Transcriptomics

Dataset Information

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Differential gene expression in nephron progenitors lacking miR-17~92


ABSTRACT: Purpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. mRNA profiles of control and mutant (=Six2-TGC; miR-17~92 flx/flx) embryonic day 16 kidneys were generated by deep sequencing, in triplicate, using Illumina HiSeq2000

ORGANISM(S): Mus musculus  

SUBMITTER: April K Marrone   Dennis Kostka  Jacqueline Ho 

PROVIDER: E-GEOD-52514 | ArrayExpress | 2014-03-07

SECONDARY ACCESSION(S): SRP033129GSE52514PRJNA229148

REPOSITORIES: GEO, ArrayExpress, ENA

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Publications

MicroRNA-17~92 is required for nephrogenesis and renal function.

Marrone April K AK   Stolz Donna B DB   Bastacky Sheldon I SI   Kostka Dennis D   Bodnar Andrew J AJ   Ho Jacqueline J  

Journal of the American Society of Nephrology : JASN 20140207 7


Deletion of all microRNAs (miRNAs) in nephron progenitors leads to premature loss of these cells, but the roles of specific miRNAs in progenitors have not been identified. Deletions in the MIR17HG cluster (miR-17~92 in mice), detected in a subset of patients with Feingold syndrome, represent the first miRNA mutations to be associated with a developmental defect in humans. Although MIR17HG is expressed in the developing kidney, and patients with Feingold syndrome caused by MYCN mutations have ren  ...[more]

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