PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32032660-0 2020 Synergistic activation of p53 by actinomycin D and nutlin-3a is associated with the upregulation of crucial regulators and effectors of innate immunity. Dactinomycin 33-46 tumor protein p53 Homo sapiens 26-29 33221336-10 2021 Moreover, triggering nucleolar stress by the chemotherapeutic agents ActinomycinD or the RNA polymeraseI inhibitor CX-5461 stimulates expression of Wnt/beta-Catenin targets, which is followed by the p53 target CDKN1A(p21). Dactinomycin 69-81 tumor protein p53 Homo sapiens 199-202 32032660-1 2020 Actinomycin D and nutlin-3a (A + N) activate p53, partly through induction of phosphorylation on Ser392. Dactinomycin 0-13 tumor protein p53 Homo sapiens 45-48 29842899-4 2018 To stimulate p53 in synergistic fashion, we exposed A549 lung cancer cells to actinomycin D and nutlin-3a (A + N). Dactinomycin 78-91 tumor protein p53 Homo sapiens 13-16 31939089-6 2020 Actinomycin D was utilized to examine the stability of p53 mRNA. Dactinomycin 0-13 tumor protein p53 Homo sapiens 55-58 30096294-0 2018 PIM2 survival kinase is upregulated in a p53-dependent manner in cells treated with camptothecin or co-treated with actinomycin D and nutlin-3a. Dactinomycin 116-129 tumor protein p53 Homo sapiens 41-44 30096294-2 2018 In a previous study, we found that actinomycin D and nutlin-3a (A + N) synergistically activate p53. Dactinomycin 35-48 tumor protein p53 Homo sapiens 96-99 29207594-3 2017 Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest. Dactinomycin 184-197 tumor protein p53 Homo sapiens 166-169 29854877-3 2018 For initial screening, we screened 5,000 genes through selection of shRNAs in p53 wild-type tumor cells that altered sensitivity to the p53 activator actinomycin D (ActD) to identify p53 regulatory genes; shRNAs targeting 322 genes were obtained. Dactinomycin 150-163 tumor protein p53 Homo sapiens 136-139 29854877-3 2018 For initial screening, we screened 5,000 genes through selection of shRNAs in p53 wild-type tumor cells that altered sensitivity to the p53 activator actinomycin D (ActD) to identify p53 regulatory genes; shRNAs targeting 322 genes were obtained. Dactinomycin 150-163 tumor protein p53 Homo sapiens 136-139 29207594-3 2017 Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest. Dactinomycin 184-197 tumor protein p53 Homo sapiens 166-169 27565728-3 2016 Here we found that four nucleocytoplasmic-shuttling RNA-binding proteins and p53 interact specifically with the YB-NLS and co-accumulate with YB-1 in the nucleus of actinomycin D-treated cells. Dactinomycin 165-178 tumor protein p53 Homo sapiens 77-80 28870911-7 2017 Mechanistically, blocking of de novo RNA synthesis by actinomycin D significantly inhibited sunitinib-induced expression of p53 mRNA, but not that of caspase-3, indicating involvement of a transcriptional mechanism. Dactinomycin 54-67 tumor protein p53 Homo sapiens 124-127 28102346-0 2017 Human p53 interacts with the elongating RNAPII complex and is required for the release of actinomycin D induced transcription blockage. Dactinomycin 90-103 tumor protein p53 Homo sapiens 6-9 26070487-3 2015 Through an unbiased genome-wide ChIP-seq analysis, we have found that 5-lipoxygenase (ALOX5, 5-LO) which is a key enzyme of leukotriene (LT) biosynthesis, is a direct target gene of p53 and its expression is induced by genotoxic stress via actinomycin D (Act.D) or etoposide (Eto) treatment. Dactinomycin 240-253 tumor protein p53 Homo sapiens 182-185 27556362-0 2016 Low-dose Actinomycin-D treatment re-establishes the tumoursuppressive function of P53 in RELA-positive ependymoma. Dactinomycin 9-22 tumor protein p53 Homo sapiens 82-85 27556362-6 2016 Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA. Dactinomycin 281-294 tumor protein p53 Homo sapiens 109-112 27556362-6 2016 Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA. Dactinomycin 281-294 tumor protein p53 Homo sapiens 109-112 27556362-9 2016 At the protein level, we validated the Actinomycin-D induced upregulation of PUMA, and of p53 interaction partners MDM2 and p21. Dactinomycin 39-52 tumor protein p53 Homo