| Literature DB >> 14983006 |
Ming-Zhi Zhang1, Weiyi Mai, Cunxi Li, Sae-youll Cho, Chuanming Hao, Gilbert Moeckel, Runxiang Zhao, Ingyu Kim, Jikui Wang, Huaqi Xiong, Hong Wang, Yasunori Sato, Yizhong Wu, Yasuni Nakanuma, Marusia Lilova, York Pei, Raymond C Harris, Song Li, Robert J Coffey, Le Sun, Dianqing Wu, Xing-Zhen Chen, Matthew D Breyer, Zhizhuang Joe Zhao, James A McKanna, Guanqing Wu.
Abstract
Mutations of the polycystic kidney and hepatic disease 1 (PKHD1) gene have been shown to cause autosomal recessive polycystic kidney disease (ARPKD), but the cellular functions of the gene product (PKHD1) remain uncharacterized. To illuminate its properties, the spatial and temporal expression patterns of PKHD1 were determined in mouse, rat, and human tissues by using polyclonal Abs and mAbs recognizing various specific regions of the gene product. During embryogenesis, PKHD1 is widely expressed in epithelial derivatives, including neural tubules, gut, pulmonary bronchi, and hepatic cells. In the kidneys of the pck rats, the rat model of which is genetically homologous to human ARPKD, the level of PKHD1 was significantly reduced but not completely absent. In cultured renal cells, the PKHD1 gene product colocalized with polycystin-2, the gene product of autosomal dominant polycystic disease type 2, at the basal bodies of primary cilia. Immunoreactive PKHD1 localized predominantly at the apical domain of polarized epithelial cells, suggesting it may be involved in the tubulogenesis and/or maintenance of duct-lumen architecture. Reduced PKHD1 levels in pck rat kidneys and its colocalization with polycystins may underlie the pathogenic basis for cystogenesis in polycystic kidney diseases.Entities:
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Year: 2004 PMID: 14983006 PMCID: PMC356947 DOI: 10.1073/pnas.0400073101
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205