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Photoinduced phenomena are of general interest for new materials. Recently, photoinduced molecular desorption of oxygen has been reported in carbon nanotubes. Here we present, using thermopower measurements, that carbon nanotubes when exposed simultaneously to UV light and oxygen exhibit photoinduced oxidation of the nanotubes. At least two plausible mechanisms for the experimentally observed photoinduced oxidation are proposed: (i) a lower energy barrier for the adsorption of photo-generated singlet oxygen, or (ii) due to the presence of defects in carbon nanotubes that may facilitate the formation of locally electron-deficient and electron-rich regions on the nanotubes which facilitate the adsorption of oxygen molecules on the nanotubes.

The K + channel KCa3.1 is required for Ca 2+ influx and the subsequent activation of CD4 T cells. The class II phosphatidylinositol 3 kinase C2β (PI3KC2β) is activated by the T-cell receptor (TCR) and is critical for KCa3.1 channel activation. Tripartite motif containing protein 27 (TRIM27) is a member of a large family of proteins that function as Really Interesting New Gene (RING) E3 ubiquitin ligases. We now show that TRIM27 functions as an E3 ligase and mediates lysine 48 polyubiquitination of PI3KC2β, leading to a decrease in PI3K enzyme activity. By inhibiting PI3KC2β, TRIM27 also functions to negatively regulate CD4 T cells by inhibiting KCa3.1 channel activity and TCR-stimulated Ca 2+ influx and cytokine production in Jurkat, primary human CD4 T cells, and Th0, Th1, and Th2 CD4 T cells generated from TRIM27 −/− mice. These findings provide a unique mechanism for regulating class II PI3Ks, and identify TRIM27 as a previously undescribed negative regulator of CD4 T cells.

Cross-linking of the IgE receptor (FcRI) on mast cells plays a critical role in؊/؊ mice are also more susceptible in vivo to acute anaphylaxis. These findings identify TRIM27 as an important negative regulator of mast cells in vivo and suggest that PI3KC2␤ is a potential new pharmacologic target to treat IgE-mediated disease.