p53 in coordinating stress response with changes in cellular metabolism. Glucose 149-156 tumor protein p53 Homo sapiens 235-238 20068143-13 2010 High glucose and palmitate increased p53 acetylation and JNK phosphorylation; these effects were abolished in siRNA SIRT1-treated cells. Glucose 5-12 tumor protein p53 Homo sapiens 37-40 19229245-6 2009 Knockdown of MDH1 significantly reduces binding of acetylated-p53 and transcription-active histone codes to the promoter upon glucose depletion. Glucose 126-133 tumor protein p53 Homo sapiens 62-65 19940145-8 2010 Further, knockdown of siah-1 prevented high glucose-induced cell death of Muller cells potentially by inhibiting p53 phosphorylation consistent with previous observations, indicating that nuclear GAPDH induces cell death via p53 activation. Glucose 44-51 tumor protein p53 Homo sapiens 113-116 19940145-8 2010 Further, knockdown of siah-1 prevented high glucose-induced cell death of Muller cells potentially by inhibiting p53 phosphorylation consistent with previous observations, indicating that nuclear GAPDH induces cell death via p53 activation. Glucose 44-51 tumor protein p53 Homo sapiens 225-228 19286634-7 2009 Introduction of SIRT1 or disruption of p53 inhibits high glucose-induced endothelial senescence and dysfunction. Glucose 57-64 tumor protein p53 Homo sapiens 39-42 19995986-10 2009 These results demonstrate that ChREBP plays a key role both in redirecting glucose metabolism to anabolic pathways and suppressing p53 activity. Glucose 75-82 tumor protein p53 Homo sapiens 131-134 17721990-8 2008 Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling. Glucose 79-86 tumor protein p53 Homo sapiens 220-223 19202066-2 2009 Recently, we have shown that p53 regulates glucose metabolism through the IKK-NF-kappaB pathway and that, in the absence of p53, the positive feedback loop between IKK-NF-kappaB and glycolysis has an integral role in oncogene-induced cell transformation. Glucose 43-50 tumor protein p53 Homo sapiens 29-32 18804536-0 2008 Simvastatin inhibits cell cycle progression in glucose-stimulated proliferation of aortic vascular smooth muscle cells by up-regulating cyclin dependent kinase inhibitors and p53. Glucose 47-54 tumor protein p53 Homo sapiens 175-178 18391940-0 2008 p53 regulates glucose metabolism through an IKK-NF-kappaB pathway and inhibits cell transformation. Glucose 14-21 tumor protein p53 Homo sapiens 0-3 18155176-1 2008 Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4]. Glucose 227-234 tumor protein p53 Homo sapiens 55-58 19202066-4 2009 In p53-deficient cells, the O-GlcNAcylated IKKbeta and the activating phosphorylation of IKK were decreased by p65/NF-kappaB knockdown or glucose depletion. Glucose 138-145 tumor protein p53 Homo sapiens 3-6 19202066-8 2009 Taken together, we propose a novel mechanism for the enhancement of NF-kappaB activity by loss of p53, which evokes positive feedback regulation from enhanced glucose metabolism to IKK in oncogenesis. Glucose 159-166 tumor protein p53 Homo sapiens 98-101 18523732-5 2008 For example deregulation of Akt, ras and MYC as well as loss of p53 function have been reported to confer increased glucose metabolic rates in cancer cells. Glucose 116-123 tumor protein p53 Homo sapiens 64-67 17721990-9 2008 Inhibition of p53 protein expression using small interfering RNA (siRNA) blocked the activation of p21 and the cell apoptosis induced by 5 microM MG/20 mM glucose. Glucose 155-162 tumor protein p53 Homo sapiens 14-17 16954562-11 2006 CONCLUSION: These data suggest that abrogation of p53 in breast cancer is associated with specific changes in glucose metabolism detected by PET. Glucose 110-117 tumor protein p53 Homo sapiens 50-53 17932466-6 2007 Our results demonstrate that the wild-type p53-expressing tumor xenografts exhibit high levels of glucose uptake, similar to those observed in p53-null