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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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The atypical PKC-interacting protein p62 is an important mediator of RANK-activated osteoclastogenesis.

The atypical PKCs (aPKCs) have been implicated genetically in at least two independent signaling cascades that control NF-kappa B and cell polarity, through the interaction with the adapters p62 and Par-6, respectively. P62 binds TRAF6, which plays an essential role in osteoclastogenesis and bone remodeling. Recently, p62 mutations have been shown to be the cause of the 5q35-linked Paget's disease of bone, a genetic disorder characterized by aberrant osteoclastic activity. Here we show that p62, like TRAF6, is upregulated during RANK-L-induced osteoclastogenesis and that the genetic inactivation of p62 in mice leads to impaired osteoclastogenesis in vitro and in vivo, as well as inhibition of IKK activation and NF-kappa B nuclear translocation. In addition, RANK-L stimulation leads to the inducible formation of a ternary complex involving TRAF6, p62, and the aPKCs. These observations demonstrate that p62 is an important mediator during osteoclastogenesis and induced bone remodeling.[1]

References

  1. The atypical PKC-interacting protein p62 is an important mediator of RANK-activated osteoclastogenesis. Durán, A., Serrano, M., Leitges, M., Flores, J.M., Picard, S., Brown, J.P., Moscat, J., Diaz-Meco, M.T. Dev. Cell (2004) [Pubmed]
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