https://www.selleckchem.com/pr....oducts/cetuximab.htm
Mechanistically, Aim2 bound Ube2i, which mediates sumoylation-based suppression of IFN-I expression; deficiency of Aim2 decreased cellular sumoylation, resulting in an augmented IFN-I signature and kidney pathogenesis. This study demonstrates a critical role for Aim2 in an optimal Ube2i-mediated sumoylation-based suppression of IFN-I generation and development of SLE, the Aim2-Ube2i axis can thus be a novel target for intervention. This study demonstrates a critical role for Aim2 in an optimal Ube2i-mediated sumoylation-based suppress
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