tumor xenografts, by quantitative PET imaging indicative of the glycolytic switch. Glucose 98-105 tumor protein p53 Homo sapiens 43-46 17979566-11 2007 CONCLUSIONS: Therefore, p53 seemed to have a significant role in cellular glucose metabolism and G2/M checkpoint, according to beta-irradiation, and could cause a different therapeutic response of (18)F-FDG uptake in cancer cells. Glucose 74-81 tumor protein p53 Homo sapiens 24-27 17481900-4 2007 Recent discoveries revealing new functions for p53 in the regulation of glucose metabolism and oxidative stress have brought together these two venerable fields of cancer biology. Glucose 72-79 tumor protein p53 Homo sapiens 47-50 18056705-2 2008 In this study, we have found that glucose depletion promotes the phosphorylation of AMP-activated protein kinase catalytic subunit alpha (AMPKalpha) in association with a significant up-regulation of p53, thereby inducing p53-dependent apoptosis in vivo and in vitro. Glucose 34-41 tumor protein p53 Homo sapiens 200-203 18056705-2 2008 In this study, we have found that glucose depletion promotes the phosphorylation of AMP-activated protein kinase catalytic subunit alpha (AMPKalpha) in association with a significant up-regulation of p53, thereby inducing p53-dependent apoptosis in vivo and in vitro. Glucose 34-41 tumor protein p53 Homo sapiens 222-225 18056705-6 2008 Small interference RNA-mediated knockdown of p53 caused an inhibition of apoptosis following glucose depletion. Glucose 93-100 tumor protein p53 Homo sapiens 45-48 15928081-6 2005 In addition, glucose starvation not only signals to shut down mTOR, but also results in the transient phosphorylation of the p53 protein. Glucose 13-20 tumor protein p53 Homo sapiens 125-128 15800853-8 2005 Evidence in support of this model, in which excess glucose metabolism inhibits expression of Pax3, thereby derepressing p53-dependent apoptosis of neuroepithelium and leading to NTD will be discussed. Glucose 51-58 tumor protein p53 Homo sapiens 120-123 15866171-6 2005 AMPK-induced p53 activation promotes cellular survival in response to glucose deprivation, and cells that have undergone a p53-dependent metabolic arrest can rapidly reenter the cell cycle upon glucose restoration. Glucose 70-77 tumor protein p53 Homo sapiens 13-16 12905708-2 2003 METHODS: The p21WAF1 and p53 gene were transfected respectively into a human lung adenocarcinoma cell line, GLC-82. Glucose 108-111 tumor protein p53 Homo sapiens 25-28 15251465-0 2004 Thymidylate synthase inhibition triggers glucose-dependent apoptosis in p53-negative leukemic cells. Glucose 41-48 tumor protein p53 Homo sapiens 72-75 12692899-6 2003 It was found that expression of p53 was induced by oxidative stress, particularly when glucose had been omitted from the culture medium. Glucose 87-94 tumor protein p53 Homo sapiens 32-35 15059920-10 2004 Mutations within the DNA-binding domain of p53, which are usually associated with malignancy, were found to impair the repressive effect of p53 on transcriptional activity of the GLUT1 and GLUT4 gene promoters, thereby resulting in increased glucose metabolism and cell energy supply. Glucose 242-249 tumor protein p53 Homo sapiens 43-46 15059920-10 2004 Mutations within the DNA-binding domain of p53, which are usually associated with malignancy, were found to impair the repressive effect of p53 on transcriptional activity of the GLUT1 and GLUT4 gene promoters, thereby resulting in increased glucose metabolism and cell energy supply. Glucose 242-249 tumor protein p53 Homo sapiens 140-143 11574421-2 2001 At a high glucose concentration, O-glycosylation of p53 occurred between 10 and 20 min, reached its peak at 1 h, and then decreased with time. Glucose 10-17 tumor protein p53 Homo sapiens 52-55 34692517-8 2021 High glucose instigated suppression in the intracellular accumulation of anticancer drug doxorubicin