PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33040724-10 2020 Simultaneously, the activities of NAD+-dependent IDH, mitochondrial aspartate aminotransferase, and two malate dehydrogenase isoenzymes, whose genes were not predicted to have the p53-binding sequences near the transcription starting points, were upregulated by cisplatin. NAD 34-37 tumor protein p53 Homo sapiens 180-183 32371497-0 2020 p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators. NAD 77-81 tumor protein p53 Homo sapiens 0-3 32371497-3 2020 Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53. NAD 117-121 tumor protein p53 Homo sapiens 252-255 32371497-3 2020 Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53. NAD 122-126 tumor protein p53 Homo sapiens 252-255 30778219-8 2019 HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-kappaB activity. NAD 65-69 tumor protein p53 Homo sapiens 128-131 32371497-3 2020 Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53. NAD 169-173 tumor protein p53 Homo sapiens 252-255 32371497-4 2020 NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation. NAD 0-4 tumor protein p53 Homo sapiens 82-85 32371497-4 2020 NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation. NAD 0-4 tumor protein p53 Homo sapiens 82-85 32371497-5 2020 We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand. NAD 140-144 tumor protein p53 Homo sapiens 111-114 32371497-5 2020 We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand. NAD 145-149 tumor protein p53 Homo sapiens 111-114 32093281-9 2020 This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD. NAD 52-55 tumor protein p53 Homo sapiens 102-105 30050056-4 2019 p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis. NAD 56-59 tumor protein p53 Homo sapiens 21-24 30050056-4 2019 p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis. NAD 56-59 tumor protein p53 Homo sapiens 108-111 30050056-4 2019 p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis. NAD 56-59 tumor protein p53 Homo sapiens 108-111 31812668-6 2020 We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity. NAD 102-105 tumor protein p53 Homo sapiens 32-35 28845527-0 2017 Extracellular NAMPT/visfatin causes p53 deacetylation via NAD production and SIRT1 activation in breast cancer cells. NAD 58-61 tumor protein p53 Homo sapiens 36-39 29476819-2 2018 SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states. NAD 28-32 tumor protein p53 Homo sapiens 19-22 29476819-2 2018 SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states. NAD 28-32 tumor protein p53 Homo sapiens 87-90 29307819-4 2018 In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy. NAD 67-71 tumor protein p53 Homo sapiens 122-125 30518708-1 2018 SIRT1, an NAD+-dependent deacetylase, causes deacetylation and down-regulation of its target p53. NAD 10-13 tumor protein p53 Homo sapiens 93-96 28845527-10 2017 In conclusion, the results show that extracellular visfatin produces NAD that causes upregulation of SIRT1 activity and p53 deacetylation. NAD 69-72 tumor protein p53 Homo sapiens 120-123 24548601-1 2014 BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses. NAD 35-38 tumor protein p53 Homo sapiens 26-29 25971446-9 2015 CAP metabolites preferentially caused double base lesion, the G and C of the ACG sequence complementary to codon 273 of the p53 gene, in the presence of NADH and Cu(II). NAD 153-157 tumor protein p53 Homo sapiens 124-127 25033286-1 2014 Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival. NAD 35-39 tumor protein p53 Homo sapiens 94-97 27816507-5 2016 Additionally, depletion of NAD+ causes sensitization of cancer cells to oxidative damage by disruption of the anti-oxidant defense system, decreased cell proliferation, and initiation of cell death through manipulation of cell signaling pathways (e.g., SIRT1 and p53). NAD 27-31 tumor protein p53 Homo sapiens 263-266 27608947-1 2016 Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO. NAD 116-122 tumor protein p53 Homo sapiens 314-317 26712469-2 2016 The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells. NAD 132-138 tumor protein p53 Homo sapiens 115-118 24819061-6 2014 Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH. NAD 90-96 tumor protein p53 Homo sapiens 53-56 24819061-6 2014 Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH. NAD 118-122 tumor protein p53 Homo sapiens 53-56 24819061-7 2014 Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+). NAD 148-152 tumor protein p53 Homo sapiens 97-100 24819061-7 2014 Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+). NAD 153-159 tumor protein p53 Homo sapiens 97-100 24819061-8 2014 This effect was specific for p53(+/+) cancer cells and correlated with (i) reduced activity of NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity. NAD 95-101 tumor protein p53 Homo sapiens 29-32 24819061-11 2014 Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes. NAD 52-56 tumor protein p53 Homo sapiens 125-128 24819061-11 2014 Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes. NAD 57-63 tumor protein p53 Homo sapiens 125-128 