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

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Mechanical stimuli induce cleavage and nuclear translocation of the polycystin-1 C terminus.

Polycystin-1, which is encoded by a gene that is mutated in autosomal dominant polycystic kidney disease (ADPKD), is involved in cell-matrix interactions as well as in ciliary signaling. The precise mechanisms by which it functions, however, remain unclear. Here we find that polycystin-1 undergoes a proteolytic cleavage that releases its C-terminal tail (CTT), which enters the nucleus and initiates signaling processes. The cleavage occurs in vivo in association with alterations in mechanical stimuli. Polycystin-2, the product of the second gene mutated in ADPKD, modulates the signaling properties of the polycystin-1 CTT. These data reveal a novel pathway by which polycystin-1 transmits messages directly to the nucleus.[1]

References

  1. Mechanical stimuli induce cleavage and nuclear translocation of the polycystin-1 C terminus. Chauvet, V., Tian, X., Husson, H., Grimm, D.H., Wang, T., Hiesberger, T., Hieseberger, T., Igarashi, P., Bennett, A.M., Ibraghimov-Beskrovnaya, O., Somlo, S., Caplan, M.J. J. Clin. Invest. (2004) [Pubmed]
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