ArticleEMBO reports2023
MARCH5 promotes STING pathway activation by suppressing polymer formation of oxidized STING.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Redox regulation of neuroinflammatory pathways contributes to damage in Alzheimer's disease brain.Cell chemical biology · 2026Article
- Mitochondria-ER contacts function as an iron supply hub.Nature cell biology · 2026Article
- STING is the scaffold protein for stress granule pre-condensation at the ER.Cell death and differentiation · 2026Article
- Pantetheinase Vanin-1 potentiates agonist-induced STING activation via S-cysteaminylation.Frontiers in immunology · 2026Article
- STING: a multifaced player in cellular homeostasis.Human molecular genetics · 2025Review
- Targeting the MARCH5-MFN2 axis to enhance mitochondrial fusion and sensitize multiple myeloma cells to venetoclax.Journal of translational medicine · 2025Article
- Article
- USP14 inhibition enhances Parkin-independent mitophagy in iNeurons.Pharmacological research · 2024Article
- Deciphering MARCH5's impact on multiple myeloma: insights into autophagy regulation and AKT-FOXO3 signaling.Blood neoplasia · 2024Article
- MARCH5 promotes STING pathway activation by suppressing polymer formation of oxidized STING.EMBO reports · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Stimulator of interferon genes (STING) is a core DNA sensing adaptor in innate immune signaling. STING activity is regulated by a variety of post-translational modifications (PTMs), including phosphorylation, ubiquitination, sumoylation, palmitoylation, and oxidation, as well as the balance between active and inactive polymer formation. It remains unclear, though, how different PTMs and higher order structures cooperate to regulate STING activity. Here, we report that the mitochondrial ubiquitin ligase MARCH5 (Membrane Associated Ring-CH-type Finger 5, also known as MITOL) ubiquitinates STING and enhances its activation. A long-term MARCH5 deficiency, in contrast, leads to the production of reactive oxygen species, which then facilitate the formation of inactive STING polymers by oxidizing mouse STING cysteine 205. We show that MARCH5-mediated ubiquitination of STING prevents the oxidation-induced STING polymer formation. Our findings highlight that MARCH5 balances STING ubiquitination and polymer formation and its control of STING activation is contingent on oxidative conditions.
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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.