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

Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses.

Proceedings of the National Academy of Sciences of the United States of America - 28 Sept 1999

Wong P M, Kang A, Chen H, Yuan Q, Fan P, Sultzer B M, Kan Y W, Chung S W

Abstract excerpt

C3H/HeJ inbred mice are defective in that they are highly resistant to endotoxic shock as compared with normal responder mice. Their B cells and macrophages do not respond significantly when exposed to lipopolysaccharide (LPS), whereas cells from the responder mice do. Using a functional assay, we previously isolated a cDNA, which encodes for Ran/TC4 GTPase. We now show that this gene is mutated in C3H/HeJ mice,...

Read the complete abstract on PubMed

Topics

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

Share to 3' Untranslated Regions
Share to Gene Transfer Techniques

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Genetic Therapy

Share to Lipopolysaccharides

Share to Mice, Inbred BALB C

Share to Mice, Inbred C3H

Share to ran GTP-Binding Protein

Share to Shock, Septic

Source

Open in PubMed Open full text

Identifiers

PMID: 10500213
DOI: 10.1073/pnas.96.20.11543
PMCID: PMC18070

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses.PMID 10500213Read ↗

Cutting edge: functional characterization of the effect of the C3H/HeJ defect in mice that lack an Lpsn gene: in vivo evidence for a dominant negative mutation.Semantic proximity Read ↗

Novel Regulators of the Systemic Response to LipopolysaccharideSemantic proximity Read ↗

CD14 is required for MyD88-independent LPS signaling.Semantic proximity Read ↗

Genes other than TLR4 are involved in the response to inhaled LPS.Semantic proximity Read ↗

Positional cloning of Lps, and the general role of toll-like receptors in the innate immune response.Semantic proximity Read ↗

Variations in LPS responsiveness among different mouse substrains of C3H lineage and their congenic derivative sublines.Semantic proximity Read ↗

Construction of a BALB/c congenic mouse, C.C3H-Lpsd, that expresses the Lpsd allele: analysis of chromosome 4 markers surrounding the Lps gene.Semantic proximity Read ↗

Construction of a lipopolysaccharide reporter cell line and its use in identifying mutants defective in endotoxin, but not TNF-alpha, signal transduction.Semantic proximity Read ↗

A high-resolution map in the chromosomal region surrounding the Lps locus.Semantic proximity Read ↗

Expression of CD14 corrects the slow response to lipopolysaccharide in the 1B8 mutant of the B cell lymphoma 70Z/3.Semantic proximity Read ↗

Paradoxical preservation of a lipopolysaccharide response in C3H/HeJ macrophages: induction of matrix metalloproteinase-9.Semantic proximity Read ↗

Presence of Lps(d) mutation influences cytokine regulation in vivo by the Mycoplasma arthritidis mitogen superantigen and lethal toxicity in mice infected with M. arthritidis.Semantic proximity Read ↗

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