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• W2971994631 abstract "The interleukin-1-receptor-associated kinase 3 (IRAK3) is known in mammals as a negative feedback regulator of NF-B-mediated innate-immune mechanisms. We identified in RNA-seq experiments a prototypic 1920-nt sequence encoding irak3 from rainbow trout (Oncorhynchus mykiss) and 20 variants hereof, which vary in length and nucleotide composition. Based on the DNA-sequence information from two closely related irak3 genes from rainbow trout and an irak3-sequence fragment from Atlantic salmon retrieved from public databases, we elucidated the underlying genetic causes for this striking irak3 diversity. Infection of rainbow trout with a lethal dose of Aeromonas salmonicida enhanced the expression of all variants in liver, head kidney and peripheral blood leucocytes. We analysed the functional impact of the full-length factor and selected structural variants by overexpressing them in mammalian HEK-293 cells. The full-length factor enhanced the basal activity of NF-κB, but did not dampen the TLR2-signalling-induced levels of NF-κB activtion. Increasing the basal NF-B-activity through Irak3 does apparently not involve its C-terminal domain. However, more severely truncated factors did not influence NF-κB activities at all. The TLR2-mediated stimulation did not alter the spatial distribution of Irak3 inside the cells. In salmonid CHSE-214 cells, we observed that the Irak3-splice variant expressing prominently the C-terminal domain quenched significantly the stimulation-dependent production of interleukin-1 and interleukin-8 but not of other immune regulators. We conclude that the different gene and splice variants of Irak3 from trout play distinct roles in the activation of immune-regulatory mechanisms." @default.
• W2971994631 created "2019-09-12" @default.
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• W2971994631 date "2019-09-20" @default.
• W2971994631 modified "2023-10-18" @default.
• W2971994631 title "At Least Two Genes Encode Many Variants of Irak3 in Rainbow Trout, but Neither the Full-Length Factor Nor Its Variants Interfere Directly With the TLR-Mediated Stimulation of Inflammation" @default.
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• W2971994631 doi "https://doi.org/10.3389/fimmu.2019.02246" @default.
• W2971994631 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6763605" @default.
• W2971994631 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31616422" @default.
• W2971994631 hasPublicationYear "2019" @default.
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