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Degradation of Id2 by the anaphase-promoting complex couples cell cycle exit and axonal growth

Author

Listed:
  • Anna Lasorella

    (Institute for Cancer Genetics
    College of Physicians and Surgeons of Columbia University
    College of Physicians and Surgeons of Columbia University)

  • Judith Stegmüller

    (Harvard Medical School)

  • Daniele Guardavaccaro

    (New York University School of Medicine)

  • Guangchao Liu

    (Institute for Cancer Genetics)

  • Maria S. Carro

    (Institute for Cancer Genetics)

  • Gerson Rothschild

    (Institute for Cancer Genetics)

  • Luis de la Torre-Ubieta

    (Harvard Medical School)

  • Michele Pagano

    (New York University School of Medicine)

  • Azad Bonni

    (Harvard Medical School)

  • Antonio Iavarone

    (Institute for Cancer Genetics
    College of Physicians and Surgeons of Columbia University
    College of Physicians and Surgeons of Columbia University)

Abstract

The anaphase-promoting complex/cyclosome (APC/C) has a key role in controlling mitosis. This paper identifies Id2 as a target of the APC/C that is responsible for its function in regulating axonal growth.

Suggested Citation

  • Anna Lasorella & Judith Stegmüller & Daniele Guardavaccaro & Guangchao Liu & Maria S. Carro & Gerson Rothschild & Luis de la Torre-Ubieta & Michele Pagano & Azad Bonni & Antonio Iavarone, 2006. "Degradation of Id2 by the anaphase-promoting complex couples cell cycle exit and axonal growth," Nature, Nature, vol. 442(7101), pages 471-474, July.
    • Handle: RePEc:nat:nature:v:442:y:2006:i:7101:d:10.1038_nature04895
    DOI: 10.1038/nature04895
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    Cited by:

    1. Sang Bae Lee & Luciano Garofano & Aram Ko & Fulvio D’Angelo & Brulinda Frangaj & Danika Sommer & Qiwen Gan & KyeongJin Kim & Timothy Cardozo & Antonio Iavarone & Anna Lasorella, 2022. "Regulated interaction of ID2 with the anaphase-promoting complex links progression through mitosis with reactivation of cell-type-specific transcription," Nature Communications, Nature, vol. 13(1), pages 1-14, December.

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