| First Author | Shen Y | Year | 2005 |
| Journal | Biochem Biophys Res Commun | Volume | 330 |
| Issue | 1 | Pages | 305-9 |
| PubMed ID | 15781265 | Mgi Jnum | J:97481 |
| Mgi Id | MGI:3575498 | Doi | 10.1016/j.bbrc.2005.02.154 |
| Citation | Shen Y, et al. (2005) Reduced STAT3 activity in mice mimics clinical disease syndromes. Biochem Biophys Res Commun 330(1):305-9 |
| abstractText | Phosphorylation on Y705 is obligatory for STAT3 activation, but full transcriptional activity of this widely expressed protein also requires phosphorylation on S727. We described earlier the STAT3 SA/- mice (SA, S727A allele) on a Black 6 (Bl6) background that showed 75% perinatal lethality and early growth retardation presumably due to the decreased transcription supported by STAT3 S727A. We now report additional analyses of long-term surviving SA/- animals which show no important tissue abnormalities. However, we have found a much greater susceptibility to doxorubicin-induced heart failure in the SA/- mice. Also we introduced the SA allele into strain 129 and found the SA/- mice showed greater susceptibility to LPS-induced toxicity. These results suggest a continued need for normal STAT3 transcriptional activity to resist two different noxious challenges that mimic the conditions necessary to induce adult diseases. |
