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Mutations in genes<jats:italic>PKD1<\/jats:italic>and<jats:italic>PKD2<\/jats:italic>account for nearly all cases of ADPKD. Increased cell proliferation is one of the key features of the disease. Several studies indicated that polycystin-1 regulates cellular proliferation through various signaling pathways, but little is known about the role played by polycystin-2, the product of<jats:italic>PKD2<\/jats:italic>. Recently, it was reported that as with polycystin-1, polycystin-2 can act as a negative regulator of cell growth by modulating the levels of the cyclin-dependent kinase inhibitor, p21 and the activity of the cyclin-dependent kinase 2, Cdk2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Here we utilized different kidney cell-lines expressing wild-type and mutant<jats:italic>PKD2<\/jats:italic>as well as primary tubular epithelial cells isolated from a PKD transgenic rat to further explore the contribution of the p21\/Cdk2 pathway in ADPKD proliferation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Surprisingly, over-expression of wild-type<jats:italic>PKD2<\/jats:italic>in renal cell lines failed to inactivate Cdk2 and consequently had no effect on cell proliferation. On the other hand, expression of mutated<jats:italic>PKD2<\/jats:italic>augmented proliferation only in the primary tubular epithelial cells of a rat model but this was independent of the STAT-1\/p21 pathway. On the contrary, multiple approaches revealed unequivocally that expression of the cyclin-dependent kinase inhibitor, p57<jats:sup>KIP2<\/jats:sup>, is downregulated, while p21 remains unchanged. This p57 reduction is accompanied by an increase in Cdk2 levels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our results indicate the probable involvement of p57<jats:sup>KIP2<\/jats:sup>on epithelial cell proliferation in ADPKD implicating a new mechanism for mutant polycystin-2 induced proliferation. Most importantly, contrary to previous studies, abnormal proliferation in cells expressing mutant polycystin-2 appears to be independent of STAT-1\/p21.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2369-9-10","type":"journal-article","created":{"date-parts":[[2008,8,26]],"date-time":"2008-08-26T06:12:55Z","timestamp":1219731175000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Mutant polycystin-2 induces proliferation in primary rat tubular epithelial cells in a STAT-1\/p21-independent fashion accompanied instead by alterations in expression of p57KIP2and Cdk2"],"prefix":"10.1186","volume":"9","author":[{"given":"Kyriacos N","family":"Felekkis","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Panayiota","family":"Koupepidou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Evdokia","family":"Kastanos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ralph","family":"Witzgall","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chang-Xi","family":"Bai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Li","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leonidas","family":"Tsiokas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norbert","family":"Gretz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Constantinos","family":"Deltas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2008,8,25]]},"reference":[{"issue":"5","key":"101_CR1","doi-asserted-by":"publisher","first-page":"332","DOI":"10.1056\/NEJM199307293290508","volume":"329","author":"PA Gabow","year":"1993","unstructured":"Gabow PA: Autosomal dominant polycystic kidney disease. 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