IndraLab

"After IAV infection, OTUB1 has been observed to translocate from the nucleus to the mitochondrial membrane and subsequently activate RIG-1 through deubiquitination and E2 suppression, thereby triggering RIG-1-dependent immune signaling and antiviral responses [ xref ]."

"The RIG-I tetramer translocates to mitochondrial membrane, where it activates downstream effectors including IRF3, IRF7, and NF-kB to produce type-I Interferon (IFN-I) ( xref ). xref found OTUB1 activates RIG-I at mitochondria and achieves this function through both DUB activity and E2-blocking activity."

"During influenza A virus (IAV) infection, OTUB1 activated RIG-I via a dual mechanism of K48-Ub hydrolysis and formation of an E2-repressive complex with UBCH5c, which stimulated the RIG-I signaling cascade and the anti -viral response ( xref )."

"Jahan et al. (2020) found OTUB1 activates RIG-I at mitochondria and achieves this function through both DUB activity and E2-blocking activity."

"After IAV infection, OTUB1 has been observed to translocate from the nucleus to the mitochondrial membrane and subsequently activate RIG-1 through deubiquitination and E2 suppression, thereby triggering RIG-1-dependent immune signaling and antiviral responses [32]."

"Collectively, our results indicate that OTUB1 deficiency inhibits NF-κB and IRF activities, suggesting that it acts upstream of these transcription factors in the RIG-I signaling cascade."

"Both human and their homologs in grouper, Epinephelus coioides (OTUB1/2 and EcOTUB1/2), interact with TRAF3 and TRAF6, deubiquitinating them to attenuate virus-induced activation of IRF3 and NF-κB and suppress virus-triggered type I interferon (IFN) induction and promote viral replication. xref , xref Meanwhile, OTUB1 also activates RIG-I (retinoic acid-inducible gene I)-dependent antiviral responses through a dual mechanism: K48 polyubiquitin hydrolysis and complex formation with UbcH5c—a process antagonized by influenza A virus (IAV) NS1 protein-mediated OTUB1 degradation. xref This evolutionary arms race between host Otubains and viral evasion strategies underscores their fundamental role in antiviral defense, while highlighting the therapeutic potential of developing targeted Otubain modulators."

"OTUD1 inhibits innate antiviral immunity in response to RNA and DNA viruses ( Zhang et al., 2018 , 2020b , 2020c ), OTUD4 promotes antiviral response by deubiquitinating and stabilizing MAVS ( Liuyu e[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Collectively, our data indicate that OTUB1-dependent activation of RIG-I is impeded by the presence of IAV NS1 by facilitating its proteasomal degradation."

"Collectively, our data indicate that OTUB1-dependent activation of RIG-I is impeded by the presence of IAV NS1 by facilitating its proteasomal degradation.RLRs are critical cytosolic sensors for patho[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"To determine the mechanism of OTUB1-dependent RIG-I activation, we adopted a cell-free system of IRF3 dimerization ( Zeng et al., 2010 ) reconstituted from purified RIG-I, mitochondria, and cytosol ex[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Our data suggest that OTUB1 participates by a dual mechanism to enable RIG-I activation; first via its conventional deubiquitylating activity and also by inhibition of E2 enzymes, most likely Ubch5c, [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"