sapiens 90-93 27556362-11 2016 Thus, Actinomycin-D could constitute a promising therapeutic option for ST-EPN-RELA ependymoma patients, whose tumours frequently exhibit p53 inactivation. Dactinomycin 6-19 tumor protein p53 Homo sapiens 138-141 27302066-7 2016 Treatment of cells with Nutlin-3 or low concentrations of actinomycin D resulted in a strong elevation of CerS6 mRNA and protein, thus demonstrating that CerS6 is a component of the non-genotoxic p53-dependent cellular stress response. Dactinomycin 58-71 tumor protein p53 Homo sapiens 196-199 25961931-4 2016 In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis. Dactinomycin 99-112 tumor protein p53 Homo sapiens 44-47 25961931-4 2016 In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis. Dactinomycin 114-118 tumor protein p53 Homo sapiens 44-47 26728659-4 2016 METHODS: Neuroblastoma cell lines with different p53 genetic background were employed to determine the response on cell viability and apoptosis of low-dose of actinomycin D. Dactinomycin 159-172 tumor protein p53 Homo sapiens 49-52 26728659-6 2016 RESULTS: Low-dose actinomycin D treatment causes a reduction of cell viability in neuroblastoma cell lines and that this effect is stronger in cells that are wild-type for p53. Dactinomycin 18-31 tumor protein p53 Homo sapiens 172-175 25989210-0 2015 Actinomycin D and nutlin-3a synergistically promote phosphorylation of p53 on serine 46 in cancer cell lines of different origin. Dactinomycin 0-13 tumor protein p53 Homo sapiens 71-74 25989210-5 2015 Actinomycin D promotes phosphorylation and accumulation of p53 via a mechanism that involves high expression of MDM2. Dactinomycin 0-13 tumor protein p53 Homo sapiens 59-62 25989210-6 2015 We hypothesized that co-treatment of cells with actinomycin D and nutlin-3a would lead to synergistic activation of p53 by stimulating kinases and preventing accumulated MDM2 from binding to p53. Dactinomycin 48-61 tumor protein p53 Homo sapiens 116-119 25989210-6 2015 We hypothesized that co-treatment of cells with actinomycin D and nutlin-3a would lead to synergistic activation of p53 by stimulating kinases and preventing accumulated MDM2 from binding to p53. Dactinomycin 48-61 tumor protein p53 Homo sapiens 191-194 25989210-7 2015 Indeed, co-treatment of various cell lines with actinomycin D and nutlin-3a resulted in a synergistic increase of p53 phosphorylation on serine 46. Dactinomycin 48-61 tumor protein p53 Homo sapiens 114-117 22743622-0 2012 Actinomycin D induces p53-independent cell death and prolongs survival in high-risk chronic lymphocytic leukemia. Dactinomycin 0-13 tumor protein p53 Homo sapiens 22-25 24525337-0 2014 AKT mediates actinomycin D-induced p53 expression. Dactinomycin 13-26 tumor protein p53 Homo sapiens 35-38 24525337-1 2014 At high cytotoxic concentrations, actinomycin D (ActD) blocks transcription, decreasing levels of MDM2 and thus causing p53 stabilization. Dactinomycin 34-47 tumor protein p53 Homo sapiens 120-123 24174547-8 2014 Longer treatment of actinomycin D increases RPL6 ubiquitination and destabilizes RPL6, and thereby putatively attenuates p53 response until the level of L6 subsides. Dactinomycin 20-33 tumor protein p53 Homo sapiens 121-124 24859470-6 2014 Actinomycin D (ActD), an activator of p53, induces the promoter and protein activities of HspB2/alphaB-crystallin. Dactinomycin 0-13 tumor protein p53 Homo sapiens 38-41 24915467-0 2014 Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D. Dactinomycin 144-157 tumor protein p53 Homo sapiens 45-48 24915467-0 2014 Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D. Dactinomycin 144-157 tumor protein p53 Homo sapiens 95-98 24915467-3 2014 Because AICAR is a relatively weak activator of p53, we investigated whether stimulation of p53 by the strong activator actinomycin D is also sensitive to the inhibitory effect of rapamycin. Dactinomycin 120-133 tumor protein p53 Homo sapiens 92-95 24915467-4 2014 In A549 lung cancer cells, activation of p53 by actinomycin D was associated with phosphorylation of p53 on Ser46. Dactinomycin 48-61 tumor protein p53 Homo sapiens 41-44 24915467-4 2014 In A549 