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PKHD1 post‐transcriptionally modulated by miR‐365‐1 inhibits cell‐cell adhesion
Author(s) -
Duan Jingjing,
Huang Huizhe,
Lv Xiaoyan,
Wang Honglian,
Tang Ziwei,
Sun Huan,
Li Qingwei,
Ai Jianzhong,
Tan Ruizhi,
Liu Yuhang,
Chen Mianzhi,
Duan Weiwei,
Wei Yuquan,
Zhou Qin
Publication year - 2012
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.2795
Subject(s) - biology , microrna , gene , genetics , three prime untranslated region , untranslated region , gene expression , regulation of gene expression , coding region , messenger rna
Autosomal recessive polycystic kidney disease (ARPKD) is a severe inherited disorder with an incidence of 1/20 000 live births. Mutations of PKHD1 (polycystic kidney and hepatic disease gene 1) gene were identified to be responsible for ARPKD. However, the underlying molecular mechanisms remain largely unknown. MicroRNAs (miRNAs) are an abundant class of small RNAs with global effect on gene expression. Up to 30% of human protein coding genes may be regulated by miRNAs. However, to date, nothing is known regarding the role of miRNAs in PKHD1 . In this study, we exploited bioinformatics to analyse the 3'UTR of PKHD1 gene and illustrated that the 3'UTR region of the gene is highly conserved in evolution. We identified about 35 candidate miRNAs within a 3738 bp window of the 3'UTR region. Of the 35 potential miRNAs, miR‐365‐1 emerged to post‐transcriptionally modulate the expression of PKHD1 . Furthermore, we demonstrated that miR‐365‐1 modulated PKHD1 suppressed cell–cell adhesion in part through E‐cadherin. Copyright © 2012 John Wiley & Sons, Ltd.