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Drp1 can be SUMOylated by both SUMO-1 and SUMO-2/3. SUMO-1-ylation and deSUMO-2/3-ylation of Drp1 promotes its association with mitochondrial outer membrane (MOM), which facilitates mitochondrial fission and activates mitophagy. On the contrary, SUMO-2/3-ylation and deSUMO-1-ylation of Drp1 lead to accumulation of defective mitochondria and cardiomyocyte apoptosis.
In the course of disease, TLR4 of the B lymphocyte membrane is stimulated by ligands to activate downstream NF-κB signaling, which eventually leads to the activation of B lymphocytes and their differentiation into plasma cells and then to the production of a large number of autoantibodies. The present work reveals that β-arr2 interacts with TLR4 and mediates its endocytosis, thus inhibiting downstream NF-κB signaling mediated by TLR4 and preventing B lymphocytes from overactivation and differentiation under stimulation with inflammatory mediators