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Nm23-M2/NDP kinase B induces endogenous c- myc and nm23-M1/NDP kinase A overexpression in BAF3 cells. Both NDP kinases protect the cells from oxidative stress-induced death
The nm23 gene family encodes nucleoside diphosphate kinases (NDPKs) which supply the cell with (d)NTPs. The human NDPKB, also known as the PuF protein, binds the c- myc promoter and transactivates the c- myc protooncogene. We have now studied the effects of mouse NDPKA and NDPKB overexpression on en...
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Published in: | Experimental cell research 2004-12, Vol.301 (2), p.293-304 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The
nm23 gene family encodes nucleoside diphosphate kinases (NDPKs) which supply the cell with (d)NTPs. The human NDPKB, also known as the PuF protein, binds the c-
myc promoter and transactivates the c-
myc protooncogene. We have now studied the effects of mouse NDPKA and NDPKB overexpression on endogenous c-
myc transactivation in the mouse BAF3 and the rat PC12 cell lines. c-
myc transcripts were found to be up-regulated by NDPKB only in the BAF3 line. This suggests that c-
myc transcriptional control via NDPKB depends on the presence of cell-specific co-factors. Unexpectedly, NDPKB also induced NDPKA expression. This new effect was found in both cell lines, suggesting that NDPKB-dependent
nm23-M1 gene transactivation requires cis and/or trans elements different from those involved in c-
myc transactivation. Moreover, the BAF3 cell proliferation capacities were found to be independent of NDPKA or B cell contents. Interestingly, cell death induced by c-
myc overexpression or H
2O
2 exposure was decreased in
nm23-transfected compared to control BAF3 cells. These data collectively suggest that NDPKs might improve cell survival by a mechanism coupling DNA repair and transcriptional regulation of genes involved in DNA damage response. |
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ISSN: | 0014-4827 1090-2422 |
DOI: | 10.1016/j.yexcr.2004.07.026 |