lung cancer cells, activation of p53 by actinomycin D was associated with phosphorylation of p53 on Ser46. Dactinomycin 48-61 tumor protein p53 Homo sapiens 101-104 24835245-6 2014 We also found that HIF-1alpha does not contribute to the protection against DNA damage that can be observed in low oxygen environments, and that there are certain DNA damaging agents, such as doxorubicin and actinomycin D, that prevent HIF-1alpha induction independently of p53. Dactinomycin 208-221 tumor protein p53 Homo sapiens 274-277 25482947-6 2014 We found that inhibitors of the mTOR pathway including rapamycin, wortmannin, and caffeine blunted the p53 response to nucleolar stress induced by actinomycin D. Dactinomycin 147-160 tumor protein p53 Homo sapiens 103-106 25482947-7 2014 Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21. Dactinomycin 79-92 tumor protein p53 Homo sapiens 103-106 22743622-4 2012 In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action. Dactinomycin 63-76 tumor protein p53 Homo sapiens 27-30 22743622-4 2012 In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action. Dactinomycin 63-76 tumor protein p53 Homo sapiens 226-229 22743622-4 2012 In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action. Dactinomycin 63-76 tumor protein p53 Homo sapiens 226-229 21685937-9 2011 Finally, we show that overexpression of SPARC renders cells more resistant to the p53-mediated cytotoxic effects of the DNA-damaging drug actinomycin-D. Dactinomycin 138-149 tumor protein p53 Homo sapiens 82-85 22081073-3 2012 We show that the RPL11 is rapidly but transiently recruited at promoter sites of p53-regulated genes upon nucleolar stress induced by actinomycin D (ActD). Dactinomycin 134-147 tumor protein p53 Homo sapiens 81-84 22051195-4 2012 In this study, we found that Mdm2 was stabilized and upregulated upon Actinomycin D (ActD) treatment in the p53-deficient H1299 cell line. Dactinomycin 70-83 tumor protein p53 Homo sapiens 108-111 22051195-4 2012 In this study, we found that Mdm2 was stabilized and upregulated upon Actinomycin D (ActD) treatment in the p53-deficient H1299 cell line. Dactinomycin 85-89 tumor protein p53 Homo sapiens 108-111 22025681-6 2012 Furthermore, PNR significantly boosted actinomycin D-stimulated p53 acetylation. Dactinomycin 39-52 tumor protein p53 Homo sapiens 64-67 21490429-3 2011 Here we analyze and compare the effects of nutlin-3, tenovin-6 and low doses of actinomycin-D on p53 and its main negative regulator, mdm2. Dactinomycin 80-93 tumor protein p53 Homo sapiens 97-100 21561866-5 2011 Knockdown of S27a significantly attenuates the p53 activation in cells in response to treatment with ribosomal stress-inducing agent actinomycin D or 5-fluorouracil. Dactinomycin 133-146 tumor protein p53 Homo sapiens 47-50 21702904-4 2011 Low and high prevalence E6 variants displayed similar abilities in abrogation of growth arrest and inhibition of p53 elevation induced by actinomycin D. Dactinomycin 138-151 tumor protein p53 Homo sapiens 113-116 19657224-0 2009 Specific activation of the p53 pathway by low dose actinomycin D: a new route to p53 based cyclotherapy. Dactinomycin 51-64 tumor protein p53 Homo sapiens 27-30 21394211-3 2011 Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively. Dactinomycin 61-74 tumor protein p53 Homo sapiens 27-30 20947454-1 2010 We have previously shown that whereas T-cells from normal individuals undergo accumulation of p53 and apoptosis when treated with the genotoxic agent Actinomycin D (ActD), those from Ataxia Telangiectasia (AT) and Nijmegen Breakage Syndrome (NBS) patients resist ActD-induced apoptosis [1]. Dactinomycin 150-163 tumor protein p53 Homo sapiens 94-97 21317459-0 2010 Evaluation of an Actinomycin D/VX-680 aurora kinase inhibitor combination in p53-based cyclotherapy. Dactinomycin 17-30 tumor protein p53 Homo sapiens 77-80 21317459-3 2010 Here we sought to evaluate whether low doses of Actinomycin D (LDActD), a clinically-approved drug and potent p53 activator, could substitute Nutlin-3 in p53-based cyclotherapy. Dactinomycin 48-61 tumor protein p53 Homo sapiens 110-113 21317459-3 2010 Here we sought to