and drug-induced chromatin compactness along with declined expression of drug efflux pump MDR-1 and transcription factors and signal transducers governing the survival, aggressiveness, and apoptotic cell death (p53, HIF-1alpha, mTOR, MYC, STAT3). Glucose 5-12 tumor protein p53 Homo sapiens 312-315 34270989-6 2021 Consistent with the in vivo findings, high glucose induced endothelial senescence, impaired endothelial function and elevated DDR1 expression, accompanied by the elevation of senescence-related genes p53 and p21 expression, and these effects were reversed by DDR1 siRNA. Glucose 43-50 tumor protein p53 Homo sapiens 200-203 34270989-9 2021 In conclusion, our data demonstrated that miR-199a-3p/DDR1/p53/p21 signaling pathway was involved in endothelial senescence under diabetic conditions, and therapeutic targeting DDR1 would be exploited to inhibit endothelial senescence owing to high glucose exposure. Glucose 249-256 tumor protein p53 Homo sapiens 59-62 11717960-0 1999 Interaction between gene p53 and oncogene mdm2 in human glandular lung cancer cell line GLC-82. Glucose 88-91 tumor protein p53 Homo sapiens 25-28 34636125-8 2022 RESULTS: Under high glucose conditions, the viability of ARPE-19 was decreased and the apoptosis rate increased, the protein expressions of Bax, Caspase-3, LC3-II/LC3-I, and p-p53 were all increased and the expressions of Bcl-2, p62, and p-mTOR decreased, and autophagic flux was increased compared with that of the controls. Glucose 20-27 tumor protein p53 Homo sapiens 176-179 34636125-11 2022 CONCLUSIONS: Our findings indicate that through the p53/mTOR autophagy pathway, PC may protect RPE cells from high glucose-induced injury. Glucose 115-122 tumor protein p53 Homo sapiens 52-55 34461288-5 2021 Using a microarray assay to detect the dysregulated genes in IDD patients with obesity, we identified 33 differentially expressed genes and verified only two proapoptotic genes, including Puma (p53 upregulated modulator of apoptosis) and BAX (BCL2 associated X) responded to glucose. Glucose 275-282 tumor protein p53 Homo sapiens 194-197 34216644-0 2021 Cytoskeleton-associated protein 2 (CKAP2) is regulated by vascular endothelial growth factor and p53 in retinal capillary endothelial cells under high-glucose conditions. Glucose 151-158 tumor protein p53 Homo sapiens 97-100 34075143-5 2021 Glucose 20 mmol/L accelerates senescence of HREC: population doubling time (+ 58%, p < 0.001) beta-galactosidase activity (+ 60%, p < 0.002) intracellular oxidative stress (+ 65%, p < 0.01), expression of p53 gene (+ 118%, p < 0.001). Glucose 0-7 tumor protein p53 Homo sapiens 205-208 34417460-2 2021 Deficiency or excess of nutrients causes cellular metabolic stress, and we hypothesized that p53 could be linked to glucose maintenance. Glucose 116-123 tumor protein p53 Homo sapiens 93-96 34417460-8 2021 Finally, protein levels of p53, as well as genes responsible of O-GlcNAcylation are elevated in the liver of type 2 diabetic patients and positively correlate with glucose and HOMA-IR. Glucose 164-171 tumor protein p53 Homo sapiens 27-30 34244606-8 2021 Overall, this study proposes a novel strategy of VM suppression through Chk2 induction, which prevents PKM2-mediated glucose flux in p53-mutated TNBC. Glucose 117-124 tumor protein p53 Homo sapiens 133-136 34369624-6 2021 Remarkably, TCF19 can form different transcription activation/repression complexes which show substantial overlap with that of p53, depending on glucose-mediated variant stress situations as obtained from IP/MS studies. Glucose 145-152 tumor protein p53 Homo sapiens 127-130 34369624-7 2021 Interestingly, we observed that TCF19/p53 complexes either have CBP or HDAC1 to epigenetically program the expression of TIGAR and SCO2 genes depending on short-term high glucose or prolonged high glucose conditions. Glucose 171-178 tumor protein p53 Homo