The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Polaris, a protein disrupted in orpk mutant mice, is required for assembly of renal cilium
Abstract
Cilia are organelles that play diverse roles, from fluid movement to sensory reception. Polaris, a protein associated with cystic kidney disease in Tg737°rpk mice, functions in a ciliogenic pathway. Here, we explore the role of polaris in primary cilia on Madin-Darby canine kidney cells. The results indicate that polaris localization and solubility change dramatically during cilia formation. These changes correlate with the formation of basal bodies and large protein rafts at the apical surface of the epithelia. A cortical collecting duct cell line has been derived from mice with a mutation in the Tg737 gene. These cells do not develop normal cilia, which can be corrected by reexpression of the wild-type Tg737 gene. These data suggest that the primary cilia are important for normal renal function and/or development and that the ciliary defect may be a contributing factor to the cystic disease in Tg737°rpk mice. Further characterization of these cells will be important in elucidating the physiological role of renal cilia and in determining their relationship to cystic disease.
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Cites
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A polycystic kidney-disease gene homologue required for male mating behaviour in C. elegans
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Cited by
Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells
Nauli, S. M., Alenghat, F. J., Luo, Y., Williams, E., Vassilev, P., Li, X., Elia, A. E. H., Lu, W., Brown, E. M., Quinn, S. J., et al. (2003) · Nature Genetics · doi:10.1038/ng1076 · Cited by 2,057
When cilia go bad: cilia defects and ciliopathies
Fliegauf, M., Benzing, T., & Omran, H. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2278 · Cited by 1,257
Yoder, B. K., Hou, X., & Guay-Woodford, L. M. (2002) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000029587.47950.25 · Cited by 935
Self-citationHaycraft, C. J., Banizs, B., Aydin-Son, Y., Zhang, Q., Michaud, E. J., & Yoder, B. K. (2005) · PLoS Genetics · doi:10.1371/journal.pgen.0010053 · Cited by 902
Self-citationGenetics and Pathogenesis of Polycystic Kidney Disease
Igarashi, P., & Somlo, S. (2002) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000028643.17901.42 · Cited by 593
Metadata
- Authors
- Yoder, B. K., Tousson, A., Millican, L., Wu, J. H., Bugg, C. E., Schafer, J. A., Balkovetz, D. F., & Watkins), (. T. T. A. O. L. L. A. M. L.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2002-03-01
- Volume
- 282
- Issue
- 3
- Pages
- F541-F552
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2147014496
- Cited by
- 240
- References
- 5
- FWCI
- 10.51
- Type
- journal article
- Language
- en
- Open access
- closed
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- Yoder, B. K., Tousson, A., Millican, L., Wu, J. H., Bugg, C. E., Schafer, J. A., Balkovetz, D. F., & Watkins), (. T. T. A. O. L. L. A. M. L. (2002). Polaris, a protein disrupted in orpk mutant mice, is required for assembly of renal cilium. American Journal of Physiology-Renal Physiology. https://doi.org/10.1152/ajprenal.00273.2001
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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