Research Output

Hyperphosphorylation of tau and neurofilaments and activation of CDK5 and ERK1/2 in PTEN-deficient cerebella

  Inherited mutations to the tumor suppressor PTEN sporadically lead to cerebellar gangliocytoma characterized by migration defects. This has been modeled by CNS-specific PTEN ablation in mice, but the underlying mechanism cannot be explained by the known role of PTEN in Akt/PKB inactivation. Here we show that the loss of PTEN in mouse cerebellar neurons causes neurodegeneration by hyperphosphorylation of tau and neurofilaments, and activation of Cdk5 and pERK1/2, suggesting that dysregulation of the PTEN/pAkt pathway can mediate neurodegeneration.

  • Type:

    Article

  • Date:

    05 January 2007

  • Publication Status:

    Published

  • Publisher

    Elsevier BV

  • DOI:

    10.1016/j.mcn.2006.11.014

  • Cross Ref:

    S1044743106002685

  • ISSN:

    1044-7431

  • Library of Congress:

    QR Microbiology

  • Dewey Decimal Classification:

    572 Biochemistry

Citation

Nayeem, N., Kerr, F., Naumann, H., Linehan, J., Lovestone, S. & Brandner, S. (2007). Hyperphosphorylation of tau and neurofilaments and activation of CDK5 and ERK1/2 in PTEN-deficient cerebella. Molecular and Cellular Neuroscience. 34(3), 400-408. doi:10.1016/j.mcn.2006.11.014. ISSN 1044-7431

Authors

Keywords

Tau phosphorylation; PTEN; Cre-LoxP system; Transgenic mice; Neurodegeneration

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