Prof. Bing SUN′s group reported that TRIM30a, a RING protein, was induced by TLR agonists and interacted with the TAB2-TAB3-TAK1 adaptor-kinase complex involved in the activation of transcription factor NF-kB. TRIM30a promoted the degradation of TAB2 and TAB3 and inhibited NF-kB activation induced by TLR signaling. In vivo studies showed that transfected or transgenic mice overexpressing TRIM30a were more resistant to endotoxic shock. Consistent with that, in vivo ‘knockdown’ of TRIM30a mRNA by small interfering RNA impaired LPS-induced tolerance.

　　This work collectively indicate that TRIM30a negatively regulates TLR-mediated NF-kB activation by targeting degradation of TAB2 and TAB3 by a ‘feedback’ mechanism. Results have been published on《Nature Immunology》in 2008.