Literature DB >> 1912403

Elevated proto-oncogene expression in polycystic kidneys of the C57BL/6J (cpk) mouse.

B D Cowley1, L J Chadwick, J J Grantham, J P Calvet.   

Abstract

Polycystic kidney disease in the C57BL/6J (cpk) mouse is an autosomal recessive disorder which leads to the rapid development of renal cysts and kidney failure during the first 3 to 4 postnatal weeks. Previously, we showed that the cystic kidneys of affected mice have abnormally elevated levels of c-myc mRNA. In the study presented here, it is shown that mRNAs for the proto-oncogenes c-fos and c-Kiras, as well as c-myc, are markedly elevated in cystic kidneys, suggesting that there is a more general abnormality in gene expression associated with the disease. It is also evident that there are two stages to this abnormal proto-oncogene expression. In the first stage, which occurs up through the second postnatal week, there are modest increases in proto-oncogene mRNA which parallel the increased cell proliferation that accompanies cyst growth at this time. In the second stage, which occurs after the second postnatal week, there are markedly elevated levels of proto-oncogene mRNA that are seen at a time when cell proliferation is declining. The development of this latter stage suggests either that there is a fundamental abnormality intrinsic to polycystic kidneys that leads to uncontrolled proto-oncogene expression later in disease progression or that there is a secondary response in the kidney to the progressive renal failure.

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Year:  1991        PMID: 1912403     DOI: 10.1681/ASN.V181048

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  32 in total

1.  The molecular basis of nephrogenesis and congenital kidney disease.

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Journal:  Arch Dis Child       Date:  1992-08       Impact factor: 3.791

Review 2.  The hallmarks of cancer: relevance to the pathogenesis of polycystic kidney disease.

Authors:  Tamina Seeger-Nukpezah; Daniel M Geynisman; Anna S Nikonova; Thomas Benzing; Erica A Golemis
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3.  Growth characteristics of cells cultured from two murine models of polycystic kidney disease.

Authors:  C A Rankin; D M Ziemer; R L Maser; I Foo; J P Calvet
Journal:  In Vitro Cell Dev Biol Anim       Date:  1996-02       Impact factor: 2.416

Review 4.  Polycystic kidney disease--a truly pediatric problem.

Authors:  M R Ogborn
Journal:  Pediatr Nephrol       Date:  1994-12       Impact factor: 3.714

5.  Homo- and heterodimeric interactions between the gene products of PKD1 and PKD2.

Authors:  L Tsiokas; E Kim; T Arnould; V P Sukhatme; G Walz
Journal:  Proc Natl Acad Sci U S A       Date:  1997-06-24       Impact factor: 11.205

Review 6.  Genetic mechanisms and signaling pathways in autosomal dominant polycystic kidney disease.

Authors:  Peter C Harris; Vicente E Torres
Journal:  J Clin Invest       Date:  2014-06-02       Impact factor: 14.808

7.  Differential rescue of the renal and hepatic disease in an autosomal recessive polycystic kidney disease mouse mutant. A new model to study the liver lesion.

Authors:  B K Yoder; W G Richards; C Sommardahl; W E Sweeney; E J Michaud; J E Wilkinson; E D Avner; R P Woychik
Journal:  Am J Pathol       Date:  1997-06       Impact factor: 4.307

Review 8.  Polycystic kidney disease: huge kidneys, huge problems, huge progress.

Authors:  J J Grantham
Journal:  Trans Am Clin Climatol Assoc       Date:  1997

9.  JunD protects against chronic kidney disease by regulating paracrine mitogens.

Authors:  Evangéline Pillebout; Jonathan B Weitzman; Martine Burtin; Carla Martino; Pierre Federici; Moshe Yaniv; Gérard Friedlander; Fabiola Terzi
Journal:  J Clin Invest       Date:  2003-09       Impact factor: 14.808

10.  Disappearance of polycystic kidney disease in revertant c-myc transgenic mice.

Authors:  M Trudel; N Chrétien; V D'Agati
Journal:  Mamm Genome       Date:  1994-03       Impact factor: 2.957

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