Abstract
A systematic analysis of the FANTOM3 mouse cDNA dataset provides transcriptional evidence of widespread alternate splicing in the Toll-like receptor signaling pathway.
Highlights
Alternate 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
This study evaluates the variation in proteins arising from these alternate splicing events using a systematic bioinformatics approach; predicts the impact a variant protein will have on signal transduction in the Tlr signaling cascade, and tests the expression of these novel proteins in a model of inflammatory macrophage activation
Identification and validation of variant members of the Tlr signaling pathway The FANTOM3 transcriptional framework (TK) defined the start, end, and splice boundaries of all of the variant transcripts arising from a gene [11]
Summary
Alternate 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
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