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Sci. Signal., 30 March 2010
Vol. 3, Issue 115, p. ra24
[DOI: 10.1126/scisignal.2000672]


Editor's Summary

Adapting to Oxidizing Environments
Reactive oxygen species (ROS) were thought for many years to be only detrimental, causing damage to DNA and proteins. However, it has become clear that ROS, particularly H2O2, can act as intracellular signaling molecules that link cellular redox state to such processes as proliferation and differentiation. Bogeski et al. have uncovered a role for ROS in regulating calcium channel activity—and intracellular Ca2+ signals crucial to the immune response—in T lymphocytes. They found that activity of ORAI1 calcium channels was blocked by H2O2, whereas that of the related ORAI3 channels was not. Redox sensitivity decreased as naïve human T helper lymphocytes differentiated into effector T helper lymphocytes, which was associated with an increase in the abundance of mRNA encoding the insensitive ORAI3 protein. The authors suggest that changes in the specific complement of ORAI channels, and thereby sensitivity to ROS, could enable T lymphocytes to fine tune cellular responses in oxidizing environments such as those found during inflammation.

Citation: I. Bogeski, C. Kummerow, D. Al-Ansary, E. C. Schwarz, R. Koehler, D. Kozai, N. Takahashi, C. Peinelt, D. Griesemer, M. Bozem, Y. Mori, M. Hoth, B. A. Niemeyer, Differential Redox Regulation of ORAI Ion Channels: A Mechanism to Tune Cellular Calcium Signaling. Sci. Signal. 3, ra24 (2010).

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B. J. Hawkins, K. M. Irrinki, K. Mallilankaraman, Y.-C. Lien, Y. Wang, C. D. Bhanumathy, R. Subbiah, M. F. Ritchie, J. Soboloff, Y. Baba, et al. (2010)
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The Nonphagocytic NADPH Oxidase Duox1 Mediates a Positive Feedback Loop During T Cell Receptor Signaling.
J. Kwon, K. E. Shatynski, H. Chen, S. Morand, X. de Deken, F. Miot, T. L. Leto, and M. S. Williams (2010)
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