Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Science Signaling

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 3 May 1996:
Vol. 272. no. 5262, pp. 719 - 722
DOI: 10.1126/science.272.5262.719

Reports

Cell Growth Arrest and Induction of Cyclin-Dependent Kinase Inhibitor p21WAF1/CIP1 Mediated by STAT1

Yue E. Chin, * Motoo Kitagawa, * Wu-Chou S. Su, Zhi-Hao You, Yoshiki Iwamoto, Xin-Yuan Fu dagger

Signal transducers and activators of transcription (STAT) proteins can be conditionally activated in response to epidermal growth factor (EGF) and interferon (IFN)-gamma . STAT activation was correlated with cell growth inhibition in response to EGF and IFN-gamma . Activated STAT proteins specifically recognized the conserved STAT-responsive elements in the promoter of the gene encoding the cyclin-dependent kinase (CDK) inhibitor p21WAF1/CIP1 and regulated the induction of p21 messenger RNA. IFN-gamma did not inhibit the growth of U3A cells, which are deficient in STAT1, but did inhibit the growth of U3A cells into which STAT1alpha was reintroduced. Thus, STAT1 protein is essential for cell growth suppression in response to IFN-gamma . The STAT signaling pathway appears to negatively regulate the cell cycle by inducing CDK inhibitors in response to cytokines.

Department of Pathology, Yale University School of Medicine, New Haven, CT 06520-8023, USA.
* These authors contributed equally to this work.
dagger To whom correspondence should be addressed.






ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)