Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

HSV1 VP1-2 deubiquitinates STING to block type I interferon expression and promote brain infection.

The Journal of experimental medicine - 6 Jul 2020

Bodda Chiranjeevi, Reinert Line S, Fruhwürth Stefanie, Richardo Timmy, Sun Chenglong, Zhang Bao-Cun, Kalamvoki Maria, Pohlmann Anja, Mogensen Trine H, Bergström Petra, Agholme Lotta, O'Hare Peter, Sodeik Beate, Gyrd-Hansen Mads, Zetterberg Henrik, Paludan Søren R

Abstract excerpt

Herpes simplex virus (HSV) is the main cause of viral encephalitis in the Western world, and the type I interferon (IFN) system is important for antiviral control in the brain. Here, we have compared Ifnb induction in mixed murine brain cell cultures by a panel of HSV1 mutants, each devoid of one mechanism to counteract the IFN-stimulating cGAS-STING pathway. We found that a mutant lacking the deubiquitinase...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cytoplasm
Share to Herpesvirus 1, Human

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interferon Type I

Share to Lysine

Share to Microglia

Share to Nucleotidyltransferases

Share to Ubiquitin

Share to Ubiquitination

Source

Open in PubMed Open full text

Identifiers

PMID: 32383759
DOI: 10.1084/jem.20191422
PMCID: PMC7336311

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

HSV1 VP1-2 deubiquitinates STING to block type I interferon expression and promote brain infection.PMID 32383759Read ↗

HSV Replication: Triggering and Repressing STING FunctionalitySemantic proximity Read ↗

HSV-2 Immediate-Early Protein US1 Inhibits IFN-β Production by Suppressing Association of IRF-3 with IFN-β PromoterSemantic proximity Read ↗

The microglia receptor protein TREM2 is essential for protective innate immune responses against herpesvirus infection in the brainSemantic proximity Read ↗

Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Semantic proximity Read ↗

TRIM23 mediates cGAS-induced autophagy in anti-HSV defenseSemantic proximity Read ↗

Herpes simplex virus 1 evades cellular antiviral response by inducing microRNA-24, which attenuates STING synthesisSemantic proximity Read ↗

Evasion of the STING DNA-Sensing Pathway by VP11/12 of Herpes Simplex Virus 1Semantic proximity Read ↗

STING is a key driver of Japanese encephalitis virus induced inflammatory responseSemantic proximity Read ↗

Herpes simplex virus 1 encodes a STING antagonist that can be therapeutically targetedSemantic proximity Read ↗

Microbial Infection Instigates Tau-Related Pathology Via Activating Neuroimmune cGAS-STING PathwaySemantic proximity Read ↗

STING-ΔN, a novel splice isoform of STING, modulates innate immunity and autophagy in response to DNA virus infectionSemantic proximity Read ↗

Tick-borne encephalitis virus NS4A ubiquitination antagonizes type I interferon-stimulated STAT1/2 signalling pathwaySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.