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The ATM protein: The importance of being active
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| Zeitschriftentitel: | Journal of Cell Biology |
|---|---|
| Personen und Körperschaften: | , |
| In: | Journal of Cell Biology, 198, 2012, 3, S. 273-275 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Rockefeller University Press
|
| Schlagwörter: |
| author_facet |
Shiloh, Yosef Ziv, Yael Shiloh, Yosef Ziv, Yael |
|---|---|
| author |
Shiloh, Yosef Ziv, Yael |
| spellingShingle |
Shiloh, Yosef Ziv, Yael Journal of Cell Biology The ATM protein: The importance of being active Cell Biology |
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shiloh, yosef |
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Shiloh, Yosef Ziv, Yael 1540-8140 0021-9525 Rockefeller University Press Cell Biology http://dx.doi.org/10.1083/jcb.201207063 <jats:p>The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics.</jats:p> The ATM protein: The importance of being active Journal of Cell Biology |
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| title |
The ATM protein: The importance of being active |
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The ATM protein: The importance of being active |
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The ATM protein: The importance of being active |
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The ATM protein: The importance of being active |
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The ATM protein: The importance of being active |
| title_short |
The ATM protein: The importance of being active |
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the atm protein: the importance of being active |
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Cell Biology |
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http://dx.doi.org/10.1083/jcb.201207063 |
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2012 |
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273-275 |
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<jats:p>The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics.</jats:p> |
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| description | <jats:p>The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics.</jats:p> |
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| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTA4My9qY2IuMjAxMjA3MDYz |
| imprint | Rockefeller University Press, 2012 |
| imprint_str_mv | Rockefeller University Press, 2012 |
| institution | DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161 |
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| spelling | Shiloh, Yosef Ziv, Yael 1540-8140 0021-9525 Rockefeller University Press Cell Biology http://dx.doi.org/10.1083/jcb.201207063 <jats:p>The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics.</jats:p> The ATM protein: The importance of being active Journal of Cell Biology |
| spellingShingle | Shiloh, Yosef, Ziv, Yael, Journal of Cell Biology, The ATM protein: The importance of being active, Cell Biology |
| title | The ATM protein: The importance of being active |
| title_full | The ATM protein: The importance of being active |
| title_fullStr | The ATM protein: The importance of being active |
| title_full_unstemmed | The ATM protein: The importance of being active |
| title_short | The ATM protein: The importance of being active |
| title_sort | the atm protein: the importance of being active |
| title_unstemmed | The ATM protein: The importance of being active |
| topic | Cell Biology |
| url | http://dx.doi.org/10.1083/jcb.201207063 |