evaluate whether low doses of Actinomycin D (LDActD), a clinically-approved drug and potent p53 activator, could substitute Nutlin-3 in p53-based cyclotherapy. Dactinomycin 48-61 tumor protein p53 Homo sapiens 154-157 20655369-4 2010 Our results revealed a significant P53-induction by actinomycin D, methyl methanesulfonate and etoposide. Dactinomycin 52-65 tumor protein p53 Homo sapiens 35-38 21467739-8 2011 We next investigated the involvement of the transcription-independent function of p53 using an RNA synthesis inhibitor, actinomycin D (ActD), and a protein synthesis inhibitor, cycloheximide (CHX), and found that the apoptosis was suppressed by CHX but not by ActD. Dactinomycin 120-133 tumor protein p53 Homo sapiens 82-85 19657224-0 2009 Specific activation of the p53 pathway by low dose actinomycin D: a new route to p53 based cyclotherapy. Dactinomycin 51-64 tumor protein p53 Homo sapiens 81-84 19657224-7 2009 We show here that low doses of actinomycin D mimic nutlin-3 in the highly specific activation of p53 dependant transcription, in the induction of a reversible protective growth arrest in normal cells and in the enhancement of the activity of chemotherapeutic drug induced killing of p53 positive human tumor cells. Dactinomycin 31-44 tumor protein p53 Homo sapiens 97-100 19657224-7 2009 We show here that low doses of actinomycin D mimic nutlin-3 in the highly specific activation of p53 dependant transcription, in the induction of a reversible protective growth arrest in normal cells and in the enhancement of the activity of chemotherapeutic drug induced killing of p53 positive human tumor cells. Dactinomycin 31-44 tumor protein p53 Homo sapiens 283-286 18315559-8 2008 Also, the general transcription inhibitor actinomycin D triggered nucleolar stress and activated p53. Dactinomycin 42-55 tumor protein p53 Homo sapiens 97-100 19509161-12 2009 A combination of vincristine or actinomycin D with nutlin-3 enhanced the antitumor activity in RMS cell lines with wild-type p53. Dactinomycin 32-45 tumor protein p53 Homo sapiens 125-128 19042971-4 2009 We show that upregulation of IRF2BP2 after treatment with actinomycin D (Act.D) is dependent on functional p53 in different cell lines. Dactinomycin 58-71 tumor protein p53 Homo sapiens 107-110 17371838-8 2007 Although comparable in level to that achieved by treatment with the p53 activators actinomycin D and nutlin-3, the increases in p53 and p21 after downregulation of Mdm2 were not sufficient to trigger cell cycle arrest. Dactinomycin 83-96 tumor protein p53 Homo sapiens 68-71 18474530-3 2008 In a genome-wide tiling ChIP-on-chip approach, we have identified and characterized 1546 binding sites of p53 upon Actinomycin D treatment. Dactinomycin 115-128 tumor protein p53 Homo sapiens 106-109 18296503-3 2008 The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53. Dactinomycin 174-187 tumor protein p53 Homo sapiens 241-244 18296503-3 2008 The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53. Dactinomycin 189-201 tumor protein p53 Homo sapiens 241-244 18025263-5 2007 LPA partially protected A549 cells from actinomycin D induction of both apoptosis and increased p53 abundance. Dactinomycin 40-53 tumor protein p53 Homo sapiens 96-99 17224908-5 2007 Disruption of transcription by actinomycin D, 5,6-dichloro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 protein. Dactinomycin 31-44 tumor protein p53 Homo sapiens 148-151 17056014-7 2006 Thus, the reduction of KAP1 levels promotes p53-dependent p21 induction and inhibits cell proliferation in actinomycin D-treated cells. Dactinomycin 107-120 tumor protein p53 Homo sapiens 44-47 16971506-10 2006 p53 phosphorylation was induced by serum withdrawal and other chemotherapeutic reagents such as actinomycin D, doxorubicin, and etoposide. Dactinomycin 96-109 tumor protein p53 Homo sapiens 0-3 17056014-4 2006 KAP1 reduction markedly enhanced the induction of p21, a product of the p53 target gene, after treatment with actinomycin D or gamma-irradiation, but not with camptothecin. Dactinomycin 110-123 tumor protein p53 Homo sapiens 72-75 17056014-5 2006 Treatment with actinomycin D, but