Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Immune response in Stat2 knockout mice.

Immunity | Dec 19, 2000

http://www.ncbi.nlm.nih.gov/pubmed/11163195

Type I IFNs induce gene expression through Stat1 and Stat2, which can in turn associate either to form Stat1 homodimers or the transcription factor ISGF-3. Stat1 homodimers also transduce signals for IFN-gamma. To explore the unique properties of Stat2 and ISGF-3 in type I IFN signaling, its gene was targeted for deletion. Stat2 null mice exhibit a number of defects in immune response. This includes an increased susceptibility to viral infection and the loss of a type I IFN autocrine/ paracrine loop, which in turn regulates several aspects of immune response. Intriguingly, Stat2-deficient fibroblasts exhibit a more significant defect in their response to type I IFNs than macrophages, highlighting tissue-specific differences in the response to this family of ligands.

Pubmed ID: 11163195 RIS Download

Mesh terms: Animals | CD4-Positive T-Lymphocytes | CD8-Positive T-Lymphocytes | DNA-Binding Proteins | GTP Phosphohydrolases | Gene Deletion | Gene Expression | Gene Targeting | Interferon Regulatory Factor-1 | Interferon-Stimulated Gene Factor 3 | Interferon-Stimulated Gene Factor 3, gamma Subunit | Interferon-alpha | Interferon-gamma | Mice | Mice, Knockout | Phosphoproteins | Rhabdoviridae Infections | STAT2 Transcription Factor | Signal Transduction | Trans-Activators | Transcription Factors | Vesicular stomatitis Indiana virus

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIGMS NIH HHS, Id: GM54686
  • Agency: NHLBI NIH HHS, Id: HL56984

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.