MAVS splicing variants associated with TRAF3 and TRAF6 in NF-κB and IRF3 signaling pathway in large yellow croaker Larimichthys crocea

Zou, Pengfei; Tang, Jun Chun; Liu, Ying; Feng, Jian; Zhang, Ziping; Wang, Yi Lei

doi:10.1016/j.dci.2021.104076

Cited by 15 publications

(7 citation statements)

References 44 publications

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“…Notably, the results of the present study showed that the co-expression of Lc-RIP3 with Lc-TRIF could significantly abolish the induction of NF-κB activity but enhance IRF3 activation although the overexpression of Lc-RIP3 alone exhibited no effect in IRF3 activation, indicating the regulation of Lc-RIP3 in Lc-TRIF-mediated signaling. Additionally, as an important adaptor, MAVS functions dominantly in RLRs-mediated antiviral signaling [21,37]. Interestingly, our results indicated that the co-expression of Lc-RIP3 with Lc-MAVS significantly down-regulated the induction of the NF-κB activity but up-regulated the IRF3 activation.…”

Section: Discussionmentioning

confidence: 73%

“…Thus, it is important to understand the basic immune mechanisms against such invading pathogens, which is meaningful for further disease control and prevention. Notably, we have previously revealed TRIF-and MAVS-mediated immune signaling in large yellow croakers [20,21], and further investigations also showed that RIP1 was associated with TRIF and MAVS in the host innate immune signaling, suggesting the pivotal regulatory function of RIP1 in the host immune defense. To further delineate the function of the RIP family member in the innate immunity, a RIP3 ortholog named Lc-RIP3 was cloned and characterized in large yellow croakers in the present study.…”

Section: Introductionmentioning

confidence: 77%

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RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

Zou

Liu

et al. 2021

Antibiotics

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Receptor-interacting protein 3 (RIP3) has been demonstrated to be a key regulator not only in cell death pathways including apoptosis and necroptosis but also in inflammation and host immune responses. In this study, a RIP3 ortholog named Lc-RIP3 is identified in large yellow croaker (Larimichthys crocea). The open reading frame (ORF) of Lc-RIP3 is 1524 bp long and encodes a protein of 507 amino acids (aa). The deduced Lc-RIP3 protein has an N-terminal kinase domain and a C-terminal RHIM domain, and the genome organization of Lc-RIP3 is conserved in teleosts with 12 exons and 11 introns but is different from that in mammals, which comprises 10 exons and 9 introns. Confocal microscopy revealed that Lc-RIP3 is a cytosolic protein. The expression analysis at the mRNA level indicated that Lc-RIP3 is ubiquitously distributed in various tissues/organs, and could be up-regulated under poly I:C, LPS, PGN, and Pseudomonas plecoglossicida stimulation in vivo. Notably, Lc-RIP3 could induce NF-κB but not IRF3 activation. In addition, Lc-RIP3 co-expression with Lc-TRIF, Lc-MAVS, or Lc-IRF3 significantly abolishes the activation of NF-κB but enhances the induction of IRF3 activity. Moreover, NF-κB activity could be up-regulated when Lc-RIP3 is co-expressed with Lc-RIP1 or Lc-IRF7. These results collectively indicate that Lc-RIP3 acts as an important regulator in host innate immune signaling in teleosts.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 77%

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

Zou

Liu

et al. 2021

Antibiotics

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“…To determine the expression profiles of SARM under various immune stimulations, the healthy fish were equally divided into five groups (four experimental groups and a control group), with each group contained 50 fish. In the experimental groups, each fish was injected intraperitoneally with 100 µL of PBS containing polyinosinic-polycytidylic acid (poly I:C) (1 mg/mL), peptidoglycan (PGN) (1 mg/mL), lipopolysaccharides (LPS) (0.5 mg/mL), or Pseudomonas plecoglossicida (5 × 10 5 CFU/mL), whereas the fish of the control group was injected intraperitoneally with 100 µL of PBS, respectively (32,33). At 6, 12, and 24 h post-injection (hpi), six fish were randomly selected and anesthetized as described above, various organs including the head kidney, gill, and intestine were gathered for total RNA extraction.…”

