Evidence map›Paper›PMID 40254425›Full record

ArticleCell structure and function2025

A quantitative method to monitor STING degradation with dual-luciferase reporters.

Tsumugi Shoji, Kanako Sato, Ayumi Shinojima, Shogo Koide, Ruri Shindo, Kazune Hongo, Kojiro Mukai, Yoshihiko Kuchitsu, Tomohiko Taguchi

Abstract read
In one paragraph

Article in Cell structure and function, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. A PI(3,5)PNature communications · 2026
    Article
  3. Cell biological insights into human STING variants.Cell structure and function · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Tsumugi ShojiLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Kanako SatoLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Ayumi ShinojimaLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Shogo KoideLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Ruri ShindoLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Kazune HongoLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Kojiro MukaiLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Yoshihiko KuchitsuLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.
Tomohiko TaguchiLaboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University.

Funding

Unraveling the molecular mechanisms of impaired central tolerance in COPA syndromeR01AI168299 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Anthony Shum · 2022 to 2026
$3.3M
NIAID NIH HHS R01 AI168299
6 · The paper itself

Abstract

Stimulator of interferon genes (STING) triggers the type I interferon and inflammatory responses against a variety of DNA pathogens, which is essential to limiting viral infection and replication. STING activates the downstream kinase TBK1 at the trans-Golgi network (TGN) and is degraded at lysosomes through a process called lysosomal microautophagy. Impaired STING targeting to lysosomes results in the prolonged inflammatory signal, which may be associated with a variety of neurodegenerative and autoinflammatory diseases. Thus, development of methods to quantify STING degradation helps understand the mechanism of lysosomal microautophagy and its related diseases. Here we report a quantitative method to monitor STING degradation with two luciferases, firefly luciferase (FLuc) and Nanoluciferase (NLuc). The expression plasmid is composed of FLuc, a P2A self-cleavage site, and NLuc-tagged STING. FLuc intensity reflects the total amount of translated protein, serving as an internal control, while NLuc intensity corresponds to the amount of STING. Comparison of the NLuc/FLuc ratios at different time points after STING stimulation revealed the kinetics of decay of STING levels in live cells. This method should provide a useful complement to western blotting and fluorescence-activated cell sorter (FACS) analysis presently used to monitor STING degradation.Key words: innate immunity, STING, membrane traffic, lysosomal degradation, luciferase.

Indexed as

LuciferasesMembrane ProteinsGenes, ReporterHEK293 CellsHumansLysosomesProteolysisSTING ProteinLuciferasesMembrane ProteinsSTING1 protein, humanSTING Proteininnate immunityluciferaselysosomal degradationmembrane trafficSTING

Identifiers

PMID40254425
PMCPMC12702679

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.