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Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ
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| Zeitschriftentitel: | Genes & Development |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Genes & Development, 18, 2004, 15, S. 1824-1837 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Cold Spring Harbor Laboratory
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| Schlagwörter: |
| author_facet |
Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. |
|---|---|
| author |
Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. |
| spellingShingle |
Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. Genes & Development Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ Developmental Biology Genetics |
| author_sort |
li, baojie |
| spelling |
Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.1223504 <jats:p>c-Abl and Atm have been implicated in cell responses to DNA damage and oxidative stress. However, the molecular mechanisms by which they regulate oxidative stress response remain unclear. In this report, we show that deficiency of c-Abl and deficiency of ATM differentially altered cell responses to oxidative stress by induction of antioxidant protein peroxiredoxin I (Prx I) via Nrf2 and cell death, both of which required protein kinase C (PKC) δ activation and were mediated by reactive oxygen species.<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl;<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>osteoblasts showed the opposite. These phenotypes correlated with increased PKC δ expression in<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts and decreased PKC δ expression in<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells, respectively. The enhanced responses of<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts could be mimicked by overexpression of PKC δ in normal cells and impeded by inhibition of PKC δ, and diminished responses of<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells could be rescued by PKC δ overexpression, indicating that PKC δ mediated the effects of c-Abl and ATM in oxidative stress response. Hence, our results unveiled a previously unrecognized mechanism by which c-Abl and Atm participate in oxidative stress response.</jats:p> Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ Genes & Development |
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Cold Spring Harbor Laboratory, 2004 |
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| title |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_unstemmed |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_full |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_fullStr |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_full_unstemmed |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_short |
Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_sort |
distinct roles of c-abl and atm in oxidative stress response are mediated by protein kinase c δ |
| topic |
Developmental Biology Genetics |
| url |
http://dx.doi.org/10.1101/gad.1223504 |
| publishDate |
2004 |
| physical |
1824-1837 |
| description |
<jats:p>c-Abl and Atm have been implicated in cell responses to DNA damage and oxidative stress. However, the molecular mechanisms by which they regulate oxidative stress response remain unclear. In this report, we show that deficiency of c-Abl and deficiency of ATM differentially altered cell responses to oxidative stress by induction of antioxidant protein peroxiredoxin I (Prx I) via Nrf2 and cell death, both of which required protein kinase C (PKC) δ activation and were mediated by reactive oxygen species.<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl;<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>osteoblasts showed the opposite. These phenotypes correlated with increased PKC δ expression in<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts and decreased PKC δ expression in<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells, respectively. The enhanced responses of<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts could be mimicked by overexpression of PKC δ in normal cells and impeded by inhibition of PKC δ, and diminished responses of<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells could be rescued by PKC δ overexpression, indicating that PKC δ mediated the effects of c-Abl and ATM in oxidative stress response. Hence, our results unveiled a previously unrecognized mechanism by which c-Abl and Atm participate in oxidative stress response.</jats:p> |
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| author | Li, Baojie, Wang, Xueying, Rasheed, Naslin, Hu, Yuanyu, Boast, Sharon, Ishii, Tetsuro, Nakayama, Keiko, Nakayama, Keiichi I., Goff, Stephen P. |
| author_facet | Li, Baojie, Wang, Xueying, Rasheed, Naslin, Hu, Yuanyu, Boast, Sharon, Ishii, Tetsuro, Nakayama, Keiko, Nakayama, Keiichi I., Goff, Stephen P., Li, Baojie, Wang, Xueying, Rasheed, Naslin, Hu, Yuanyu, Boast, Sharon, Ishii, Tetsuro, Nakayama, Keiko, Nakayama, Keiichi I., Goff, Stephen P. |
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| description | <jats:p>c-Abl and Atm have been implicated in cell responses to DNA damage and oxidative stress. However, the molecular mechanisms by which they regulate oxidative stress response remain unclear. In this report, we show that deficiency of c-Abl and deficiency of ATM differentially altered cell responses to oxidative stress by induction of antioxidant protein peroxiredoxin I (Prx I) via Nrf2 and cell death, both of which required protein kinase C (PKC) δ activation and were mediated by reactive oxygen species.<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl;<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>osteoblasts showed the opposite. These phenotypes correlated with increased PKC δ expression in<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts and decreased PKC δ expression in<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells, respectively. The enhanced responses of<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts could be mimicked by overexpression of PKC δ in normal cells and impeded by inhibition of PKC δ, and diminished responses of<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells could be rescued by PKC δ overexpression, indicating that PKC δ mediated the effects of c-Abl and ATM in oxidative stress response. Hence, our results unveiled a previously unrecognized mechanism by which c-Abl and Atm participate in oxidative stress response.</jats:p> |
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| imprint | Cold Spring Harbor Laboratory, 2004 |
| imprint_str_mv | Cold Spring Harbor Laboratory, 2004 |
| 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 |
| issn | 0890-9369, 1549-5477 |
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| language | English |
| last_indexed | 2024-03-01T16:51:20.544Z |
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| physical | 1824-1837 |
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| publisher | Cold Spring Harbor Laboratory |
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| series | Genes & Development |
| source_id | 49 |
| spelling | Li, Baojie Wang, Xueying Rasheed, Naslin Hu, Yuanyu Boast, Sharon Ishii, Tetsuro Nakayama, Keiko Nakayama, Keiichi I. Goff, Stephen P. 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.1223504 <jats:p>c-Abl and Atm have been implicated in cell responses to DNA damage and oxidative stress. However, the molecular mechanisms by which they regulate oxidative stress response remain unclear. In this report, we show that deficiency of c-Abl and deficiency of ATM differentially altered cell responses to oxidative stress by induction of antioxidant protein peroxiredoxin I (Prx I) via Nrf2 and cell death, both of which required protein kinase C (PKC) δ activation and were mediated by reactive oxygen species.<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl;<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>osteoblasts showed the opposite. These phenotypes correlated with increased PKC δ expression in<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts and decreased PKC δ expression in<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells, respectively. The enhanced responses of<jats:italic>c-abl</jats:italic><jats:sup>-/-</jats:sup>osteoblasts could be mimicked by overexpression of PKC δ in normal cells and impeded by inhibition of PKC δ, and diminished responses of<jats:italic>Atm</jats:italic><jats:sup>-/-</jats:sup>cells could be rescued by PKC δ overexpression, indicating that PKC δ mediated the effects of c-Abl and ATM in oxidative stress response. Hence, our results unveiled a previously unrecognized mechanism by which c-Abl and Atm participate in oxidative stress response.</jats:p> Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ Genes & Development |
| spellingShingle | Li, Baojie, Wang, Xueying, Rasheed, Naslin, Hu, Yuanyu, Boast, Sharon, Ishii, Tetsuro, Nakayama, Keiko, Nakayama, Keiichi I., Goff, Stephen P., Genes & Development, Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ, Developmental Biology, Genetics |
| title | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_full | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_fullStr | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_full_unstemmed | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_short | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| title_sort | distinct roles of c-abl and atm in oxidative stress response are mediated by protein kinase c δ |
| title_unstemmed | Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ |
| topic | Developmental Biology, Genetics |
| url | http://dx.doi.org/10.1101/gad.1223504 |