ArticleNature immunology2020
STEEP mediates STING ER exit and activation of signaling.
Article in Nature immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 105 papers.
What it found
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Who cites it
105 citing papers in PubMed, 162 citations in OpenAlex.
- The cGAS-STING pathway in inflammaging and neuroinflammation.Science China. Life sciences · 2026Review
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- The ER-Golgi intermediate compartment: a central hub integrating membrane trafficking and stress responses.EMBO reports · 2026Review
- Article
- STING signalling as a mediator between lipid metabolism and innate immunity.Nature reviews. Molecular cell biology · 2026Article
- Detection of nuclear STING in cultured human cells and in the normal and cancer tissues.iScience · 2026Article
- Article
- HCMV-pUS2 Disrupts cGAS-STING Signaling through LMAN2L Degradation.PLoS pathogens · 2026Article
- SCD1 licenses STING signaling through fatty acid desaturation-mediated membrane remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A unique Z-shaped tetramer mediates the autoinhibition of waterfowl STING.PLoS pathogens · 2026Article
- STING is the scaffold protein for stress granule pre-condensation at the ER.Cell death and differentiation · 2026Article
- Deltex E3 ubiquitin ligase 2 potentiates STING-mediated type I interferon response by K63-linked ubiquitination.Cell death & disease · 2026Article
- A CRISPR-Cas9 screen Reveals STEEP1 as a Key Host Dependency Factor for Epstein-Barr Virus Latent Membrane Protein 1 Trafficking and Signaling.bioRxiv : the preprint server for biology · 2026Article
- Low-dose radiotherapy remodels the tumor immune microenvironment via the cGAS-STING pathway: mechanisms, challenges, and combination therapy strategies.Molecular cancer · 2026Review
- Article
- An additional site mutation in MITA/STING gain-of-function mutants abolishes the autoimmune SAVI phenotypes and directs a therapeutic strategy.Cell insight · 2026Article
- Dual roles of TRPV2 in the innate immune response to cytosolic DNA: Arresting dormant and boosting activated STING.Cell reports · 2026Article
- STING Innate Immunity Signalling from the Golgi.Sub-cellular biochemistry · 2026Review
- Targeting cGAS-STING-macrophage axis: a novel therapeutic horizon for renal fibrosis.Frontiers in immunology · 2026Review
- Ubiquitination by HRD1 is essential for TLR3 trafficking and its innate immune signaling.Nature communications · 2025Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
31 authors at 7 institutions in 5 countries.
Funding
Abstract
STING is essential for control of infections and for tumor immunosurveillance, but it can also drive pathological inflammation. STING resides on the endoplasmic reticulum (ER) and traffics following stimulation to the ERGIC/Golgi, where signaling occurs. Although STING ER exit is the rate-limiting step in STING signaling, the mechanism that drives this process is not understood. Here we identify STEEP as a positive regulator of STING signaling. STEEP was associated with STING and promoted trafficking from the ER. This was mediated through stimulation of phosphatidylinositol-3-phosphate (PtdIns(3)P) production and ER membrane curvature formation, thus inducing COPII-mediated ER-to-Golgi trafficking of STING. Depletion of STEEP impaired STING-driven gene expression in response to virus infection in brain tissue and in cells from patients with STING-associated diseases. Interestingly, STING gain-of-function mutants from patients interacted strongly with STEEP, leading to increased ER PtdIns(3)P levels and membrane curvature. Thus, STEEP enables STING signaling by promoting ER exit.
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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.