Evidence map›Paper›PMID 32715615›Full record

ArticleEMBO reports2020

Autoimmunity gene IRGM suppresses cGAS-STING and RIG-I-MAVS signaling to control interferon response.

Kautilya Kumar Jena, Subhash Mehto, Parej Nath, Nishant Ranjan Chauhan, Rinku Sahu, Kollori Dhar, Saroj Kumar Das, Srinivasa Prasad Kolapalli, Krushna C Murmu, Ashish Jain and 7 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
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

59 citing papers in PubMed, 87 citations in OpenAlex.

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  19. Autophagy and Bacterial infections.Autophagy reports · 2025
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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

17 authors at 3 institutions in 2 countries.

Kautilya Kumar Jena *Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Subhash Mehto *Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Parej Nath *Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Nishant Ranjan ChauhanCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Rinku SahuCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Kollori DharCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Saroj Kumar DasCentre for Biotechnology, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, India.ORCID 0000-0002-5717-5333
Srinivasa Prasad KolapalliCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Krushna C MurmuEpigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-5568-680X
Ashish JainCentre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Sivaram KrishnaCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Bhabani Sankar SahooInstitute of Life Sciences, Bhubaneswar, India.
Soma ChattopadhyayMolecular Virology Lab, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Tor Erik RustenCentre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-9150-2676
Punit PrasadEpigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.
Swati ChauhanInstitute of Life Sciences, Bhubaneswar, India.
Santosh ChauhanCell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0001-9167-5107
Institute of Life Sciences · INOslo University Hospital · NOSiksha O Anusandhan University · IN

Funding

Department of Biotechnology, Ministry of Science and Technology (DBT) BT/HRD/35/02/2006Norewegian Research Council #262652Norewegian Research Council #276070The Wellcome Trust DBT India Alliance (India Alliance) IA/I/15/2/502071Wellcome Trust
6 · The paper itself

Abstract

Activation of the type 1 interferon response is extensively connected to the pathogenesis of autoimmune diseases. Loss of function of Immunity Related GTPase M (IRGM) has also been associated to several autoimmune diseases, but its mechanism of action is unknown. Here, we found that IRGM is a master negative regulator of the interferon response. Several nucleic acid-sensing pathways leading to interferon-stimulated gene expression are highly activated in IRGM knockout mice and human cells. Mechanistically, we show that IRGM interacts with nucleic acid sensor proteins, including cGAS and RIG-I, and mediates their p62-dependent autophagic degradation to restrain interferon signaling. Further, IRGM deficiency results in defective mitophagy leading to the accumulation of defunct leaky mitochondria that release cytosolic DAMPs and mtROS. Hence, IRGM deficiency increases not only the levels of the sensors, but also those of the stimuli that trigger the activation of the cGAS-STING and RIG-I-MAVS signaling axes, leading to robust induction of IFN responses. Taken together, this study defines the molecular mechanisms by which IRGM maintains interferon homeostasis and protects from autoimmune diseases.

Indexed as

Autoimmune DiseasesAutoimmunityAnimalsAutophagyMiceNucleotidyltransferasesSignal TransductionNucleotidyltransferasesautophagycGAS-STINGIRGMmitophagyRIG-I-MAVS

Identifiers

PMID32715615
PMCPMC7507369
OpenAlexW3045109118

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.