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Rb regulates fate choice and lineage commitment in vivo

Author

Listed:
  • Eliezer Calo

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

  • Jose A. Quintero-Estades

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

  • Paul S. Danielian

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

  • Simona Nedelcu

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

  • Seth D. Berman

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

  • Jacqueline A. Lees

    (David H. Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology)

Abstract

Rb suppressor and cell fate The tumour suppressor Rb (retinoblastoma protein) is mutated in about one-third of human tumours. It suppresses the activity of certain transcription factors and potentiates the activity of others, and has been shown to affect the differentiation of different cell lineages in vitro. Jacqueline Lees and colleagues now show that Rb plays a role in determining fate choice between bone cell and brown adipose tissue formation in vivo in mouse osteosarcoma models, acting via the bone and fat master regulators Runx2 and PPARγ

Suggested Citation

  • Eliezer Calo & Jose A. Quintero-Estades & Paul S. Danielian & Simona Nedelcu & Seth D. Berman & Jacqueline A. Lees, 2010. "Rb regulates fate choice and lineage commitment in vivo," Nature, Nature, vol. 466(7310), pages 1110-1114, August.
    • Handle: RePEc:nat:nature:v:466:y:2010:i:7310:d:10.1038_nature09264
    DOI: 10.1038/nature09264
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    Cited by:

    1. Chao-Hui Chang & Feng Liu & Stefania Militi & Svenja Hester & Reshma Nibhani & Siwei Deng & James Dunford & Aniko Rendek & Zahir Soonawalla & Roman Fischer & Udo Oppermann & Siim Pauklin, 2024. "The pRb/RBL2-E2F1/4-GCN5 axis regulates cancer stem cell formation and G0 phase entry/exit by paracrine mechanisms," Nature Communications, Nature, vol. 15(1), pages 1-29, December.

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