sapiens 38-41 34369624-7 2021 Interestingly, we observed that TCF19/p53 complexes either have CBP or HDAC1 to epigenetically program the expression of TIGAR and SCO2 genes depending on short-term high glucose or prolonged high glucose conditions. Glucose 197-204 tumor protein p53 Homo sapiens 38-41 33982778-0 2021 Isoquercitrin protects HUVECs against high glucose-induced apoptosis through regulating p53 proteasomal degradation. Glucose 43-50 tumor protein p53 Homo sapiens 88-91 35118064-5 2021 In this review, we focus on recent advances in our understanding of the interplay between p53 and metabolism of glucose, fatty acid as well as amino acid, and discuss how the deregulation of p53 in these processes could lead to cancer. Glucose 112-119 tumor protein p53 Homo sapiens 90-93 35118064-5 2021 In this review, we focus on recent advances in our understanding of the interplay between p53 and metabolism of glucose, fatty acid as well as amino acid, and discuss how the deregulation of p53 in these processes could lead to cancer. Glucose 112-119 tumor protein p53 Homo sapiens 191-194 35501580-4 2022 We further demonstrate that RIP140 reduces the transcription of the glucose transporter GLUT3 gene, by inhibiting the transcriptional activity of hypoxia inducible factor HIF-2alpha in cooperation with p53. Glucose 68-75 tumor protein p53 Homo sapiens 202-205 35456022-0 2022 Apoptotic and DNA Damage Effect of 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose in Cisplatin-Resistant Non-Small Lung Cancer Cells via Phosphorylation of H2AX, CHK2 and p53. Glucose 68-75 tumor protein p53 Homo sapiens 165-168 35220706-16 2022 At 48 h after seeding, the expression levels of senescence-related proteins p16 and p53 both were significantly higher in HDFs of high glucose group than those in low glucose group (with t values of 11.85 and 3.02, respectively, P<0.05 or P<0.01). Glucose 167-174 tumor protein p53 Homo sapiens 84-87 33137455-1 2021 The manner in which p53 maintains redox homeostasis and the means by which two key metabolic elements, glucose and glutamine, contribute to p53-dependent redox stability remain unclear. Glucose 103-110 tumor protein p53 Homo sapiens 140-143 33754057-17 2021 The in vitro and in vivo findings further demonstrated that high glucose may promote plakoglobin-dependent cooperation of p53 with HIF-1alpha and Smad3, subsequently increasing the expression of TGF-beta1 and the pro-EndMT target genes of the TGF-beta1/Smad signaling pathway in a KLK8-dependent manner. Glucose 65-72 tumor protein p53 Homo sapiens 122-125 34044006-4 2021 Herein, by proposing a mathematical model of glucose-mediated Nanog regulation, we showed that the differential proliferation behavior of CSCs and cell-type similar to CSCs can be explained by considering the experimentally observed varied expression levels of key positive (STAT3) and negative (p53) regulators of Nanog. Glucose 45-52 tumor protein p53 Homo sapiens 296-299 33995069-7 2021 More importantly, compounds M1, 6b, and 6d could resist high glucose-induced apoptosis of HK-2 cells by activating SIRT1 and deacetylation of p53. Glucose 61-68 tumor protein p53 Homo sapiens 142-145 33785447-7 2021 In this review, we will summarize the roles of p53 in the regulation of glucose, lipid, amino acid, nucleotide, iron metabolism, and ROS production. Glucose 72-79 tumor protein p53 Homo sapiens 47-50 33137455-2 2021 To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified. Glucose 48-55 tumor protein p53 Homo sapiens 33-36 33137455-7 2021 Collectively, our findings suggest that p53 governs the alternative utilization of metabolic ingredients, such as glucose and glutamine, in ROS-prone conditions. Glucose 114-121 tumor protein p53 Homo sapiens 40-43 31792920-7 2020 Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21. Glucose 15-22 tumor protein p53 Homo sapiens 55-58 