fig 3 (IMAGE)
Caption
UPS regulates immune cells in the TME. DCs contact T cells via MHC to transmit antigen information. The dashed box proximal to DCs depicts the mechanism by which ubiquitination modulates DCs. Ubiquitin enzymes MARCH 1, UCH-L1, MARCH9, and HRD1 regulate MHC-I and MHC-Ⅱ respectively. The results of MARCH1 regulating MHC-Ⅱ may affect the stabilization of MHC-Ⅰ. Ubiquitin-editing enzyme A20, which exerts a deubiquitinating function, mediates the maturation of DCs by regulating NEMO in the NF-κB signaling pathway of DCs. UBR5 also mediated the antigen presentation function of DCs through the regulation of IFN-γ protein stability. PD-1/PD-L1 could be regulated by DUBs and E3 ubiquitin ligases such as USP22, OTUB1, and USP12. USP can regulate T cells by autophagy and NF-κB signaling which ultimately regulate their anti-tumor immune response of them. DCs, dendritic cells; TLR, Toll-like receptor; NF-κB, nuclear factor kappa B; NEMO, nuclear factor-kappa B essential modulator; MARCH, membrane-associated ring–CH–type finger 1; HRD, 3-hydroxy-3-methylglutaryl reductase degradation1; UBR, the ubiquitin-binding region; UCH, ubiquitin carboxy-terminal hydrolases; MHC-Ⅰ/Ⅱ, major histocompatibility complex Ⅰ/Ⅱ; IFN-γ, interferon-γ; USP, ubiquitin-specific protease; OTU, ovarian tumor proteases; RNF, RING finger protein 1; TRIM, tripartite motif-containing; LRRK, eucine-rich repeat kinase; FBOX, F-box-containing protein 38; KLHL, Kelch-like family member; MDM, mouse double minute; UBA, ubiquitin-like modifier activating enzyme.
Image link: https://ars.els-cdn.com/content/image/1-s2.0-S2352304224000370-gr3_lrg.jpg
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