Evidence map›Paper›PMID 41673009›Full record

ArticleNature communications2026

Negative feedback regulation of STING signaling by TAX1BP1-directed Golgiphagy.

Sujit Suklabaidya, Suchitra Mohanty, Irene E Reider, Jesse White, Dominic Colter, Sarah M McCormick, Noula Shembade, Young Bong Choi, Christopher C Norbury, Edward W Harhaj

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
    Review
  2. Review
  3. Article
  4. 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

10 authors.

Sujit Suklabaidya *Department of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Suchitra Mohanty *Department of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Irene E ReiderDepartment of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Jesse WhiteDepartment of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Dominic ColterDepartment of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Sarah M McCormickDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Noula ShembadeDepartment of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Young Bong ChoiDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Christopher C NorburyDepartment of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA.
Edward W HarhajDepartment of Cell and Biological Systems, Penn State College School of Medicine, Hershey, PA, USA. ewh110@psu.edu.ORCID http://orcid.org/0000-0003-1197-6765

Funding

Negative regulation of innate immune signaling pathways by the selective autophagy receptor TAX1BP1R01AI162815 · NIAID · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HARHAJ, EDWARD W · 2021 to 2025
$3.3M
NIAID NIH HHS R01 AI162815
6 · The paper itself

Abstract

The cGAS-STING pathway is a critical regulator of type I Interferon (IFN) and inflammation upon cytosolic DNA-sensing. cGAS-STING signaling termination is regulated by lysosomal-mediated degradation of STING; however, the mechanisms controlling the inhibitory targeting of STING are incompletely understood. Here, we identify the selective autophagy receptor TAX1BP1 as a negative regulator of the cGAS-STING pathway. TAX1BP1-deficient macrophages activated by cGAS or STING agonists accumulate higher-order STING aggregates, exhibit heightened STING signaling, and increased production of type I IFN and proinflammatory cytokines. Mechanistically, TAX1BP1 promotes STING degradation through microautophagy by facilitating the interaction of STING with the ESCRT-0 protein HGS. Furthermore, STING activation is associated with the swelling and fragmentation of the Golgi apparatus, and TAX1BP1 and p62/SQSTM1 are essential for the autophagic degradation of fragmented Golgi (Golgiphagy). Our findings suggest that STING activation at the Golgi is coupled to its downregulation by Golgiphagy to restrict innate immune responses.

Indexed as

Golgi ApparatusIntracellular Signaling Peptides and ProteinsMembrane ProteinsAnimalsAutophagycGAS-STING Signaling PathwayFeedback, PhysiologicalHumansImmunity, InnateInterferon Type IMacrophagesMiceNeoplasm ProteinsSignal TransductionSTING ProteinInterferon Type IIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeoplasm ProteinsSTING1 protein, humanSting1 protein, mouseSTING ProteinTAX1BP1 protein, human

Identifiers

PMID41673009
PMCPMC13018473

What OpenQuestion holds

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Registered trials

None linked

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.