33160987-0 2021 SIRT3 protects endothelial cells from high glucose-induced senescence and dysfunction via the p53 pathway. Glucose 43-50 tumor protein p53 Homo sapiens 94-97 33160274-0 2020 p53 coordinates glucose and choline metabolism during the mesendoderm differentiation of human embryonic stem cells. Glucose 16-23 tumor protein p53 Homo sapiens 0-3 33160274-4 2020 Collectively, our study reveals the indispensable role of p53 in orchestrating both glucose and lipid metabolism to maintain proper hESC identity. Glucose 84-91 tumor protein p53 Homo sapiens 58-61 33028529-3 2020 Here, we found that DSBs in oxygen/glucose-deprived (OGD) neurons spatiotemporally correlated with the up-regulation of WRAP53 (WD40-encoding p53-antisense RNA), which translocated to the nucleus to activate the DSB repair response. Glucose 35-42 tumor protein p53 Homo sapiens 142-145 31792920-7 2020 Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21. Glucose 15-22 tumor protein p53 Homo sapiens 67-70 32266931-2 2020 Both c-Jun and p53 are phosphorylated at Ser63 and Thr18, respectively, in response to low glucose (40 mg/dL of medium) but not high glucose (140 mg/dL of medium) in human hepatoma-derived Huh-7 cells. Glucose 91-98 tumor protein p53 Homo sapiens 15-18 32266639-6 2020 Moreover, GSPE was able to avoid mitochondria dysfunction and the increased in p53 and poly-(ADP-ribose) polymerase expression induced by high glucose exposition. Glucose 143-150 tumor protein p53 Homo sapiens 79-82 32266931-2 2020 Both c-Jun and p53 are phosphorylated at Ser63 and Thr18, respectively, in response to low glucose (40 mg/dL of medium) but not high glucose (140 mg/dL of medium) in human hepatoma-derived Huh-7 cells. Glucose 133-140 tumor protein p53 Homo sapiens 15-18 32266931-6 2020 A correlation of this low glucose response phosphorylation of Thr386 with the phosphorylation of c-Jun and p53 suggests that VRK1 phosphorylated at Thr386 catalyzes this phosphorylation. Glucose 26-33 tumor protein p53 Homo sapiens 107-110 31668020-16 2019 TP53, EGFR and KRAS mutations are associated with expression of glucose and glutamine metabolism-related markers in NSCLC. Glucose 64-71 tumor protein p53 Homo sapiens 0-4 31892967-2 2020 p53-induced glycolysis and apoptosis regulator (TIGAR) is a protein regulates glycolytic activity and glucose metabolism. Glucose 102-109 tumor protein p53 Homo sapiens 0-3 31597953-0 2020 Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway. Glucose 101-108 tumor protein p53 Homo sapiens 72-75 31657880-2 2020 p53 is activated by glucose limitation and maintains cell survival via triggering metabolic checkpoint. Glucose 20-27 tumor protein p53 Homo sapiens 0-3 31657880-5 2020 The current study demonstrated that glucose limitation transcriptionally suppressed BAG3 expression in a p53-dependent manner. Glucose 36-43 tumor protein p53 Homo sapiens 105-108 30902332-0 2019 Detection of p53 DNA using commercially available personal glucose meters based on rolling circle amplification coupled with nicking enzyme signal amplification. Glucose 59-66 tumor protein p53 Homo sapiens 13-16 31119778-13 2019 P53 antagonist also inhibited the glucose-induced senescence of cardiac c-kit positive cells. Glucose 34-41 tumor protein p53 Homo sapiens 0-3 31119778-14 2019 In conclusion, bradykinin prevents the glucose-induced premature senescence of cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways. Glucose 39-46 tumor protein p53 Homo sapiens 138-141 30902332-2 2019 Herein, on the basis of rolling circle amplification (RCA) coupled with nicking endonuclease-assisted signal amplification (NESA), a simple, sensitive and portable biosensor was developed for the determination of p53 DNA by using the personal glucose meter (PGM) as readout. Glucose 243-250 tumor protein p53 Homo sapiens 213-216 31000199-1 2019 Glucose limitation activates p53, which