TRIM28, also named KRAB-associated protein 1 (KAP1), acts as the E3 ligase of IRF7 to induce the SUMOylation of IRF7, which suppresses the transcriptional activity of IRF7 and, thus, negatively regulates cellular antiviral immune responses .

Jan 23, 2017 · TRIM28 interacts with the SUMO E2 enzyme and increases SUMOylation of IRF7 followed by the repression of transcriptional activity of TRF7, suggesting that TRIM28 is a specific SUMO E3 ligase and negative regulator of IRF7 .

Interaction networks analysis identified that IRF3, IRF7, OAS1, OAS2, OAS3, OASL, GBP1, PML, BTBD1 and BTBD2 proteins were contacted with TRIM5. Moreover, KEGG revealed that apoptosis and cancer- and immune-related pathways were enriched with elevated TRIM5.

TLR7 and TLR9, which recognize viral RNA and DNA, respectively, activate IRF7 via MyD88. TRIM30α negatively regulates NF-κB activation by targeting the TAK1 complex for degradation. TRIM23 activates NEMO and TRIM27 inhibits IKKα/IKKβ and TBK1/IKKi.

Aug 18, 2023 · TRIM5 expression levels were negatively correlated with naive CD4 (+) T cells but positively correlated with M2 macrophages. Our data indicated that TRIM5 might be a key factor that modulates SLE etiology, possibly through naive CD4 (+) T cells and M2 macrophages. Keywords: differential gene expression analysis, gene, virus, autoimmune disease.

We have demonstrated that repression of IRF7 by TRIM28 is mediated by the RING domain–dependent SUMOylation of IRF7 that requires the N-terminal RBCCM domain, an effect distinct from the general repressor activity that requires the PHD and BR domains in the C …

Jan 15, 2025 · TRIM21 interacts with IRF7 and ubiquitinates IFR7 in a dose-dependent manner, which lowers the level of IRF7 protein expression and, consequently, inhibits the generation of IFN-I [27].

Jun 25, 2020 · Tripartite motif 5 (TRIM5) plays a significant function in autophagy and involves in immune and tumor processes. While the function of TRIM5 remains poorly understood in glioma. We purpose to evaluate the possible prognostic role of …

Aug 18, 2023 · Our data indicated that TRIM5 might be a key factor that modulates SLE etiology, possibly through naive CD4(+) T cells and M2 macrophages.

Jan 7, 2021 · IRF3, IRF5, and IRF7 have been identified as the substrates of Trim21. In this regard, Trim21 limits the TLR-induced type I IFN production by degradation of IRF family members. In response to virus and TLR stimulation, Trim21 expression is activated, which ubiquitylates and directs IRF3 for degradation, thus limiting the type I IFN production ...