not with camptothecin, augmented the interaction of p53 with Mdm2 and KAP1. Dactinomycin 15-28 tumor protein p53 Homo sapiens 86-89 15308643-8 2004 Actinomycin D-induced p53 was inhibited by small interference RNA against L5. Dactinomycin 0-13 tumor protein p53 Homo sapiens 22-25 16906043-4 2006 Whole blood (part 1+2) was stimulated (24 hr) with eight different concentrations of actinomycin-D (0-800 nM), an apoptosis inductor acting via p53-pathway. Dactinomycin 85-98 tumor protein p53 Homo sapiens 144-147 16380082-3 2006 We previously demonstrated that an N-terminal portion of NS3 formed a complex with the tumor suppressor p53 and suppressed actinomycin D-induced apoptosis. Dactinomycin 123-136 tumor protein p53 Homo sapiens 104-107 16024796-3 2005 In this report, we demonstrate that the mitochondrial ribosomal protein L41 (MRPL41) enhances p53 stability and contributes to p53-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation. Dactinomycin 201-214 tumor protein p53 Homo sapiens 94-97 16024796-3 2005 In this report, we demonstrate that the mitochondrial ribosomal protein L41 (MRPL41) enhances p53 stability and contributes to p53-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation. Dactinomycin 201-214 tumor protein p53 Homo sapiens 127-130 15310756-3 2004 We found here that knock-down of Tip60 affects the p53-dependent response following actinomycin D treatment, most likely because it inhibits p21 (CDKN1A) accumulation. Dactinomycin 84-97 tumor protein p53 Homo sapiens 51-54 14612427-8 2003 Interference with ribosomal biogenesis by a low concentration of actinomycin D is associated with an increased L11-HDM2 interaction and subsequent p53 stabilization. Dactinomycin 65-78 tumor protein p53 Homo sapiens 147-150 15314173-5 2004 The interaction of L23 with MDM2 was enhanced by treatment with actinomycin D but not by gamma-irradiation, leading to p53 activation. Dactinomycin 64-77 tumor protein p53 Homo sapiens 119-122 15152193-3 2004 In search of mechanisms controlling L11-HDM2 interaction, we found that the induction of p53 under growth inhibitory conditions, such as low dose of actinomycin D or serum depletion, can be significantly attenuated by knocking down L11, indicating the importance of L11 in mediating these growth inhibitory signals to p53. Dactinomycin 149-162 tumor protein p53 Homo sapiens 89-92 11250899-2 2001 Here we demonstrate that, unlike phosphorylation, p53 invariably undergoes acetylation in cells exposed to a variety of stress-inducing agents including hypoxia, anti-metabolites, nuclear export inhibitor and actinomycin D treatment. Dactinomycin 209-222 tumor protein p53 Homo sapiens 50-53 12374798-9 2002 In MCF7 breast cancer and A427 lung cancer cells, MUC2 expression was increased along with the endogenous p53 level by actinomycin D, UVC, and x-ray, but not in RERF-LC-MS lung cancer cells carrying a mutated p53. Dactinomycin 119-132 tumor protein p53 Homo sapiens 106-109 12127985-6 2002 MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes. Dactinomycin 9-22 tumor protein p53 Homo sapiens 61-64 11807952-4 2002 Western immunoblot analyses of MCF7 human mammary cancer cells exposed to actinomycin D (used as a positive control for G(1) cell-cycle arrest) or hydrocarbon carcinogens revealed that while all of these chemicals caused an increase in p53, only trace levels of p21(waf1/cip1) protein were observed in the hydrocarbon carcinogen-treated samples. Dactinomycin 74-87 tumor protein p53 Homo sapiens 236-239 11384212-6 2001 However, lung H441 adenocarcinoma cells, with a mutation in exon 5, codon 158 of p53, exhibited partial G1 arrest after the diol epoxides as well as actinomycin D, and H2030 adenocarcinoma cells did not show G1 arrest after any of the chemicals despite a normal p53. Dactinomycin 149-162 tumor protein p53 Homo sapiens 81-84 12927789-4 2003 It was found that induction of apoptosis (characterized by DNA laddering) by actinomycin D was accompanied by a stimulation of the expression of active (phosphorylated) form of p53. Dactinomycin 77-90 tumor protein p53 Homo sapiens 177-180 12481433-9 2002 When p53 expression was