We have updated our privacy policy. If you have any question, contact us at privacy@scicrunch.org. Dismiss and don't show again

Searching across hundreds of databases

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

Forgot Password

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

Targeted disruption of the mouse Stat1 gene results in compromised innate immunity to viral disease.

Cell | Feb 9, 1996

The STAT1 transcription factor is activated in response to many cytokines and growth factors. To study the requirement for STAT1 in vivo, we disrupted the Stat1 gene in embryonic stem (ES) cells and in mice. Stat1(-1-)ES cells were unresponsive to interferon (IFN), but retained responsiveness to leukemia inhibitory factor (LIF) and remained LIF dependent for undifferentiated growth. Stat1(-1-1) animals were born at normal frequencies and displayed no gross developmental defects. However, these animals failed to thrive and were extremely susceptible to viral disease. Cells and tissues from Stat1(-1-) mice were unresponsive to IFN, but remained responsive to all other cytokines tested. Thus, STAT1 appears to be specific for IFN pathways that are essential for viability in the face of otherwise innocuous pathogens.

Pubmed ID: 8608598 RIS Download

Mesh terms: Animals | Cytokines | DNA-Binding Proteins | Female | Gene Targeting | Growth Inhibitors | Interferons | Interleukin-6 | Leukemia Inhibitory Factor | Lymphokines | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Opportunistic Infections | Phenotype | STAT1 Transcription Factor | Signal Transduction | Stem Cells | Trans-Activators | Vesicular stomatitis Indiana virus | Virus Diseases

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


Mouse Genome Informatics (Data, Gene Annotation)

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.

We have not found any resources mentioned in this publication.