Genetic inactivation of p62 leads to accumulation of hyperphosphorylated tau and neurodegeneration.

@article{Babu2008GeneticIO,
  title={Genetic inactivation of p62 leads to accumulation of hyperphosphorylated tau and neurodegeneration.},
  author={Jeganathan Ramesh Babu and M Lamar Seibenhener and Junmin Peng and A David G Strom and Robert J. Kemppainen and Nancy Cox and Haining Zhu and Michael Wooten and M T Diaz-Meco and J Moscat},
  journal={Journal of neurochemistry},
  year={2008},
  volume={106 1},
  pages={
          107-20
        }
}
The signaling adapter p62 plays a coordinating role in mediating phosphorylation and ubiquitin-dependent trafficking of interacting proteins. However, there is little known about the physiologic role of this protein in brain. Here, we report age-dependent constitutive activation of glycogen synthase kinase 3beta, protein kinase B, mitogen-activated protein kinase, and c-Jun-N-terminal kinase in adult p62(-/-) mice resulting in hyperphosphorylated tau, neurofibrillary tangles, and… CONTINUE READING

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