functions as an adaptive response to maintain cell survival. Glucose 0-7 tumor protein p53 Homo sapiens 29-32 29808718-3 2019 Results: We observed that high glucose (HG), via activation of nuclear phosphatase PP2Cdelta, suppresses p53 function, and consequently promotes BC cell proliferation, migration, and invasion. Glucose 31-38 tumor protein p53 Homo sapiens 105-108 31089945-4 2019 RESULTS: High glucose led to premature senescence of HGMCs, as evident from the increase in the percentage of SA-beta-gal-positive cells, decrease in telomere length, cell cycle arrest at G1 phase,decrease in the expression of miR-126 and p-Akt and increase in the expression of p53, p21 and Rb proteins in the HG group. Glucose 14-21 tumor protein p53 Homo sapiens 279-282 31089945-6 2019 CONCLUSIONS: High glucose induces the senescence of HGMCs in vitro via the miR-126 and Akt-p53-p21 signaling pathways. Glucose 18-25 tumor protein p53 Homo sapiens 91-94 30341510-15 2018 High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways. Glucose 5-12 tumor protein p53 Homo sapiens 39-42 30341510-15 2018 High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways. Glucose 5-12 tumor protein p53 Homo sapiens 134-137 30093705-5 2018 Simultaneously, it caused mitochondrial translocation of p53 and effectively inhibited glucose uptake, expression of GLUT transporters as well as hexokinase (HK II) - a key glycolytic enzyme that most cancer cells thrive on. Glucose 87-94 tumor protein p53 Homo sapiens 57-60 30121551-3 2018 In human renal proximal tubule (human kidney 2 [HK-2]) cells, inhibition of p53 by PIF reduced the high glucose (HG)-induced extracellular matrix (ECM) accumulation and reversed the inhibitory effect of HG on mRNA expression levels of lncRNA zinc finger E-box binding homeobox1-antisense RNA 1 (ZEB1-AS1) and ZEB1. Glucose 104-111 tumor protein p53 Homo sapiens 76-79 29422776-8 2018 p53 transcriptional activity was assayed by qPCR, apoptosis by flow cytometry and glycolysis by glucose and lactate measurements, with quantification of glycolytic enzymes expression. Glucose 96-103 tumor protein p53 Homo sapiens 0-3 30128492-8 2018 Results: Expression levels of ANGPTL3, IL-1beta, IL-6, Bax, P53, VEGF, and integrin alphaVbeta3 were found to be upregulated after high-glucose stimulation or ANGPTL3 overexpression in HRMECs or diabetic retinal tissue. Glucose 136-143 tumor protein p53 Homo sapiens 60-63 29717634-7 2018 Notch signaling was also involved in glucose metabolism through p53 inactivation. Glucose 37-44 tumor protein p53 Homo sapiens 64-67 31938352-0 2018 High glucose concentration induces retinal endothelial cell apoptosis by activating p53 signaling pathway. Glucose 5-12 tumor protein p53 Homo sapiens 84-87 31938352-10 2018 Further research indicated that the protein levels of p53, pro-apoptotic cleaved-caspase-3, and bax were significantly upregulated, and the level of bcl-2 was decreased after treating with glucose at 30 mmol/L. Glucose 189-196 tumor protein p53 Homo sapiens 54-57 31938352-12 2018 In conclusion, high glucose concentration induces apoptosis in retinal endothelial cells by activating p53 signaling pathway. Glucose 20-27 tumor protein p53 Homo sapiens 103-106 29572435-9 2018 Up-regulated beta-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. Glucose 138-145 tumor protein p53 Homo sapiens 63-66 29572435-9 2018 Up-regulated beta-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. Glucose 138-145 tumor protein p53 Homo sapiens 119-122 29867024-6 2018 As a result, the oncogenic characteristics of miR-483-3p are linked to the effect of some of the most relevant cancer-related genes, TP53 and CTNNB1, as well as to one of the most important cancer hallmark: the aberrant glucose metabolism of tumor cells. Glucose 220-227 tumor protein p53 Homo sapiens 133-137 29848325-14 2018 RESULTS: Under high glucose