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Gigantism in mice lacking suppressor of cytokine signalling-2

Author

Listed:
  • Donald Metcalf

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Christopher J. Greenhalgh

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Elizabeth Viney

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Tracy A. Willson

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Robyn Starr

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Nicos A. Nicola

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Douglas J. Hilton

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

  • Warren S. Alexander

    (The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Post Office, Royal Melbourne Hospital)

Abstract

Suppressor of cytokine signalling-2 (SOCS-2) is a member of the suppressor of cytokine signalling family, a group of related proteins implicated in the negative regulation of cytokine action through inhibition of the Janus kinase (JAK) signal transducers and activators of transcription (STAT) signal-transduction pathway1. Here we use mice unable to express SOCS-2 to examine its function in vivo. SOCS-2-/- mice grew significantly larger than their wild-type littermates. Increased body weight became evident after weaning and was associated with significantly increased long bone lengths and the proportionate enlargement of most organs. Characteristics of deregulated growth hormone and insulin-like growth factor-I (IGF-I) signalling, including decreased production of major urinary protein, increased local IGF-I production, and collagen accumulation in the dermis, were observed in SOCS-2-deficient mice, indicating that SOCS-2 may have an essential negative regulatory role in the growth hormone/IGF-I pathway.

Suggested Citation

  • Donald Metcalf & Christopher J. Greenhalgh & Elizabeth Viney & Tracy A. Willson & Robyn Starr & Nicos A. Nicola & Douglas J. Hilton & Warren S. Alexander, 2000. "Gigantism in mice lacking suppressor of cytokine signalling-2," Nature, Nature, vol. 405(6790), pages 1069-1073, June.
    • Handle: RePEc:nat:nature:v:405:y:2000:i:6790:d:10.1038_35016611
    DOI: 10.1038/35016611
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    Cited by:

    1. Edmond M. Linossi & Kunlun Li & Gianluca Veggiani & Cyrus Tan & Farhad Dehkhoda & Colin Hockings & Dale J. Calleja & Narelle Keating & Rebecca Feltham & Andrew J. Brooks & Shawn S. Li & Sachdev S. Sid, 2021. "Discovery of an exosite on the SOCS2-SH2 domain that enhances SH2 binding to phosphorylated ligands," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    2. Sarath Ramachandran & Nikolai Makukhin & Kevin Haubrich & Manjula Nagala & Beth Forrester & Dylan M. Lynch & Ryan Casement & Andrea Testa & Elvira Bruno & Rosaria Gitto & Alessio Ciulli, 2023. "Structure-based design of a phosphotyrosine-masked covalent ligand targeting the E3 ligase SOCS2," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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