Literature DB >> 11106764

Polycystin-1, the gene product of PKD1, induces resistance to apoptosis and spontaneous tubulogenesis in MDCK cells.

A Boletta1, F Qian, L F Onuchic, A K Bhunia, B Phakdeekitcharoen, K Hanaoka, W Guggino, L Monaco, G G Germino.   

Abstract

The major form of autosomal dominant polycystic kidney disease (ADPKD) results from mutation of a gene (PKD1) of unknown function that is essential for the later stages of renal tubular differentiation. In this report, we describe a novel cell culture system for studying how PKD1 regulates this process. We show that expression of human PKD1 in MDCK cells slows their growth and protects them from programmed cell death. MDCK cells expressing PKD1 also spontaneously form branching tubules while control cells form simple cysts. Increased cell proliferation and apoptosis have been implicated in the pathogenesis of cystic diseases. Our study suggests that PKD1 may function to regulate both pathways, allowing cells to enter a differentiation pathway that results in tubule formation.

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Year:  2000        PMID: 11106764     DOI: 10.1016/s1097-2765(00)00123-4

Source DB:  PubMed          Journal:  Mol Cell        ISSN: 1097-2765            Impact factor:   17.970


  84 in total

Review 1.  Polycystic kidney disease: In danger of being X-rated?

Authors:  J J Grantham; J P Calvet
Journal:  Proc Natl Acad Sci U S A       Date:  2001-01-30       Impact factor: 11.205

2.  Regulation of integrin expression by Gα12: An additional potential mechanism modulating cell attachment.

Authors:  Tianqing Kong; Daosong Xu; Mei Tran; Bradley M Denker
Journal:  Cell Adh Migr       Date:  2010-07-01       Impact factor: 3.405

3.  Loss of PKD1 and loss of Bcl-2 elicit polycystic kidney disease through distinct mechanisms.

Authors:  P Hughes; M Robati; W Lu; J Zhou; A Strasser; P Bouillet
Journal:  Cell Death Differ       Date:  2005-11-11       Impact factor: 15.828

Review 4.  Potential pharmacological interventions in polycystic kidney disease.

Authors:  Amirali Masoumi; Berenice Reed-Gitomer; Catherine Kelleher; Robert W Schrier
Journal:  Drugs       Date:  2007       Impact factor: 9.546

5.  The isolated polycystin-1 COOH-terminal can activate or block polycystin-1 signaling.

Authors:  Uma Basavanna; Kimberly M Weber; Qinghua Hu; Roy C Ziegelstein; Gregory G Germino; Michael Sutters
Journal:  Biochem Biophys Res Commun       Date:  2007-05-25       Impact factor: 3.575

6.  Caspase-3 gene deletion prolongs survival in polycystic kidney disease.

Authors:  Yunxia Tao; Iram Zafar; Jun Kim; Robert W Schrier; Charles L Edelstein
Journal:  J Am Soc Nephrol       Date:  2008-02-13       Impact factor: 10.121

7.  Evaluating the clinical utility of a molecular genetic test for polycystic kidney disease.

Authors:  Miguel A Garcia-Gonzalez; Jeffrey G Jones; Susan K Allen; Christopher M Palatucci; Sat D Batish; William K Seltzer; Zheng Lan; Erica Allen; Feng Qian; Xose M Lens; York Pei; Gregory G Germino; Terry J Watnick
Journal:  Mol Genet Metab       Date:  2007-06-18       Impact factor: 4.797

8.  Polycystin-1 and Gα12 regulate the cleavage of E-cadherin in kidney epithelial cells.

Authors:  Jen X Xu; Tzong-Shi Lu; Suyan Li; Yong Wu; Lai Ding; Bradley M Denker; Joseph V Bonventre; Tianqing Kong
Journal:  Physiol Genomics       Date:  2014-12-09       Impact factor: 3.107

9.  Loss of polycystin-1 causes centrosome amplification and genomic instability.

Authors:  Lorenzo Battini; Salvador Macip; Elena Fedorova; Steven Dikman; Stefan Somlo; Cristina Montagna; G Luca Gusella
Journal:  Hum Mol Genet       Date:  2008-06-19       Impact factor: 6.150

10.  Bardet-Biedl syndrome proteins 1 and 3 regulate the ciliary trafficking of polycystic kidney disease 1 protein.

Authors:  Xuefeng Su; Kaitlin Driscoll; Gang Yao; Anas Raed; Maoqing Wu; Philip L Beales; Jing Zhou
Journal:  Hum Mol Genet       Date:  2014-06-16       Impact factor: 6.150

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