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July 23, 1996Proceedings of the National Academy of SciencesOpen Access

Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon alpha and interferon gamma.

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Authors

JBJacqueline BrombergCHCurt M. HorvathRSRobert D. Schreiber

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Overview

Experimental study demonstrates differential Stat1 requirements for interferon-mediated growth arrest in human and mouse cells, indicating pathway-specific transcriptional activation demands.

Key Points

  • To determine whether transcriptionally active Stat1 is necessary for the antiproliferative effects of type I and type II interferons.
  • Evaluated growth inhibition in Stat1-deficient U3A cells stably expressing wild-type Stat1alpha or mutant variants, including Stat1beta and a partial-activity transcriptional mutant.
  • Assessed interferon-alpha and interferon-gamma responses in wild-type versus Stat1-deficient primary mouse embryonic fibroblasts.
  • IFN-gamma required fully functional Stat1alpha to suppress cell proliferation; a mutant maintaining 20% to 30% transcriptional activity failed to induce growth arrest.
  • IFN-alpha mediated cell growth restraint in cells expressing Stat1beta despite its lack of transcriptional activation potential.
  • Primary mouse embryonic fibroblasts lacking Stat1 were entirely resistant to IFN-induced growth restraint compared to growth-inhibited wild-type fibroblasts.

Cite This Study

Bromberg et al. (1996) studied this question.

synapsesocial.com/papers/6a7fe71bd18094eb686c7245https://doi.org/10.1073/pnas.93.15.7673
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