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Start Over Author "Chauvet V" Journal journal of clinical investigation
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2. Mechanical stimuli induce cleavage and nuclear translocation of the polycystin-1 C terminus.

Author

Chauvet V, Tian X, Husson H, Grimm DH, Wang T, Hiesberger T, Igarashi P, Bennett AM, Ibraghimov-Beskrovnaya O, Somlo S, and Caplan MJ

Subjects
Amino Acid Sequence, Animals, CHO Cells, COS Cells, Cell Line, Chlorocebus aethiops, Cricetinae, Cricetulus, Dogs, Embryo, Mammalian, Epithelial Cells cytology, Kidney Tubules cytology, Kidney Tubules embryology, Membrane Proteins metabolism, Mice, Mice, Transgenic, Polycystic Kidney, Autosomal Dominant genetics, Polycystic Kidney, Autosomal Dominant pathology, Proteins genetics, Sequence Deletion, Stress, Mechanical, TRPP Cation Channels, Transcription Factor AP-1 metabolism, Cell Nucleus metabolism, Proteins chemistry, Proteins metabolism, Signal Transduction
Abstract

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.

Published
2004
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