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. Author manuscript; available in PMC: 2014 Feb 2.
Published in final edited form as: J Cell Biochem. 2013 Oct;114(10):2284–2292. doi: 10.1002/jcb.24573

Figure 4. Ubc13 is required for H. pylori-induced activation of NF-κB.

Figure 4

(A) IL-8-luciferase, Renilla, and TAK1 were expressed in HEK293T cells with and without CagA along with increasing amounts of Ubc13-C87A. Luciferase activity was measured 30 hrs post-transfection. (B) Ubc13 or control siRNA was transfected into AGS cells, along with IL-8-luciferase and Renilla. Cells were infected with H. pylori for 6 hrs, then lysates were assayed for luciferase activity. Statistical analysis was performed using a student’s t-test for 2 variables. (C) AGS cells were transfected with control or Ubc13 siRNA, then infected with H. pylori as indicated. mRNA was collected from cells and RT-PCR was performed to determine NF-κB gene transcription. (D) CagA is injected by H. pylori into host epithelial cells, where it interacts with TAK1 and TRAF6. This interaction induces the TRAF6- and Ubc13-dependent ubiquitination of TAK1 at lysine 158. This ubiquitination is required for the activation of the downstream NF-κB pathway by TAK1.