Section: Immune Stimulation and Qrt-pcr Analysismentioning

confidence: 99%

SARM suppresses TRIF, TRAF3, and IRF3/7 mediated antiviral signaling in large yellow croaker Larimichthys crocea

et al. 2023

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As a TIR domain-containing molecular, sterile α-and armadillo motif-containing protein (SARM) acts as an adaptor in Toll-like receptor (TLR) signaling, and also plays important roles in mediating apoptosis and neuronal injury. In the present study, the ortholog of SARM, named as Lc-SARM, was cloned and identified in large yellow croaker (Larimichthys crocea). The full-length ORF of Lc-SARM consists of 2,154 bp, encoding a protein of 717 amino acids (aa), which is comprised of an N-terminal ARM domain, two SAM domains, and a C-terminal TIR domain. Confocal microscopy revealed that Lc-SARM was mainly distributed in the cytoplasm, and the mRNA expression level of Lc-SARM was broadly distributed in all the detected organs/tissues, with the highest expression level found in the brain. The expression patterns of Lc-SARM could be induced in response to poly I:C, LPS, PGN stimulations, and Pseudomonas plecoglossicida infection. Notably, although the overexpression of Lc-SARM could significantly induce NF-κB, IRF3, IRF7, and type I IFN promoter activation, whereas the co-expression of Lc-SARM with Lc-TRIF, Lc-TRAF3, Lc-IRF3, or Lc-IRF7 significantly down-regulated the induction of NF-κB, IRF3, IRF7, or type I IFN promoter activation, and suppressed the antiviral effects as well as the downstream antiviral-related genes expression compared to the only overexpression of Lc-TRIF, Lc-TRAF3, Lc-IRF3, or Lc-IRF7. Co-immunoprecipitation (Co-IP) assays also demonstrated that Lc-SARM interacts separately with Lc-TRIF, Lc-TRAF3, Lc-IRF3, and Lc-IRF7. It is thus collectively suggested that Lc-SARM functions as a negative regulator in Lc-TRIF, Lc-TRAF3, and Lc-IRF3/7 involved antiviral signaling.

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“…RIG-I-MAVS signal transduction pathway plays a key role in the immune response of cells in response to RNA virus infection (Zhou et al, 2021). Studies have shown that MAVS molecules, after being activated by upstream RIG-I, will form prion-like aggregates and further activate downstream signaling pathways, eventually activating transcription factors IRF3 and NF-κB and inducing cells to express IFN-β, thereby inhibiting the proliferation of the virus in the body (Liu et al, 2020;Zou et al, 2021). Further studies found that Postmastectomy Radiation Therapy 9 (PMRT9), localized to mitochondria, directly binds to MAVS and catalyzes the symmetric dimethylation of MAVS, thereby inhibiting the aggregation and activation of MAVS.…”

Section: Mitochondrial Proteins and Innate Immunity Pathwaymentioning

confidence: 99%

Crosstalk between mitophagy and innate immunity in viral infection

Chen

Liu

et al. 2022

Front. Microbiol.

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Mitochondria are important organelles involved in cell metabolism and programmed cell death in eukaryotic cells and are closely related to the innate immunity of host cells against viruses. Mitophagy is a process in which phagosomes selectively phagocytize damaged or dysfunctional mitochondria to form autophagosomes and is degraded by lysosomes, which control mitochondrial mass and maintain mitochondrial dynamics and cellular homeostasis. Innate immunity is an important part of the immune system and plays a vital role in eliminating viruses. Viral infection causes many physiological and pathological alterations in host cells, including mitophagy and innate immune pathways. Accumulating evidence suggests that some virus promote self-replication through regulating mitophagy-mediated innate immunity. Clarifying the regulatory relationships among mitochondria, mitophagy, innate immunity, and viral infection will shed new insight for pathogenic mechanisms and antiviral strategies. This review systemically summarizes the activation pathways of mitophagy and the relationship between mitochondria and innate immune signaling pathways, and then discusses the mechanisms of viruses on mitophagy and innate immunity and how viruses promote self-replication by regulating mitophagy-mediated innate immunity.

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MAVS splicing variants associated with TRAF3 and TRAF6 in NF-κB and IRF3 signaling pathway in large yellow croaker Larimichthys crocea

Cited by 15 publications

References 44 publications

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

SARM suppresses TRIF, TRAF3, and IRF3/7 mediated antiviral signaling in large yellow croaker Larimichthys crocea

Crosstalk between mitophagy and innate immunity in viral infection

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