PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28265856-0 2018 DRAM Is Involved in Regulating Nucleoside Analog-Induced Neuronal Autophagy in a p53-Independent Manner. Nucleosides 31-41 tumor protein p53 Homo sapiens 81-84 32467171-9 2020 These results demonstrate that DRS induced by a nucleoside analog-type chemotherapeutic drug suppresses tumor growth irrespective of p53 status by directing tumor cell fate toward cellular senescence or apoptotic cell death according to p53 status. Nucleosides 48-58 tumor protein p53 Homo sapiens 237-240 32427989-7 2020 However, depleting Mdm4 sensitized p53-/- cells to the nucleoside analog gemcitabine, raising the future perspective of using Mdm4 inhibitors as chemosensitizers. Nucleosides 55-65 tumor protein p53 Homo sapiens 35-38 33075425-1 2021 Most nucleoside anticancer drugs show a primary resistance to p53-deficient or p53-mutated cancer cells and are limited in the clinic to the treatment of hematological malignancies. Nucleosides 5-15 tumor protein p53 Homo sapiens 62-65 33075425-1 2021 Most nucleoside anticancer drugs show a primary resistance to p53-deficient or p53-mutated cancer cells and are limited in the clinic to the treatment of hematological malignancies. Nucleosides 5-15 tumor protein p53 Homo sapiens 79-82 19287302-0 2009 Excision of nucleoside analogs in mitochondria by p53 protein. Nucleosides 12-22 tumor protein p53 Homo sapiens 50-53 26431163-11 2015 We conclude that the pre-activation of p53 through Mdm2 antagonists serves as a viable option to selectively protect p53-proficient cells against the cytotoxic effects of Wee1 inhibitors, especially when combined with a nucleoside analogue. Nucleosides 220-230 tumor protein p53 Homo sapiens 39-42 23017148-1 2012 BACKGROUND: Nucleoside analogs used in the chemotherapy of solid tumors, such as the capecitabine catabolite 5"-deoxy-5-fluorouridine (5"-DFUR) trigger a transcriptomic response that involves the aquaglyceroporin aquaporin 3 along with other p53-dependent genes. Nucleosides 12-22 tumor protein p53 Homo sapiens 242-245 20515947-1 2010 Previously, we reported that the nucleoside analogue/transcriptional inhibitor ARC (4-amino-6-hydrazino-7-beta-D-ribofuranosyl-7H-pyrrolo(2,3-d)-pyrimidine-5-carboxamide) was able to induce p53-independent apoptosis in multiple cancer cell lines of different origins. Nucleosides 33-43 tumor protein p53 Homo sapiens 190-193 19287302-7 2009 RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H. Nucleosides 67-77 tumor protein p53 Homo sapiens 271-274 19287302-8 2009 The amount of nucleoside analogs incorporated into the elongated DNA with mitochondrial fractions of human colon carcinoma 116 (HCT116)(p53+/+) cells was lower than that of HCT116(p53-/-) cells. Nucleosides 14-24 tumor protein p53 Homo sapiens 136-139 19287302-8 2009 The amount of nucleoside analogs incorporated into the elongated DNA with mitochondrial fractions of human colon carcinoma 116 (HCT116)(p53+/+) cells was lower than that of HCT116(p53-/-) cells. Nucleosides 14-24 tumor protein p53 Homo sapiens 180-183 19287302-9 2009 Furthermore, mitochondrion-localized elevation of p53 in HCT116(p53+/+) cells, following the irradiation-stress stimuli, correlates with the reduction in incorporation of nucleoside analogs and wrong nucleotides. Nucleosides 171-181 tumor protein p53 Homo sapiens 50-53 19287302-9 2009 Furthermore, mitochondrion-localized elevation of p53 in HCT116(p53+/+) cells, following the irradiation-stress stimuli, correlates with the reduction in incorporation of nucleoside analogs and wrong nucleotides. Nucleosides 171-181 tumor protein p53 Homo sapiens 64-67 19287302-10 2009 CONCLUSION: p53 in mitochondria may functionally interact with DNA polymerase gamma, thus providing a proofreading function during mitochondrial DNA replication for excision of nucleoside analogs and polymerization errors. Nucleosides 177-187 tumor protein p53 Homo sapiens 12-15 19287302-4 2009 In the present study, we investigated the ability of p53 to excise incorporated nucleoside analogs from DNA in mitochondria. Nucleosides 80-90 tumor protein p53 Homo sapiens 53-56 19287302-5 2009 DESIGN: The functional interaction of p53 and DNA polymerase gamma during the incorporation of nucleoside analog was examined in mitochondrial fractions of p53-null H1299 cells, as the source of DNA polymerase