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. 2013 Nov 16;62(12):4247–4256. doi: 10.2337/db13-0751

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© 2013 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 8. — ONOO⁻ is involved in GTPCH1 inhibition and GTPCH1 ubiquitination in diabetic mouse aortas in vivo. Control (11 mice) and STZ-induced diabetic mice (12 mice) were fed Tempo as described in research design and methods. A: Tempo treatment normalizes the maximal endothelium-dependent vasorelaxation in diabetic mice. B: Effects of Tempo treatment on total eNOS and the serine 1177 phosphorylation of eNOS in control and STZ-injected diabetic mice. C: Tempo treatment suppresses diabetes-enhanced superoxide production. D: Tempo ablates 3-NT formation in diabetic mouse aortas. E: Tempo abolishes diabetes-induced GTPCH1 inhibition in diabetic mouse aortas. F: Effects of diabetes and Tempo treatment on GTPCH1 ubiquitination in vivo. The total GTPCH1 and ubiquitinated GTPCH1 were assayed in isolated mouse aortas. The blot is a representative of six blots obtained from six independent experiments. n = 6. G: Schematic description for ONOO⁻-induced GTPCH1 inhibition and eNOS uncoupling. Ub, ubiquitin. *P < 0.05 STZ vs. control; #P < 0.05 control + Tempo or L-NAME vs. STZ; †P < 0.05 STZ vs. STZ plus Tempo or L-NAME.

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