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Updated: Jan 7, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
TNIP1 and autophagy receptors regulate STING signaling
Eric N Bunker1, Tara D Fischer1, Peng-Peng Zhu1
1Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health; Bethesda, MD 20892.
The cGAS-STING pathway regulates innate immunity. Autophagy receptors and TNIP1 bind to STING-associated vesicles, influencing immune signaling independently of autophagy.
Area of Science:
- Cellular Biology
- Immunology
- Molecular Biology
Background:
- The cGAS-STING pathway is crucial for innate immune responses.
- Ubiquitylation at Golgi-related vesicles regulates immune signaling, but mechanisms are unclear.
Purpose of the Study:
- Investigate the role of ubiquitin- and LC3B-binding proteins in STING-mediated immune signaling.
- Elucidate the mechanisms of Golgi-localized polyubiquitin chain regulation.
Main Methods:
- Co-immunoprecipitation assays to identify protein interactions.
- Confocal microscopy to visualize subcellular localization.
- Functional assays to assess immune signaling modulation.
Main Results:
- TNIP1 and autophagy receptors (p62, NBR1, NDP52, TAX1BP1, OPTN) associate with STING-induced Ub/LC3B vesicles.
- p62 and NBR1 redundantly cluster these vesicles in the perinuclear region.
- TBK1 kinase activity is involved in vesicle sequestration, and TNIP1 negatively regulates IRF3-mediated gene expression.
Conclusions:
- Autophagy receptors and TNIP1 regulate STING-mediated immunity through autophagy-independent mechanisms.
- These proteins play unanticipated roles in innate immune signaling pathways.
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