conditions, miR-155 was detected in HK-2 cells in concentration gradient, increased expression of p53 and down-regulated expression of sirt1 and autophagy-associated proteins LC3II, ATG5 and ATG7. Glucose 20-27 tumor protein p53 Homo sapiens 126-129 30250886-1 2018 We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation). Glucose 134-141 tumor protein p53 Homo sapiens 28-32 30250886-1 2018 We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation). Glucose 134-141 tumor protein p53 Homo sapiens 43-46 30250886-1 2018 We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation). Glucose 134-141 tumor protein p53 Homo sapiens 91-95 30250886-2 2018 With the aid of TRINGS, p53 was shown to prevent cancer cells against necroptosis under glucose starvation. Glucose 88-95 tumor protein p53 Homo sapiens 24-27 29046333-0 2017 The p53-inducible long noncoding RNA TRINGS protects cancer cells from necrosis under glucose starvation. Glucose 86-93 tumor protein p53 Homo sapiens 4-7 29189925-0 2018 Overexpression of Sirtuin2 prevents high glucose-induced vascular endothelial cell injury by regulating the p53 and NF-kappaB signaling pathways. Glucose 41-48 tumor protein p53 Homo sapiens 108-111 29174981-7 2018 Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition. Glucose 187-194 tumor protein p53 Homo sapiens 154-157 29094329-8 2018 Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy. Glucose 57-64 tumor protein p53 Homo sapiens 20-23 29094329-8 2018 Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy. Glucose 57-64 tumor protein p53 Homo sapiens 30-33 29094329-8 2018 Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy. Glucose 57-64 tumor protein p53 Homo sapiens 30-33 29046333-4 2017 Here, we show that under glucose starvation condition, p53 directly upregulates a novel lncRNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation) in human tumor cells. Glucose 25-32 tumor protein p53 Homo sapiens 55-58 28886153-2 2017 Although SUVmax reflects increased glucose uptake and metabolism possibly induced by activation of growth factor signaling or TP53 dysfunction, tumor characteristics of SUVmax-high breast cancers remain to be elucidated. Glucose 35-42 tumor protein p53 Homo sapiens 126-130 28649131-10 2017 In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis. Glucose 194-201 tumor protein p53 Homo sapiens 130-133 28709868-0 2017 Protective effect of p53 on the viability of intervertebral disc nucleus pulposus cells under low glucose condition. Glucose 98-105 tumor protein p53 Homo sapiens 21-24 28709868-4 2017 In this study, we found that p53 decreased and leaked to the cytoplasm in NP cells as the glucose level decreases, in contrast to cancer cells in which p53 increases and concentrates to the nuclei. Glucose 90-97 tumor protein p53 Homo sapiens 29-32 27048255-6 2017 RESULTS: Treatment with high concentrations of glucose induced GMC senescence accompanied by shortened telomere length and increase of beta-galactosidase staining as well as P53 protein, which was abrogated after application of caveolin-1-siRNA. Glucose 47-54 tumor protein p53 Homo sapiens 174-177 29035366-0 2017 Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma. Glucose 40-47 tumor protein p53 Homo sapiens 12-15 29035366-3 2017 Mechanistic studies revealed that after attenuated glucose consumption, Bcl-xL blocks cytoplasmic p53 from triggering intrinsic apoptosis. Glucose 51-58 tumor protein p53 Homo sapiens 98-101 29035366-7 2017 Together, these studies identify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic p53, which may potentially be exploited for combination therapy in GBM and possibly other malignancies. Glucose 74-81 tumor protein p53 Homo sapiens 110-113 28673515-0 2017 High glucose-induced p53 phosphorylation contributes to impairment of endothelial antioxidant system. Glucose 5-12 tumor protein p53 Homo sapiens 21-24