24819061-11 2014 Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes. NAD 210-216 tumor protein p53 Homo sapiens 125-128 24548601-1 2014 BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses. NAD 35-38 tumor protein p53 Homo sapiens 172-175 22735644-1 2012 Human DBC1 (deleted in breast cancer-1; KIAA1967) is a nuclear protein that, in response to DNA damage, competitively inhibits the NAD(+)-dependent deacetylase SIRT1, a regulator of p53 apoptotic functions in response to genotoxic stress. NAD 131-137 tumor protein p53 Homo sapiens 182-185 24552824-0 2014 The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target. NAD 4-7 tumor protein p53 Homo sapiens 94-97 24552824-4 2014 This notion led us to examine whether p53 can regulate NAD(+) biosynthesis in the cell. NAD 55-61 tumor protein p53 Homo sapiens 38-41 24552824-8 2014 Furthermore, knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53-mediated signaling. NAD 65-71 tumor protein p53 Homo sapiens 199-202 24552824-9 2014 Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate. NAD 46-52 tumor protein p53 Homo sapiens 23-26 24552824-9 2014 Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate. NAD 46-52 tumor protein p53 Homo sapiens 81-84 24009628-1 2013 BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin. NAD 78-81 tumor protein p53 Homo sapiens 150-153 24512730-1 2013 It has been reported that upregulated SIRT1 (NAD(+)-dependent class III histone deacetylase) deacetylates the p53 protein, represses its function, and allows for tumor cell growth in various cancers. NAD 45-51 tumor protein p53 Homo sapiens 110-113 23798621-7 2013 DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628. NAD 38-41 tumor protein p53 Homo sapiens 17-20 21807113-4 2011 Sirt1, a NAD-dependent class III histone deacetylase, has a paradoxical role in tumorigenesis by deacetylating several transcription factors, including p53, E2F1 and forkhead proteins. NAD 9-12 tumor protein p53 Homo sapiens 152-155 21979946-0 2012 Germline SDHx variants modify breast and thyroid cancer risks in Cowden and Cowden-like syndrome via FAD/NAD-dependant destabilization of p53. NAD 105-108 tumor protein p53 Homo sapiens 138-141 21979946-11 2012 This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells. NAD 170-203 tumor protein p53 Homo sapiens 13-16 21245319-1 2011 Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53. NAD 62-95 tumor protein p53 Homo sapiens 167-170 21245319-1 2011 Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53. NAD 62-95 tumor protein p53 Homo sapiens 214-217 21245319-1 2011 Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53. NAD 97-103 tumor protein p53 Homo sapiens 167-170 21245319-1 2011 Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53. NAD 97-103 tumor protein p53 Homo sapiens 214-217 22180829-1 2011 NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones. NAD 0-3 tumor protein p53 Homo sapiens 233-236 20975832-1 2010 BACKGROUND: The NAD-dependent deacetylase SIRT1 is a nutrient-sensitive coordinator of stress-tolerance, multiple homeostatic processes and healthspan, while p53 is a stress-responsive transcription factor and our paramount tumour suppressor. NAD 16-19 tumor protein p53 Homo sapiens 158-161 20471503-1 2010 NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones. NAD 0-6 tumor protein p53 Homo sapiens 211-214 20631301-1 2010 The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG. NAD 24-28 tumor protein p53 Homo sapiens 180-183 19188449-1 2009 The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription. NAD 4-10 tumor protein p53 Homo sapiens 107-110 19682970-1 2009 Sirtuins are nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylases that catalyze the deacetylation of proteins such as histones and p53. NAD 13-46 tumor protein p53 Homo sapiens 144-147 19833096-4 2009 These effects were associated with decreased 8-iso-prostaglandin F(2alpha) and peroxynitrite formation, enhanced protein expression of NAD(+)-dependent class III histone deacetylase sirtuin (SIRT) 1, and downregulated protein expression of histone senescence factor p53. NAD 135-141 tumor protein p53 Homo sapiens 266-269 16082197-4 2005 Recent findings suggest that p53 also undergoes ubiquitin-independent degradation by the 20S proteasomes and that this process is regulated by NAD(P)H quinone oxidoreductase 1 (NQO1) together with NADH. NAD 197-201 tumor protein p53 Homo sapiens 29-32 17454128-2 2007 We demonstrated that UVA-irradiated NADH induced damage to (32)P-labeled DNA fragments obtained from the p53 gene in the presence of Cu(II). NAD 36-40 tumor protein p53 Homo sapiens 105-108 17806102-1 2007 The NAD(+)-dependent protein deacetylase SIRT1 is linked to cellular survival pathways by virtue of keeping the tumor suppressor gene p53 and members of the forkhead transcription factor family deacetylated. NAD 4-10 tumor protein p53 Homo sapiens 134-137 17595514-1 2007 It has been reported that p53 acetylation, which promotes cellular senescence, can be regulated by the NAD(+)-dependent deacetylase SIRT1, the