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

An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection.

Genes and immunity - 1 Jan 2000

Lafferty E I, Flaczyk A, Angers I, Homer R, d'Hennezel E, Malo D, Piccirillo C A, Vidal S M, Qureshi S T

Abstract excerpt

Genetic and immunological analysis of host-pathogen interactions can reveal fundamental mechanisms of susceptibility and resistance to infection. Modeling human infectious diseases among inbred mouse strains is a proven approach but is limited by naturally occurring genetic diversity. Using N-ethyl-N-nitrosourea mutagenesis, we created a recessive loss-of-function point mutation in Unc93b1 (unc-93 homolog B1 (C....

Read the complete abstract on PubMed

Topics

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

Share to Chemokine CXCL10
Share to Ethylnitrosourea

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Influenza A Virus, H1N1 Subtype

Share to Interferon Type I

Share to L-Selectin

Share to Macrophage Activation

Share to Orthomyxoviridae Infections

Share to Toll-Like Receptors

Source

Open in PubMed Open full text

Identifiers

PMID: 24848930
DOI: 10.1038/gene.2014.22
PMCID: PMC4978536

Genes

CXCL10
TLR7
TLR9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection.PMID 24848930Read ↗

Unc93B1 restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 and 9 trafficking.Semantic proximity Read ↗

UNC93B1 and nucleic acid-sensing Toll-like receptors mediate host resistance to infection with Leishmania major.Semantic proximity Read ↗

The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9.Semantic proximity Read ↗

Large-scale mutational analysis identifies UNC93B1 variants that drive TLR-mediated autoimmunity in mice and humans.Semantic proximity Read ↗

A novel <i>UNC93B1</i> gain-of-function mutation leads to TLR7 and TLR8 hyperactivation and systemic lupus erythematosusSemantic proximity Read ↗

UNC93B1 delivers nucleotide-sensing toll-like receptors to endolysosomes.Semantic proximity Read ↗

Unraveling innate immunity using large scale N-ethyl-N-nitrosourea mutagenesis.Semantic proximity Read ↗

Genetic variants in UNC93B1 predispose to childhood-onset systemic lupus erythematosusSemantic proximity Read ↗

An essential checkpoint for TLR9 signaling is release from Unc93b1 in endosomesSemantic proximity Read ↗

Genome-wide ENU mutagenesis to reveal immune regulators.Semantic proximity Read ↗

Mutation of the ER retention receptor KDELR1 leads to cell-intrinsic lymphopenia and a failure to control chronic viral infection.Semantic proximity Read ↗

Genetic variants in UNC93B1 predispose to childhood-onset systemic lupus erythematosus.Semantic proximity Read ↗

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