
DOI . ORG {
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Title[redir]:
Programmed cell death and Bcl-2 protection in very low oxygen | Nature
Description:
PROGRAMMED cell death (PCD) is a fundamental feature of animal cells1, but the mechanism remains unknown. Similarly, the Bcl-2 oncoprotein can suppress PCD in a variety of cell types and circumstances2, but it is not known how it does so. It has been suggested that PCD involves the generation of reactive oxygen species (ROS) and that Bcl-2 protects against PCD by inhibiting the generation or action of ROS3β6. To determine whether ROS are required for PCD, we cultured cells in a near-anaerobic atmosphere where the generation of ROS would be expected not to occur, or at least to be greatly reduced. We find that these conditions inhibit PCD induced by ROS-generating agents but do not inhibit PCD induced by other means. Furthermore, we show that Bcl-2 can protect cells from PCD in these anaerobic conditions. These results suggest that ROS are not required for PCD, and that Bcl-2 protects against PCD in ways that do not depend on the inhibition of ROS production or activity.
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nature portfolio permissions reprints research progress privacy policy advertising subscribe nature social media breast cancer cells nature 361 nature 356 nature 374 nature programmed cell death personal data data protection springerlink instant access permissions privacy molecular cell biology explore content subscription content cell death european economic area institutional subscriptions read drug delivery system treat skin fibrosarcoma lung apoptosis markers male rats exposed accepting optional cookies article jacobson inhibit pcd induced reactive oxygen species journals search log issue learn bio-mediated synthesis manage preferences mechanism remains unknown university college london low oxygen michael ros-generating agents content article purchase anaerobic conditions article cite access https 1038/374814a0 raff rights cell types cell prolif
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headline:Programmed cell death and Bcl-2 protection in very low oxygen
description:PROGRAMMED cell death (PCD) is a fundamental feature of animal cells1, but the mechanism remains unknown. Similarly, the Bcl-2 oncoprotein can suppress PCD in a variety of cell types and circumstances2, but it is not known how it does so. It has been suggested that PCD involves the generation of reactive oxygen species (ROS) and that Bcl-2 protects against PCD by inhibiting the generation or action of ROS3Γ’ΒΒ6. To determine whether ROS are required for PCD, we cultured cells in a near-anaerobic atmosphere where the generation of ROS would be expected not to occur, or at least to be greatly reduced. We find that these conditions inhibit PCD induced by ROS-generating agents but do not inhibit PCD induced by other means. Furthermore, we show that Bcl-2 can protect cells from PCD in these anaerobic conditions. These results suggest that ROS are not required for PCD, and that Bcl-2 protects against PCD in ways that do not depend on the inhibition of ROS production or activity.
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headline:Programmed cell death and Bcl-2 protection in very low oxygen
description:PROGRAMMED cell death (PCD) is a fundamental feature of animal cells1, but the mechanism remains unknown. Similarly, the Bcl-2 oncoprotein can suppress PCD in a variety of cell types and circumstances2, but it is not known how it does so. It has been suggested that PCD involves the generation of reactive oxygen species (ROS) and that Bcl-2 protects against PCD by inhibiting the generation or action of ROS3Γ’ΒΒ6. To determine whether ROS are required for PCD, we cultured cells in a near-anaerobic atmosphere where the generation of ROS would be expected not to occur, or at least to be greatly reduced. We find that these conditions inhibit PCD induced by ROS-generating agents but do not inhibit PCD induced by other means. Furthermore, we show that Bcl-2 can protect cells from PCD in these anaerobic conditions. These results suggest that ROS are not required for PCD, and that Bcl-2 protects against PCD in ways that do not depend on the inhibition of ROS production or activity.
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