From cerebellar proliferation to tumorigenesis: New insights into the role of Mad3

Gustavo Barisone, Jun Soo Yun, Elva D Diaz

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


During development, Sonic hedgehog (Shh) regulates the proliferation of cerebellar granule neuron precursors (GNPs) in part via expression of Nmyc. Mutations in the Shh signaling pathway lead to brain tumors in mice and humans. We have recently identified a novel role for the Mad family member Mad3 in GNP proliferation and Nmyc expression. Interestingly, Mad3 expression is upregulated in mouse models of medulloblastoma, the most common brain tumor in children. These results are surprising because current models suggest that Mad proteins should antagonize Myc proteins by competition for direct DNA binding via Max heterodimerization to inhibit cellular proliferation and potentially tumor progression. Here, we discuss our recent work in the context of candidate Mad3-interacting proteins and Mad3 expression in human brain tumors that together suggest interesting insights into the role of Mad3 in cellular proliferation and tumorigenesis.

Original languageEnglish (US)
Pages (from-to)423-427
Number of pages5
JournalCell Cycle
Issue number4
StatePublished - Feb 15 2008


  • Cerebellum
  • Mad3
  • Medulloblastoma
  • Nmyc
  • Proliferation
  • Sonic hedgehog

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry
  • Molecular Biology


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