ArticleGenome biology2006
Alternate transcription of the Toll-like receptor signaling cascade.
Article in Genome biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
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- The N-terminally truncated helper NLR NRG1C antagonizes immunity mediated by its full-length neighbors NRG1A and NRG1B.The Plant cell · 2022Article
- An alternative downstream translation start site in the non-TIR adaptor Scimp enables selective amplification of CpG DNA responses in mouse macrophages.Immunology and cell biology · 2022Article
- Mechanism of MyD88S mediated signal termination.Cell communication and signaling : CCS · 2022Article
- KDmarkers: A biomarker database for investigating epigenetic methylation and gene expression levels in Kawasaki disease.Computational and structural biotechnology journal · 2022Article
- Alternative pre-mRNA splicing as a mechanism for terminating Toll-like Receptor signaling.Frontiers in immunology · 2022Review
- RNA metabolism and links to inflammatory regulation and disease.Cellular and molecular life sciences : CMLS · 2021Review
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- Aberrant Expression ofJournal of clinical medicine · 2021Article
- Identification of Yak'sAnimals : an open access journal from MDPI · 2020Article
- NF-κB mediates lipopolysaccharide-induced alternative pre-mRNA splicing ofThe Journal of biological chemistry · 2020Article
- Inflammation-Induced Alternative Pre-mRNA Splicing in Mouse Alveolar Macrophages.G3 (Bethesda, Md.) · 2020Article
- Effects of 1,25-Dihydroxy vitamin DMolecular and cellular biochemistry · 2020Article
- The germ cell marker dead end reveals alternatively spliced transcripts with dissimilar expression.Scientific reports · 2019Article
- Increased Alternative Splicing as a Host Response to Edwardsiella ictaluri Infection in Catfish.Marine biotechnology (New York, N.Y.) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlternate splicing of key signaling molecules in the Toll-like receptor (Tlr) cascade has been shown to dramatically alter the signaling capacity of inflammatory cells, but it is not known how common this mechanism is. We provide transcriptional evidence of widespread alternate splicing in the Toll-like receptor signaling pathway, derived from a systematic analysis of the FANTOM3 mouse data set. Functional annotation of variant proteins was assessed in light of inflammatory signaling in mouse primary macrophages, and the expression of each variant transcript was assessed by splicing arrays.
resultsA total of 256 variant transcripts were identified, including novel variants of Tlr4, Ticam1, Tollip, Rac1, Irak1, 2 and 4, Mapk14/p38, Atf2 and Stat1. The expression of variant transcripts was assessed using custom-designed splicing arrays. We functionally tested the expression of Tlr4 transcripts under a range of cytokine conditions via northern and quantitative real-time polymerase chain reaction. The effects of variant Mapk14/p38 protein expression on macrophage survival were demonstrated.
conclusionMembers of the Toll-like receptor signaling pathway are highly alternatively spliced, producing a large number of novel proteins with the potential to functionally alter inflammatory outcomes. These variants are expressed in primary mouse macrophages in response to inflammatory mediators such as interferon-gamma and lipopolysaccharide. Our data suggest a surprisingly common role for variant proteins in diversification/repression of inflammatory signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.