ArticleCell communication and signaling : CCS2026
Non-canonical STING activation by calcium influx paired to endoplasmic reticulum stress.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
STING plays a pivotal role in initiating antiviral and proinflammatory responses in vertebrates. cGAS detection of cytosolic dsDNA, leads to the synthesis of 2'3'-cGAMP that subsequently binds to STING, mediating its canonical activation. Activation of STING triggers a signaling cascade that mediates the expression of antiviral and proinflammatory genes. Due to the known effects of STING activation, this protein has been related with several situations as antitumor immunity and managing cellular stress responses. While dsDNA is the best-known mediator of STING responses, recent studies have proposed alternative non-canonical activations of this protein. In this study, we explore the non-canonical activation of STING by thapsigargin, a known SERCA inhibitor commonly utilized to provoke ER stress and initiate the unfolded protein response (UPR). Our research reveals that thapsigargin can elicit functional antiviral and pro-inflammatory responses independently of other agonists. Remarkably, thapsigargin can induce Type I IFN and proinflammatory responses as early as 30 min post-treatment. This activation is STING-dependent but occurs independently of its well-known inducers, cGAS and IFI16. This activation also depends on SERCA inhibition and Ca
Indexed as
Identifiers
What OpenQuestion holds
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.