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

Bromberg, J F, Horvath, C M, Wen, Z, Schreiber, R D, Darnell, J E·1996·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.93.15.7673
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Abstract

Type I (alpha, beta) and type II (gamma) interferons (IFNs) can restrict the growth of many cell types. INF-stimulated gene transcription, a key early event in IFN response, acts through the Janus kinase-signal transducers and activators of transcription pathway, in which both IFN-alpha and IFN-gamma activate the transcription factor Stat1. A cell line lacking Stat1 (U3A) was not growth-arrested by IFN-alpha or IFN-gamma, and experiments were carried out with U3A cells permanently expressing normal or various mutant forms of Stat1 protein. Only cells in which complete Stat1 activity was available (Stat1alpha) were growth-inhibited by IFN-gamma. A mutant that supports 20-30% normal transcription did not cause growth restraint. In contrast, IFN-alpha growth restraint was imposed by cells producing Stat1beta, which lacks transcriptional activation potential. This parallels earlier results showing the truncated Stat1 can function in IFN-alpha gene activation. In addition to experiments on long-term cultured cells, we also found that wild-type primary mouse embryonic fibroblasts were inhibited by IFNs, but fibroblasts from Stat1-deficient mouse embryos were not inhibited by IFNs.

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Cited by

Metadata

Authors
Bromberg, J. F., Horvath, C. M., Wen, Z., Schreiber, R. D., & Darnell, J. E.
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1996-07-23
Volume
93
Issue
15
Pages
7673-7678
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.93.15.7673
Cited by
422
References
1
Language
en

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