Recently, Prof. Gao Chengjiang’s team published the paper “TRIM26 positively regulates the inflammatory immune response through K11-linked ubiquitination of TAB1” in the journal Cell Death & Differentiation (IF:10.717). Zhao Jian and Cai Baoshan, doctoral candidates are the co-first authors of this paper, and Professor Gao Chengjiang and Assistant researcher Liu Bingyu are the co-corresponding authors. Shandong University is the first author unit and the only corresponding author.

The TRIM31, TRIM26 and TRIM38 members of the trim-protein family of ubiquitin ligases have been identified to play a key role in antiviral natural immune regulation by Professor Gao Chengjiang's team (Nat Immunol 2017, 18:214-224; PLoS Pathog 2015, 11:e1004726, J Immunol 2012, 188:5311-5318; J Immunol 2012, 188:2567-2574), but the function and mechanism of TRIM family members in the inflammatory response is unclear. This research found that TRIM26 also plays a key regulatory role in natural immune TLRs-mediated inflammatory response. And knocking out the TRIM26 gene in mice significantly improved LPS-mediated endotoxin shock. In-depth mechanism research has found that TRIM26 can bind to TAB1, the key downstream node protein of TLRs signaling pathway, catalyze its k11-type non-classical polyubiquitin modification, promote the formation of TAK1-Tabs complex and the kinase activation of TAK1, and finally positively regulate TLRS-mediated inflammatory cytokine production. This research reveals a new mechanism of TRIM26-mediated inflammatory response and provides a new target and theoretical basis for the treatment of inflammatory diseases.

Paper link: https://www.nature.com/articles/s41418-021-00803-1