{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T02:36:52Z","timestamp":1768531012657,"version":"3.49.0"},"reference-count":48,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2006,8,25]],"date-time":"2006-08-25T00:00:00Z","timestamp":1156464000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:p>A tubule system is an important component of the nephron, which is the structural and functional unit of the kidney. Expansion of renal tubules results in renal cysts. Hereditary forms of renal cystic diseases suggest that tubular size is determined genetically. The <jats:italic>inv<\/jats:italic> was discovered as a mutant with renal cysts and <jats:italic>situs inversus<\/jats:italic>. <jats:italic>Inv<\/jats:italic>\/<jats:italic>inv<\/jats:italic>, <jats:italic>inv<\/jats:italic>\u0394C::GFP (<jats:italic>inv<\/jats:italic>\u0394C) mouse was created by the introduction of the <jats:italic>inv<\/jats:italic> gene lacking the C\u2010terminus (<jats:italic>inv<\/jats:italic>\u0394C) into <jats:italic>inv<\/jats:italic>\/<jats:italic>inv<\/jats:italic> mice. The mouse develops multiple renal cysts without <jats:italic>situs<\/jats:italic> abnormality, giving us an opportunity to study inv function in renal tubular structure maintenance. In the present study, we showed that <jats:italic>inv<\/jats:italic> suppresses cyst progression in a dose\u2010dependent manner and that the <jats:italic>inv<\/jats:italic>\u0394C cystic kidneys showed increased cell proliferation and apoptosis. Cell cycle regulators for G1\u2010S progression were activated in the cystic kidney. Furthermore, cDNA microarray and semiquantitative RT\u2010PCR analysis showed that growth\u2010related genes maintained a high level of expression in the cystic kidney at 4\u00a0weeks of age whereas they were decreased in control kidneys, suggesting that cells in <jats:italic>inv<\/jats:italic>\u0394C kidney are still active in the cell cycle. One of the inv protein functions may provide a stop signal for renal epithelial cell proliferation.<\/jats:p>","DOI":"10.1111\/j.1365-2443.2006.01011.x","type":"journal-article","created":{"date-parts":[[2006,8,25]],"date-time":"2006-08-25T19:50:01Z","timestamp":1156535401000},"page":"1213-1224","source":"Crossref","is-referenced-by-count":15,"title":["Sustained cell proliferation of renal epithelial cells in mice with <i>inv<\/i> mutation"],"prefix":"10.1111","volume":"11","author":[{"given":"Noriyuki","family":"Sugiyama","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takahiko","family":"Yokoyama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,8,25]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddl107"},{"key":"e_1_2_6_3_1","first-page":"2210","article-title":"c\u2010myc\u2010induced apoptosis in polycystic kidney disease is independent of FasL\/Fas interaction","volume":"62","author":"Couillard M.","year":"2002","journal-title":"Cancer Res."},{"key":"e_1_2_6_4_1","first-page":"73","article-title":"Altered extracellular matrix component gene expression in murine polycystic kidney","volume":"18","author":"Ebihara I.","year":"1995","journal-title":"Ren. 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