This study examines the tissue-specific turnover rates and abundance of the Stimulator of Interferon Genes (STING) protein in both wild-type (WT) mice and those carrying the Trex1 D18N mutation, a model for STING-dependent inflammation. The research employs metabolic labeling with deuterium oxide and high-resolution mass spectrometry to measure STING protein synthesis rates and degradation across different tissues.
STING protein half-life varies significantly across tissues, ranging from 4 days in the colon and lymph nodes to 24 days in skeletal muscle. Despite increased STING abundance in Trex1 D18N mice, the protein’s degradation and resynthesis kinetics were similar to WT mice. The extent of interferon-stimulated gene transcription correlated with STING levels and was inversely proportional to its turnover rate.
Trex1 D18N Knockin mouse model, in which the endogenous Trex1 gene carries the D18N point mutation, leading to a chronic STING-dependent inflammatory response. This model mimics Aicardi-Goutières syndrome and is used to study autoimmune and inflammatory diseases.
Inflammation, STING pathway, Protein turnover, Aicardi-Goutières syndrome, Autoimmunity
Knockin mouse model, Trex1 D18N mutation, STING-dependent inflammation, Metabolic labeling, Deuterium oxide tracing, Mass spectrometry, Point mutation
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