human homolog of yeast Sir2, a protein that modulates lifespan. NAD 103-109 tumor protein p53 Homo sapiens 26-29 16618762-1 2006 SIRT1 and other NAD-dependent deacetylases have been implicated in control of cellular responses to stress and in tumorigenesis through deacetylation of important regulatory proteins, including p53 and the BCL6 oncoprotein. NAD 16-19 tumor protein p53 Homo sapiens 194-197 12867035-6 2003 This interaction, and consequent repression of p53-dependent transcription, is relieved under hypoxia or hypoxia-mimicking conditions that are known to increase levels of intracellular NADH. NAD 185-189 tumor protein p53 Homo sapiens 47-50 15509798-0 2004 NAD+ modulates p53 DNA binding specificity and function. NAD 0-4 tumor protein p53 Homo sapiens 15-18 15509798-7 2004 Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro. NAD 104-110 tumor protein p53 Homo sapiens 31-34 15509798-7 2004 Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro. NAD 104-110 tumor protein p53 Homo sapiens 120-123 15509798-7 2004 Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro. NAD 104-110 tumor protein p53 Homo sapiens 120-123 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 51-57 tumor protein p53 Homo sapiens 61-64 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 51-57 tumor protein p53 Homo sapiens 139-142 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 51-57 tumor protein p53 Homo sapiens 139-142 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 112-118 tumor protein p53 Homo sapiens 61-64 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 112-118 tumor protein p53 Homo sapiens 139-142 15509798-9 2004 These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity. NAD 112-118 tumor protein p53 Homo sapiens 139-142 12918120-8 2003 NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P<0.05). NAD 0-4 tumor protein p53 Homo sapiens 155-158 12918120-10 2003 CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS. NAD 12-16 tumor protein p53 Homo sapiens 145-148 34919052-5 2021 Mechanistic analysis suggests that NMNAT interferes with DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD+-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53. NAD 123-127 tumor protein p53 Homo sapiens 68-71 12390773-4 2002 RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P<0.01). NAD 8-12 tumor protein p53 Homo sapiens 162-165 12390773-6 2002 CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions. NAD 12-16 tumor protein p53 Homo sapiens 157-160 10945628-4 2000 Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL. NAD 52-56 tumor protein p53 Homo sapiens 212-215 10331640-2 1999 We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells. NAD 53-56 tumor protein p53 Homo sapiens 124-127 10331640-5 1999 Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis. NAD 6-9 tumor protein p53 Homo sapiens 135-138 10331640-5 1999 Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis. NAD 180-183 tumor protein p53 Homo sapiens 135-138 9823314-8 1998 Although p53 was not endogenously poly (ADP-ribosyl)ated in situ, incubation of cell extracts with full-length PARP from calf thymus and [32P]beta NAD+ resulted in its time-dependent poly(ADP-ribosyl)ation. NAD 147-151 tumor protein p53 Homo sapiens 9-12 11672522-3 2001 Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo. NAD 38-41 tumor protein p53 Homo sapiens 52-55 11672523-0 2001 hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase. NAD 29-32 tumor protein p53 Homo sapiens 43-46 10697561-5 1999 The identification of DNA-fragmentation and p53 and Ki-67 genes expression suggest that the mechanism of NADH action is different from disregulation of genes considered as check-points in cell cycle. NAD 105-109 tumor protein p53 Homo sapiens 44-47 10334203-5 1999 Using 32P-5"-end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene, we showed that PBQ plus NADH, and also PHQ, induced DNA damage frequently at thymine residues, in the presence of Cu(II). NAD 139-143 tumor protein p53 Homo sapiens 59-62 34919052-7 2021 Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth. NAD 98-102 tumor protein p53 Homo sapiens 89-92 34919052-7 2021 Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth. NAD 130-134 tumor protein p53 Homo sapiens 89-92 34562089-6 2022 DOX activates nicotinamide adenine dinucleotide phosphate NADPH oxidase (NOX) in the heart, resulting in excessive reactive oxygen species that can induce cardiomyocyte apoptosis through phosphorylation of p53, DNA damage and/or mitogen-activated protein kinases-mediated cardiomyocyte apoptosis. NAD 14-47 tumor protein p53 Homo sapiens 206-209 34130091-9 2021 Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress. NAD 191-195 tumor protein p53 Homo sapiens 88-91 34130091-9 2021 Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress. NAD 191-195 tumor protein p53 Homo sapiens 217-220 34130091-0 2021 Restoring NAD+ by NAMPT is essential for the SIRT1/p53-mediated survival of UVA- and UVB-irradiated epidermal keratinocytes. NAD 10-14 tumor protein p53 Homo sapiens 51-54