TRIM22 can activate the noncanonical NF-κB pathway by affecting IKKα

Abstract

Tripartite motif 22 (TRIM22) is involved in various cellular processes. It has been reported that TRIM22 can activate nuclear factor-κB (NF-κB) pathway, but the precise mechanism remains unclear. In this study, we explored the exact role of TRIM22 in activating the NF-κB pathway. Different to tumor necrosis factor-α (TNF-α) induction, we found that the overexpression of TRIM22 could induce the processing of p100 to p52 in HEK293T cells. Furthermore, based on the results of co-immunoprecipitation and co-localization experiments, we demonstrated that TRIM22 could interact with IκB kinase (IKK)α but not IKKβ and could increase the level and phosphorylation of IKKα through its really interesting new gene (RING) and spla-ryanodine receptor (SPRY) domains. These results suggest that TRIM22 is able to activate the noncanonical but not the canonical NF-κB pathway by activating IKKα. This finding will aid our understanding of the biological function of TRIM22.

• IKKα
• NF-κB
• TRIM22

Acknowledgements

We thank Dr. Hong-Bing Shu (Wuhan University, Wuhan, China) for providing the plasmids of Flag-IKKα and Flag-IKKβ.

Declaration of interest

The authors report no declarations of interest.

This work was supported by a grant from the Key Projects in the National Science & Technology Pillar Program during the twelfth Five-Year Plan Period of China (2012ZX10001006) and grants from the International Science & Technology Cooperation Program of China (2011DFA31030) and Deutsche Forschungsgemeinschaft (SFB/Transregio TRR60).

Supplementary material available online