induced, cells became chemosensitive to actinomycin D in the presence or absence of MDM2 expression; this result suggests that MDM2 cannot inhibit p53-mediated chemosensitivity. Dactinomycin 64-77 tumor protein p53 Homo sapiens 5-8 11593403-3 2001 In contrast, agents that inhibit the elongation phase of transcription, such as UV light, camptothecin or actinomycin D, induced the accumulation of nuclear p53 proteins that were modified at both of these sites. Dactinomycin 106-119 tumor protein p53 Homo sapiens 157-160 10998350-6 2000 PDTC treatment prevented actinomycin D-mediated up-regulation of two p53 effector gene products, murine double minute clone 2 oncoprotein and p21(WAF1/CIP1) (where WAF1 corresponds to wild-type p53-activated fragment 1 and CIP1 corresponds to cyclin-dependent kinase-interacting protein 1). Dactinomycin 25-38 tumor protein p53 Homo sapiens 194-197 10998350-7 2000 Actinomycin D treatment led to accumulation of p53 protein in the nucleus. Dactinomycin 0-13 tumor protein p53 Homo sapiens 47-50 10998350-8 2000 However, when cells were simultaneously treated with PDTC and actinomycin D, p53 accumulated in both the nucleus and the cytoplasm. Dactinomycin 62-75 tumor protein p53 Homo sapiens 77-80 10545796-5 1999 Western analyses revealed that, though both actinomycin D and 5-MeCDE treatment stabilized p53, only trace levels of p21(waf1/cip1) were seen in the latter case. Dactinomycin 44-57 tumor protein p53 Homo sapiens 91-94 10757806-5 2000 Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested. Dactinomycin 91-104 tumor protein p53 Homo sapiens 36-39 10597242-6 1999 Inhibition of transcription by Actinomycin D blocks both KILLER/DR5 and p21 induction in cells undergoing p53-dependent apoptosis. Dactinomycin 31-44 tumor protein p53 Homo sapiens 106-109 10900010-4 2000 Here we show that treatment with the small molecule nuclear export inhibitor, leptomycin B, and actinomycin D leads to the accumulation of transcriptionally active p53 in the nucleus of HeLa, CaSki, and SiHa cells. Dactinomycin 96-109 tumor protein p53 Homo sapiens 164-167 10531375-4 1999 Cadmium at 10-30 microM impairs the p53 induction in response to DNA-damaging agents such as actinomycin D, methylmethane sulfonate, and hydrogen peroxide. Dactinomycin 93-106 tumor protein p53 Homo sapiens 36-39 9770348-13 1998 Although inhibitors of transcription, such as actinomycin D, also damage DNA, reduction of Mdm-2 or other putative "sensor" proteins may contribute to their p53-stabilizing activity. Dactinomycin 46-59 tumor protein p53 Homo sapiens 157-160 10099829-3 1999 In contrast, UV light or actinomycin D induced a modest G1 arrest that was p53-dependent only at lower doses. Dactinomycin 25-38 tumor protein p53 Homo sapiens 75-78 10029405-2 1999 In this study, we showed that the p53 response to a chemotherapeutic drug, actinomycin D, was reversible in both normal and tumor cells, even when a substantial proportion of tumor cells were undergoing apoptosis. Dactinomycin 75-88 tumor protein p53 Homo sapiens 34-37 10029405-3 1999 Despite the clear reversibility of the p53-induced cell-cycle arrest after removal of actinomycin D, a substantial proportion of the cells arrested in G2 failed to resume normal cell-cycle progression and underwent another round of DNA synthesis. Dactinomycin 86-99 tumor protein p53 Homo sapiens 39-42 14646475-8 1998 Two other agents known to induce apoptosis, vinblastine and actinomycin D, induced a similar pattern of acidic p53 species as that observed for 2-MeOE2. Dactinomycin 60-73 tumor protein p53 Homo sapiens 111-114 9891062-7 1999 Induction of p53 in response to actinomycin D or hypoxic stress decreases AFP expression. Dactinomycin 32-45 tumor protein p53 Homo sapiens 13-16 9989808-3 1999 Here we report on the correlation between inhibition of mRNA synthesis and the induction of p53, p21WAF1 and apoptosis in diploid human fibroblasts treated with either UV light, cisplatin or the RNA synthesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin. Dactinomycin 220-233 tumor protein p53 Homo sapiens 92-95 9664074-5 1998 We found that treatment of Molt-4 cells with