Rb binding protein Che-1 interacts with Tau in cerebellar granule neurons: Modulation during neuronal apoptosis

Christian Barbato, Nicoletta Corbi, Nadia Canu, Maurizio Fanciulli, Annalucia Serafino, MariaTeresa Ciotti, Valentina Libri, Tiziana Bruno, Giuseppina Amadoro, Roberta De Angelis, Pietro Calissano, Claudio Passananti

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Che-1 is a recently identified human Rb binding protein that inhibits the Rb growth-suppressing function and regulates cell proliferation. Che-1 contacts the Rb and competes with HDAC1 for Rb-binding site, removing HDAC1 from the Rb/E2F cell cycle-regulated promoters. We have investigated the expression of Che-1 in neuronal cells and we showed that Che-1 directly interacts with Tau. Tau is a microtubule-associated protein involved in the assembly and stabilization of neuronal microtubules network that plays a crucial role modulating neuronal morphogenesis, axonal shape, and transport. In rat cerebellar granule neurons (CGNs) Che-1 partially colocalizes with Tau in the cytoplasm. Che-1 binds the amino-terminal region of Tau protein, which is not involved in microtubule interactions. Tau and Che-1 endogenous proteins coimmunoprecipitate from CGNs cellular lysates. In addition, Che-1/Tau interaction was demonstrated both in overexpressing COS-7 cells and CGNs by FRET analysis. Finally, we observed that Tau/Che-1 interaction is modulated during neuronal apoptosis.

Original languageEnglish
Pages (from-to)1038-1050
Number of pages13
JournalMolecular and Cellular Neuroscience
Issue number4
Publication statusPublished - Dec 2003


ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Developmental Neuroscience

Cite this

Barbato, C., Corbi, N., Canu, N., Fanciulli, M., Serafino, A., Ciotti, M., Libri, V., Bruno, T., Amadoro, G., De Angelis, R., Calissano, P., & Passananti, C. (2003). Rb binding protein Che-1 interacts with Tau in cerebellar granule neurons: Modulation during neuronal apoptosis. Molecular and Cellular Neuroscience, 24(4), 1038-1050. https://doi.org/10.1016/j.mcn.2003.08.002