Evidence map›Paper›PMID 41792265›Full record

ArticleNature cell biology2026

Lysine-11 ubiquitination drives type-I/III interferon induction by cGAS-STING and Toll-like receptors 3 and 4.

Alexis Betrancourt, M Talha Cinko, Ana Beatriz Varanda, Maykel Arias, Iratxe Uranga-Murillo, Natacha Peña, Lucia-Maria Kaps, Long Fung Chau, Bianca Buratti, Johannes Brägelmann and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature cell biology, 2026. 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. Review
  3. 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

19 authors.

Alexis Betrancourt *Cell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0008-5365-9454
M Talha Cinko *Cell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-8503-9120
Ana Beatriz VarandaCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.
Maykel AriasCIBER de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Iratxe Uranga-MurilloCIBER de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Natacha PeñaCIBER de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Lucia-Maria KapsCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0006-8977-2390
Long Fung ChauDepartment of Pathology, University of Cambridge, Cambridge, UK.
Bianca BurattiCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0000-3545-9290
Johannes BrägelmannMildred Scheel School of Oncology, University of Cologne, Faculty of Medicine and University Hospital Cologne, Department of Translational Genomics, Cologne, Germany.ORCID http://orcid.org/0000-0002-1306-2169
Diego de MiguelCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-8486-8514
Kerstin BeckerCologne Centre for Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Ramona CasperCologne Centre for Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Rocio MartinCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain.
Antonio AlcamiCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain.ORCID http://orcid.org/0000-0002-3333-6016
Brian J FergusonDepartment of Pathology, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-6873-1032
Julian PardoCIBER de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Eva RieserCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany. erieser@uni-koeln.de.ORCID http://orcid.org/0000-0002-9954-8097
Henning WalczakCell Death, Inflammation and Immunity Laboratory, Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Cologne, Germany. h.walczak@uni-koeln.de.ORCID http://orcid.org/0000-0002-6312-4591

Funding

Cancer Research UK (CRUK) A27323Deutsche Forschungsgemeinschaft (German Research Foundation) project 407493903Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1399-413326622Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1403-414786233Deutsche Krebshilfe (German Cancer Aid) 70113307Gobierno de Aragón BOA-2018-06-15-027Gobierno de Aragón Group B29_23RRCUK | Medical Research Council (MRC) MR/S00811X/1Wellcome Trust (Wellcome) 214342/Z/18/Z
6 · The paper itself

Abstract

Pattern recognition receptor (PRR)-induced interferon (IFN) is critical for effective immunity. The PRRs Toll-like receptor (TLR) 3, TLR4 and cyclic GMP-AMP synthase (cGAS), together with the stimulator of IFN genes (STING), signal through TANK-binding kinase 1 (TBK1), which activates the type-I/III IFN-inducing transcription factor interferon-response factor 3 (IRF3). The mechanism by which these PRRs activate TBK1 remains unresolved. Here we show that lysine-11 (K11)-linked ubiquitination drives TBK1 activation by these PRRs. The E3 ligase ANKIB1 attaches K11-linked ubiquitin chains to components of the TLR3- and cGAS-STING-induced signalosomes. This facilitates Optineurin recruitment to these complexes, in turn enabling recruitment and activation of TBK1 and IRF3, defining an uncharacterized signalling axis. In mice, ANKIB1 deficiency dampens IFN induction via TLR3 and cGAS-STING, reducing interferonopathy and compromising protection against HSV-1, respectively. Together, our results demonstrate an unanticipated and critical role for ANKIB1-generated K11-linked ubiquitination in the immune response activated by cGAS-STING, TLR3 and TLR4.

Indexed as

InterferonsInterferon Type ILysineMembrane ProteinsNucleotidyltransferasesToll-Like Receptor 3Toll-Like Receptor 4AnimalscGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHEK293 CellsHumansInnate Immunity RecognitionInterferon Regulatory Factor-3MiceMice, Inbred C57BLcGAS protein, humancGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseInterferon Regulatory Factor-3InterferonsInterferon Type IIrf3 protein, mouseLysineMembrane ProteinsNucleotidyltransferasesProtein Serine-Threonine KinasesSTING1 protein, humanSting1 protein, mouseSTING ProteinTBK1 protein, humanTbk1 protein, mouseTlr4 protein, mouseToll-Like Receptor 3Toll-Like Receptor 4

Identifiers

PMID41792265
PMCPMC12992118

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.