low concentrations of actinomycin D or gamma-irradiation, which activate p53-dependent apoptosis, induces apoptosis only in cells expressing normal levels of p53. Dactinomycin 67-80 tumor protein p53 Homo sapiens 118-121 9764849-4 1998 Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis. Dactinomycin 47-60 tumor protein p53 Homo sapiens 75-78 9764849-4 1998 Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis. Dactinomycin 47-60 tumor protein p53 Homo sapiens 154-157 9764849-4 1998 Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis. Dactinomycin 47-60 tumor protein p53 Homo sapiens 154-157 9664074-5 1998 We found that treatment of Molt-4 cells with low concentrations of actinomycin D or gamma-irradiation, which activate p53-dependent apoptosis, induces apoptosis only in cells expressing normal levels of p53. Dactinomycin 67-80 tumor protein p53 Homo sapiens 203-206 9395239-7 1997 Actinomycin D or cycloheximide prevented cell death, suggesting that, in this system, p53-induced apoptosis depends upon macromolecule biosynthesis. Dactinomycin 0-13 tumor protein p53 Homo sapiens 86-89 9499413-0 1998 Metaphase fragility of the human RNU1 and RNU2 loci is induced by actinomycin D through a p53-dependent pathway. Dactinomycin 66-79 tumor protein p53 Homo sapiens 90-93 9499413-4 1998 Remarkably, we now find that very low doses of actinomycin D (5-50 ng/ml) can phenocopy Ad12 infection: metaphase fragility of the RNU1 and RNU2 loci is induced specifically in the absence of virus, and induction also requires U2 promoter elements and p53 function. Dactinomycin 47-60 tumor protein p53 Homo sapiens 252-255 9499413-6 1998 We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci. Dactinomycin 32-45 tumor protein p53 Homo sapiens 168-171 9516963-6 1998 Data demonstrated p53-dependent sensitization (> or = 4-fold) to bleomycin, actinomycin D, and 5-fluorouracil and considerably less p53-dependence (< or = 2-fold) for doxorubicin, topotecan, etoposide, and cisplatin in Cl.#27 compared to an equivalent clone containing the pGRE5-EBV vector alone (VC#3). Dactinomycin 79-92 tumor protein p53 Homo sapiens 18-21 9681825-6 1998 Actinomycin D, a potent inhibitor of transcription, as well as a DNA damaging agent, abrogated the restraint apoptosis mediated by mutant p53. Dactinomycin 0-13 tumor protein p53 Homo sapiens 138-141 9506540-3 1998 When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11. Dactinomycin 115-128 tumor protein p53 Homo sapiens 5-8 9528853-5 1998 By 8 days after a brief exposure to DNA strand breaking agents, bleomycin or actinomycin D, p53 protein is at baseline levels, while the p53 transactivation level is only slightly above its baseline. Dactinomycin 77-90 tumor protein p53 Homo sapiens 92-95 9450475-2 1997 While these cells, which express wild-type p53, were arrested in G1 after treatment with actinomycin D (a positive control), treatment with the mammary carcinogen did not cause G1 arrest but instead delayed the cells in the DNA synthesis phase. Dactinomycin 89-102 tumor protein p53 Homo sapiens 43-46 9450475-3 1997 In concert with the absence of a G1 arrest, it was found that though both chemical treatments led to increased levels of p53, only the p53 induced by actinomycin D was transcriptionally active and increased the levels of the cyclin dependent kinase inhibitor, p21(waf1/cip1). Dactinomycin 150-163 tumor protein p53 Homo sapiens 135-138 9223475-8 1997 Induction of DNA damage in normal, uninfected fibroblasts (FB) or FB expressing IE86 by actinomycin D (Act D) resulted in increased p53 levels, a predominance of the hypophosphorylated form of Rb, and increased expression of both p21(CIP1/WAF1) and mdm-2. Dactinomycin 88-101 tumor protein p53 Homo sapiens 132-135 8622872-5 1996 To further investigate the mechanisms underlying p53-independent regulation of p21, the transcription inhibitor, Actinomycin D (AMD), was used to block p21 expression. Dactinomycin 113-126 tumor protein p53 Homo sapiens 49-52 8954979-4 1996 We also observed that induction of p53 expression by actinomycin D treatment was weaker in the NS3DeltaC-expressing cells than in the control