In these studies, we have used both targeted and unbiased approaches to interrogate the role of MIB2 in a mouse model of inflammatory skin disease. Mind bomb 2 (MIB2) is an inhibitor of cell death in cancer cells, but its role in other pathologies has not been explored. The tightly controlled checkpoints on cell death and nuclear factor kappa B (NF-κB) signaling are crucial regulators of skin homeostasis. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. Instead, MIB2 enhances the production of wound-healing molecules, granulocyte colony-stimulating factor, and Eotaxin, within the skin. Surprisingly, the role of MIB2 in limiting skin inflammation is independent of its known pro-survival function and E3 ligase activity. Here, we demonstrate that MIB2 antagonizes inflammatory dermatitis in the context of the cpd mutation. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of Sharpin cpdm mice however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. The chronic proliferative dermatitis (cpd) phenotype driven by the cpd mutation (cpdm) in the Sharpin gene is characterized by dermal inflammation and epidermal abnormalities. Skin inflammation is a complex process implicated in various dermatological disorders.
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