Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10770901 | Biochemical and Biophysical Research Communications | 2005 | 5 Pages |
Abstract
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/â 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/â animals which show no important tissue abnormalities. However, we have found a much greater susceptibility to doxorubicin-induced heart failure in the SA/â mice. Also we introduced the SA allele into strain 129 and found the SA/â 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.
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Authors
Yuhong Shen, Krista M.D La Perle, David E. Levy, James E. Jr.,