Letter | Published:

Cooperation of Stat2 and p300/CBP in signalling induced by interferon-α

Nature volume 383, pages 344347 (26 September 1996) | Download Citation

Subjects

Abstract

THE transcription factor ISGF3 transduces interferon (IFN)-α signals and activates the transcription of cellular antiviral defence genes1,2. Adenovirus E1A blocks the IFN-α response, allowing unhindered viral replication3–5. ISGF3 consists of Statl, Stat2 and p48. Here we show that p300 and/or CBP (CREB-binding protein), which are transcription adaptors targeted by E1A, interact specifically with Stat2. Binding occurs between the first cysteine–histidine-rich region of p300/CBP and the carboxy-terminal segment of Stat2, a domain essential for ISGF3 function6. We find that this domain of Stat2 has transactivation potential, which correlates with its binding to p300/CBP. Moreover, E1A represses Stat2 transactivation and IFN-α-activated transcription by inhibiting p300/CBP function. This provides a new mechanism for inhibition of the IFN-α-activated antiviral response by E1A, and supports the view that E1A binding to p300/CBP has functional significance for adenovirus replication in its natural host.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1.

    , & Science 264, 1415–1421 (1994).

  2. 2.

    , , & Pharmacol. Ther. 65, 415–442 (1995).

  3. 3.

    , , & Proc. Natl Acad. Sci. USA 88, 7459–7463 (1991).

  4. 4.

    & Proc. Natl Acad. Sci. USA 88, 7913–7917 (1991).

  5. 5.

    et al. Nucleic Acids Res. 19, 4387–4393 (1991).

  6. 6.

    , , , & Mol. Cell. Biol. 16, 288–293 (1996).

  7. 7.

    et al. Nature 370, 223–226 (1994).

  8. 8.

    & EMBO J. 14, 4758–4762 (1995).

  9. 9.

    , & J. Biol. Chem. 271, 2373–2375 (1996).

  10. 10.

    et al. Cell 85, 403–414 (1996).

  11. 11.

    et al. Genes Dev. 10, 528–540 (1996).

  12. 12.

    , , , & Nature 374, 81–84 (1995).

  13. 13.

    , , , & Nature 374, 81–84 (1995).

  14. 14.

    , , , & Mol. Cell. Biol. 15, 1312–1317 (1995).

  15. 15.

    & Int. J. Oncol. 5, 425–444 (1994).

  16. 16.

    , , , & J. Virol. 64, 4421–4427 (1990).

  17. 17.

    , & Cell 84, 825–830 (1996).

  18. 18.

    & Exp. Cell Res. 216, 143–148 (1995).

  19. 19.

    , , , & Nucleic Acids Res. 23, 459–463 (1995).

  20. 20.

    , & EMBO J. 13, 158–167 (1994).

  21. 21.

    et al. EMB0 J. 12, 4221–4228 (1993).

  22. 22.

    et al. Cell 70, 351–364 (1992).

  23. 23.

    , , & Science 257, 809–813 (1992).

  24. 24.

    et al. Cell 78, 161–172 (1994).

  25. 25.

    , & Genes Dev. 2, 718–729 (1988).

  26. 26.

    , , , & EMBO J. 7, 1411–1419 (1988).

  27. 27.

    & Mol. Cell. Biol. 7, 2745–2752 (1987).

  28. 28.

    , & Mol. Cell. Biol. 12, 4391–4399 (1992).

  29. 29.

    , & Cell 56, 67–75 (1989).

Download references

Author information

Author notes

    • Richard Eckner

    Present address: Institute for Molecular Biology, University of Zurich, CH-8057 Zurich, Switzerland.

Affiliations

  1. Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA

    • Shoumo Bhattacharya
    • , Richard Eckner
    • , Steven Grossman
    • , Elizabeth Oldread
    • , Zoltan Arany
    • , Alan D'Andrea
    •  & David M. Livingston

Authors

  1. Search for Shoumo Bhattacharya in:

  2. Search for Richard Eckner in:

  3. Search for Steven Grossman in:

  4. Search for Elizabeth Oldread in:

  5. Search for Zoltan Arany in:

  6. Search for Alan D'Andrea in:

  7. Search for David M. Livingston in:

About this article

Publication history

Received

Accepted

Published

DOI

https://doi.org/10.1038/383344a0

Further reading

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.