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Related Experiment Videos

RIP2, a checkpoint in myogenic differentiation.

Barbara Munz1, Eberhard Hildt, Matthew L Springer

  • 1Baxter Laboratory for Genetic Pharmacology, Stanford University Medical Center, Stanford, California 94305-5175, USA.

Molecular and Cellular Biology
|July 26, 2002
PubMed
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Receptor interacting protein 2 (RIP2) inhibits muscle cell differentiation. This gene

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Receptor interacting protein 2 (RIP2) is a tumor necrosis factor receptor 1 (TNFR-1)-associated factor.
  • RIP2 has domains including kinase and caspase activation and recruitment domain (CARD).
  • RIP2 can induce apoptosis and activate NF-kappa B in some cell types.

Purpose of the Study:

  • To analyze the function of RIP2 during myogenic differentiation.
  • To investigate the role of RIP2 in regulating cell cycle withdrawal and differentiation marker expression.

Main Methods:

  • Subtractive cDNA library hybridization was used to identify RIP2.
  • C2C12 myoblasts were transduced with retroviral vectors to overexpress RIP2.
  • Deletion mutants and kinase-deficient mutants of RIP2 were analyzed.

Related Experiment Videos

  • RIP2 homolog expression was examined in dystrophic mdx mouse muscle tissues.

    • Main Results:

    • Constitutive high-level RIP2 production in C2C12 myoblasts inhibited differentiation.
    • RIP2-expressing cells continued to proliferate when switched to differentiation medium.
    • The complete RIP2 protein, but not its kinase domain or CARD, was necessary to inhibit differentiation.
    • A decrease in RIP2 homolog expression was observed in mdx mouse muscle.

    Conclusions:

    • RIP2 acts as a novel early-acting gene that inhibits myogenic proliferation and differentiation.
    • RIP proteins can modulate downstream signaling pathways independently of TNFR-1 stimulation.
    • RIP2 functions as a checkpoint for myogenic proliferation and differentiation.