It is able to complement the radiosensitivity defect of an ataxia telangiectasia (AT) fibroblast cell line. Plays a crucial role in the regulation of macrophage activation in response to viral or bacterial infections within the respiratory tract. Mechanistically, TRIM29 interacts with IKBKG/NEMO in the lysosome where it induces its Lys-48 ubiquitination and subsequent degradation. In turn, the expression of type I interferons and the production of proinflammatory cytokines are inhibited. Additionally, induces the Lys-48 ubiquitination of STING1 in a similar way, leading to its degradation.
