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| Main Authors: | , , , , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
Fish & shellfish immunology
2025
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| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41015165/ |
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Table of Contents:
- Evolutionary analysis and immune-induced expression and mA modification of RIPK1 and RIPK2 in the miiuy croaker. Xing, Qianru Geng, Shang Lv, Xing Sun, Yuena Xu, Tianjun Animals Fish Proteins Poly I-C Perciformes Immunity, Innate Receptor-Interacting Protein Serine-Threonine Kinases Lipopolysaccharides Receptor-Interacting Protein Serine-Threonine Kinase 2 Gene Expression Regulation Adenosine Phylogeny Gene Expression Profiling Evolution, Molecular Receptor Interacting Protein Kinases (RIPKs), including RIPK1 and RIPK2, are key mediators of inflammatory signaling and inflammatory cell death. In this study, we identified the RIPK1 and RIPK2 genes in the miiuy croaker (Miichthys miiuy) and analyzed their evolutionary conservation and structural characteristics using bioinformatics approaches, highlighting their potential immune functions. Notably, research on the role of N6-methyladenosine (mA) modification in regulating RIPKs remains limited. Here, methylated RNA immunoprecipitation sequencing (MeRIP-seq) revealed significant mA enrichment near the stop codons of RIPK1 and RIPK2 of Miichthys miiuy, which was further confirmed by MeRIP-PCR. Expression analyses showed that RIPK1 and RIPK2 were markedly upregulated after poly(I:C) and LPS stimulation. Interestingly, poly(I:C) increased the mA modification level of RIPK1, whereas LPS reduced the mA level of RIPK2. Moreover, treatment with the methylation inhibitor cycloleucine further elevated their expression. These findings suggest that mA modification may participate in fine-tuning the immune regulatory networks involving RIPK1 and RIPK2, potentially modulating their expression dynamics in response to diverse immune stimuli. This work provides valuable insights into the epigenetic regulation of RIPK family members and offers a foundation for exploring mA-mediated control of fish innate immunity.