Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells

By S. Nauli, F. Alenghat, Ying Luo, E. Williams, P. Vassilev, Xiaogang Li, A. Elia, Weining Lu, E. Brown, S. Quinn and 2 more. Nature Genetics, 2003

2,079 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/65b71020b0aa4d2417e8c6ed06050e7b8b98d5f9

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Citations in the corpus

Mechanical control of tissue and organ development (2010, background): “cilia, which is mediated by polycystin-1/2 mechanosensitive ion channels on the cell surface, can affect mitotic alignment, cause renal tubular enlargement and result in cyst formation, as observed in mice with polycystic kidney disease (Fischer et al., 2006; Nauli et al., 2003).”
The Primary Cilium as a Complex Signaling Center (2009, background): “This is supported by the loss of a calcium (Ca) signal induced by cilia deflection in the absence of these proteins [23], despite normal cilia structure (Figure 2).”
An introduction to TRP channels. (2006, background): “PKD1 and TRPP2 both appear to be targeted to primary cilia of renal epithelial cells, where the channel complex may be gated by fluid flow (178).”
Cellular mechanotransduction: putting all the pieces together again (2006, background): “The importance of mechanical forces for organ development is made clear by the finding that mutation or deletion of the polycystin genes that encode mechanosensitive ion channels that mediate urine flow sensation in kidney epithelium leads to the development of polycystic kidney disease (97).”
The TRP Superfamily of Cation Channels (2005, background): “Consistent with this proposal, cultured kidney cells from wildtype, but not TRPP1 mutant, cells display an increase in Ca2+ influx in response to fluid flow (222).”
Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways (2005, background): “In inner medullary collecting duct (IMCD) cells, a flow rate equivalent to that of urine flo”
Basal body dysfunction is a likely cause of pleiotropic Bardet–Biedl syndrome (2003, background): “, whereas failure of mechanosensation at the primary cilium of renal tubular cells causes polycystic kidney disease (PKD”
Mechanotransduction gone awry (2009, background): “Similarly, mutations in the genes that encode the ciliary proteins polycystin 1 or the transient receptor potential channel family protein polycystin 2 (TRPP2) provide direct evidence for defects in mechanotransduction that result in kidney diseas”