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. 2009 May 15;284(20):13686–13695. doi: 10.1074/jbc.M809275200

FIGURE 5.

FIGURE 5.

SUMO-1 modification of IκBα controls NFκB-mediated transcription. A, wild type, knockdown, and overexpressing SUMO-1 cells were assayed for IL-6 mRNA transcript levels using real time PCR at base-line normoxia or after 24 h of hypoxia. Control and SUMO-1 knockdown cells demonstrated remarkable increase in IL-6 expression in hypoxia (*, p < 0.005) compared with Normoxic cells. SUMO-1-overexpressing cells showed impressive attenuation of IL-6 expression despite hypoxia (**, p < 0.005). B, IL-6 mRNA levels of whole lung tissue lysates from C57BL/6 or CD 73 null mice exposed to hypoxia or in vivo protocols of H/R. In wild type mice (WT), H/R induced attenuation of IL-6 expression (*, p < 0.05, compared with hypoxia) similar to the effect observed in vitro. In CD 73 (-/-) tissue, the absence of Ado signaling produced a substantial increase (10-fold; **, p < 0.01) in base-line normoxic levels of IL-6 and 11-fold (***, p < 0.01, compared with normoxic WT) increase during hypoxia. C, protein levels of SUMO-1/IκBα. WT animals exposed to H/R showed restoration of SUMO-1/IκBα compared with degraded levels in animals exposed to hypoxia (p < 0.01). Basal levels of SUMO-1/IκBα in CD 73 null mice were substantially lower (p < 0.001) compared with WT animals and no increase was observed despite H/R.