gamma. Nucleosides 95-105 tumor protein p53 Homo sapiens 38-41 19287302-7 2009 RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H. Nucleosides 67-77 tumor protein p53 Homo sapiens 178-181 19287302-7 2009 RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H. Nucleosides 67-77 tumor protein p53 Homo sapiens 271-274 19287302-7 2009 RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H. Nucleosides 67-77 tumor protein p53 Homo sapiens 271-274 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. Nucleosides 0-10 tumor protein p53 Homo sapiens 143-146 17977830-2 2008 However, whether cellular responses to nucleoside analogue-induced DNA damage also operate through p53 posttranslational modification has not been reported. Nucleosides 39-49 tumor protein p53 Homo sapiens 99-102 15793143-0 2005 Excision of nucleoside analogs from DNA by p53 protein, a potential cellular mechanism of resistance to inhibitors of human immunodeficiency virus type 1 reverse transcriptase. Nucleosides 12-22 tumor protein p53 Homo sapiens 43-46 16505115-2 2006 However, it is also known that nucleosides are efficient activators of apoptosis in tumor cells that do not express a functional p53. Nucleosides 31-42 tumor protein p53 Homo sapiens 129-132 16505115-11 2006 Together, these studies indicate that c-Abl-independent p73 stabilization pathways could account for the p53-independent mechanisms in nucleoside-induced apoptosis. Nucleosides 135-145 tumor protein p53 Homo sapiens 105-108 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. Nucleosides 0-10 tumor protein p53 Homo sapiens 102-105 15793143-1 2005 We investigated the ability of p53 in cytoplasm to excise nucleoside analogs (NAs). Nucleosides 58-68 tumor protein p53 Homo sapiens 31-34 15793143-2 2005 A decrease in incorporation of NAs by human immunodeficiency virus type 1 reverse transcriptase and their excision from DNA by p53, provided by the cytoplasmic fraction of LCC2 cells, suggest that p53 in cytoplasm may act as an external proofreader for NA incorporation. Nucleosides 31-34 tumor protein p53 Homo sapiens 197-200 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. Nucleosides 98-108 tumor protein p53 Homo sapiens 212-215 11751391-0 2001 Interaction of p53 and DNA-PK in response to nucleoside analogues: potential role as a sensor complex for DNA damage. Nucleosides 45-55 tumor protein p53 Homo sapiens 15-18 11751391-11 2001 These data suggest that DNA-PK and p53 may form a sensor complex that detects the disruption of DNA replication caused by nucleoside analogue incorporation and may subsequently signal for apoptosis. Nucleosides 122-132 tumor protein p53 Homo sapiens 35-38 10945628-3 2000 Whereas p53 can contribute to the nucleoside-induced killing of CLL cells, recent work from this laboratory and elsewhere has shown that such killing can also occur by p53-independent mechanisms. Nucleosides 34-44 tumor protein p53 Homo sapiens 8-11 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. Nucleosides 241-251 tumor protein p53 Homo sapiens 212-215 10945628-10 2000 This indicates that PARP activity can occasionally be central to nucleoside-induced killing and that such PARP-mediated killing is p53 independent. Nucleosides 65-75 tumor protein p53 Homo sapiens 131-134 10772725-6 2000 The hypothesis on an important role of the 3"-to-5" exonuclease activity of p53 protein in the action of nucleoside analogs was proposed. Nucleosides 105-115 tumor protein p53 Homo sapiens 76-79 10520012-2 1999 Cases of CLL with p53 dysfunction (n = 7) displayed slight, but significant, resistance to nucleoside-induced cell killing when compared with cases with functionally intact p53 (n = 12). Nucleosides 91-101 tumor protein p53 Homo sapiens 18-21 10520012-4 1999 These findings suggest that the poor therapeutic response to purine analogues observed in patients with p53 defects is likely to be caused by the emergence, on a background of genomic instability, of CLL-cell clones that are resistant to nucleoside-induced killing for reasons unrelated to p53. Nucleosides 238-248 tumor protein p53 Homo sapiens 104-107 9031099-14 1996 Finally, whereas CLB and nucleoside analogs may produce cell death in CLL by a P53 dependent pathway other agents, such as dexamethasone or vincristine, may act through P53-independent pathways. Nucleosides 25-35 tumor protein p53 Homo sapiens 79-82