eagle-i Harvard UniversityHarvard University
See it in Search
This page is a preview of the following resource. Continue onto eagle-i search using the button on the right to see the full record.


eagle-i ID


Resource Type

  1. Mus musculus


  1. Exchange facilitator
    <a href=http://jaxmice.jax.org/strain/005037.html target=_window><img src=https://eagle-i.net/images/jacksonlabs-button-large.png alt='Order from Jackson Laboratory'></a>
  2. Resource Description
    "Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This single base pair deletion mutation was induced by ENU mutagenesis. Unlike wildtype macrophages, macrophages derived from these animals fail to respond to synthetic lipid A, endotoxin lipopolysaccharide (LPS), and dsRNA with production of tumor necrosis factor (TNF). Macrophages are less susceptible to LPS-induced cytotoxicity. Nitrous oxide and type I interferon production in activated macrophages is impaired. Homozygotes exhibit increased susceptibility to mouse cytomegalovirus. Although homozygotes are resistant to challenges with LPS, the mice will become ill and some may die."
  3. Additional Name
  4. Contact
    Lederer, James Ph.D.
  5. Related Disease
    Wernicke encephalopathy
  6. Related Publication or Documentation
    Identification of Lps2 as a key transducer of MyD88-independent TIR signalling
  7. Biological process studied
    Inflammatory response
  8. Genetic Alteration(s)
  9. Developed by
    Beutler, Bruce, M.D.
  10. Location
    Lederer Lab
Provenance Metadata About This Resource Record

Copyright © 2016 by the President and Fellows of Harvard College
The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016