ArticleThe American journal of pathology2003
Susceptibility to anthrax lethal toxin is controlled by three linked quantitative trait loci.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- Fine mapping of the Bmgr5 quantitative trait locus for allogeneic bone marrow engraftment in mice.Immunogenetics · 2013Article
- Review
- Anthrax and the inflammasome.Microbes and infection · 2012Review
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Identification of Orch3, a locus controlling dominant resistance to autoimmune orchitis, as kinesin family member 1C.PLoS genetics · 2012Article
- Article
- Allelic variation on murine chromosome 11 modifies host inflammatory responses and resistance to Bacillus anthracis.PLoS pathogens · 2011Article
- Multigenic control and sex bias in host susceptibility to spore-induced pulmonary anthrax in mice.Infection and immunity · 2011Article
- AMPD3 is involved in anthrax LeTx-induced macrophage cell death.Protein & cell · 2011Article
- Activation of the latent PlcR regulon in Bacillus anthracis.Microbiology (Reading, England) · 2010Article
- Susceptibility to anthrax lethal toxin-induced rat death is controlled by a single chromosome 10 locus that includes rNlrp1.PLoS pathogens · 2010Article
- Cellular and systemic effects of anthrax lethal toxin and edema toxin.Molecular aspects of medicine · 2009Review
- Identification of a major susceptibility locus for lethal graft-versus-host disease in MHC-matched mice.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Suppression of dendritic cell activation by anthrax lethal toxin and edema toxin depends on multiple factors including cell source, stimulus used, and function tested.DNA and cell biology · 2008Article
- Transcriptional and apoptotic responses of THP-1 cells to challenge with toxigenic, and non-toxigenic Bacillus anthracis.BMC immunology · 2008Article
- Rat survival to anthrax lethal toxin is likely controlled by a single gene.The pharmacogenomics journal · 2008Article
- A mathematical simulation of the inflammatory response to anthrax infection.Shock (Augusta, Ga.) · 2008Article
- Anthrax edema toxin sensitizes DBA/2J mice to lethal toxin.Infection and immunity · 2007Article
- Cisplatin inhibition of anthrax lethal toxin.Antimicrobial agents and chemotherapy · 2006Article
- Oxidized ATP protection against anthrax lethal toxin.Infection and immunity · 2006Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Anthrax lethal toxin (LT) is the principal virulence factor associated with lethal pathologies following infection with Bacillus anthracis. Macrophages are the primary effector cells mediating lethality since macrophage-depleted mice are resistant to LT challenge. Recently, Ltxs1, the gene controlling differential susceptibility of murine macrophages to cytolysis following in vitro exposure to LT, was identified as Kif1c. To directly assess the in vivo role of Kif1c alleles in mortality, we studied a panel of interval-specific recombinant congenic lines carrying various segments of central chromosome 11 derived from LT-resistant DBA/2 mice on the LT-susceptible BALB/c background. The results of this study reveal that mortality is controlled by three linked quantitative trait loci (QTL): Ltxs1/Kif1c (42-43 cM), Ltxs2 (35-37 cM), and Ltxs3 (45-47 cM). The Ltxs3 interval encompasses Nos2, which is an attractive candidate gene for Ltxs3. In this regard, we demonstrate that selective, pharmacologically based inhibition of Nos2 activity in vivo partially overrides genetic resistance to LT and that Nos2 expression as determined by reverse transcription-polymerase chain reaction differs significantly between DBA/2 and BALB/c macrophages. Additionally, to recapitulate dominant resistance to mortality as seen in (BALB/c x DBA/2) F(1) hybrids, DBA/2 alleles are required at all three QTL.
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Registered trials
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.