cells. Dactinomycin 53-66 tumor protein p53 Homo sapiens 35-38 8570169-7 1995 In addition, cycloheximide and actinomycin D inhibited wt p53-induced apoptosis. Dactinomycin 31-44 tumor protein p53 Homo sapiens 58-61 8542574-5 1996 Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D. Dactinomycin 66-79 tumor protein p53 Homo sapiens 38-41 8542574-5 1996 Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D. Dactinomycin 167-180 tumor protein p53 Homo sapiens 142-145 8485705-2 1993 Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin. Dactinomycin 88-101 tumor protein p53 Homo sapiens 14-17 8579493-1 1995 The ability of exogenous p53 tumor-suppressor and activated N-PAS oncogene to influence differentiation state of human colon carcinoma LIM 1215 cells and their derivatives with acquired resistance to actinomycin D or methotrexate was analysed Introduction of retroviral construct expressing human wild-type (wt) p53 into LIM 1215 cells induced electron microscopic manifestations of enterocytic differentiation, i.e. caused an increase in the numbers of cells with microvilli, desmosomes and glandular-like lumens. Dactinomycin 200-213 tumor protein p53 Homo sapiens 25-28 21559675-0 1994 Effect of actinomycin-d on the cell-cycle progression and the expression of p53, waf1/cip1, gadd45, and mdm-2 genes in human oral keratinocytes - implication of human papillomavirus infection. Dactinomycin 10-23 tumor protein p53 Homo sapiens 76-79 21559675-4 1994 Actinomycin D significantly increased the levels of intranuclear wild-type p53 and mdm-2 proteins and the transcripts of WAF1/CIP1, gadd45 and mdm-2 in normal cells, but it did not increase them in the HPV-immortalized cells. Dactinomycin 0-13 tumor protein p53 Homo sapiens 75-78 21559675-5 1994 These data indicate that actinomycin D-induced transient cell cycle arrest may be associated with enhanced level of wild-type p53 protein and the transcripts of WAF1/CIP1 and gadd45 in normal human oral keratinocytes. Dactinomycin 25-38 tumor protein p53 Homo sapiens 126-129 8057451-0 1994 The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest. Dactinomycin 128-141 tumor protein p53 Homo sapiens 58-61 8057451-5 1994 Expression of HPV-16 E6 or mutated E6 proteins that bound and targeted p53 for degradation in vitro sharply reduced the level of intracellular p53 induced by actinomycin D in human keratinocytes. Dactinomycin 158-171 tumor protein p53 Homo sapiens 71-74 8057451-5 1994 Expression of HPV-16 E6 or mutated E6 proteins that bound and targeted p53 for degradation in vitro sharply reduced the level of intracellular p53 induced by actinomycin D in human keratinocytes. Dactinomycin 158-171 tumor protein p53 Homo sapiens 143-146 8057451-6 1994 A perfect correlation between the ability of E6 proteins to reduce the level of intracellular p53 and their ability to block actinomycin D-induced cellular growth arrest was observed. Dactinomycin 125-138 tumor protein p53 Homo sapiens 94-97 34577545-0 2021 Actinomycin D Arrests Cell Cycle of Hepatocellular Carcinoma Cell Lines and Induces p53-Dependent Cell Death: A Study of the Molecular Mechanism Involved in the Protective Effect of IRS-4. Dactinomycin 0-13 tumor protein p53 Homo sapiens 84-87 8387205-6 1993 We treated primary keratinocytes with the DNA-damaging agent actinomycin D and demonstrated inhibition of replicative DNA synthesis and a significant increase in p53 protein levels. Dactinomycin 61-74 tumor protein p53 Homo sapiens 162-165 34681730-0 2021 Transcriptome Analysis of Cells Exposed to Actinomycin D and Nutlin-3a Reveals New Candidate p53-Target Genes and Indicates That CHIR-98014 Is an Important Inhibitor of p53 Activity. Dactinomycin 43-56 tumor protein p53 Homo sapiens 93-96 34681730-0 2021 Transcriptome Analysis of Cells Exposed to Actinomycin D and Nutlin-3a Reveals New Candidate p53-Target Genes and Indicates That CHIR-98014 Is an Important Inhibitor of p53 Activity. Dactinomycin 43-56 tumor protein p53 Homo sapiens 169-172 34681730-1 2021 Co-treatment with actinomycin D and nutlin-3a (A + N) strongly activates p53. Dactinomycin 18-31 tumor protein p53 Homo sapiens 73-76