Ontology highlight
ABSTRACT:
PROVIDER: PRJNA773192 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16508143.fastq.gz | Fastqsanger.gz | |||
| SRR16508144_1.fastq.gz | Fastqsanger.gz | |||
| SRR16508144_2.fastq.gz | Fastqsanger.gz | |||
| SRR16508145_1.fastq.gz | Fastqsanger.gz | |||
| SRR16508145_2.fastq.gz | Fastqsanger.gz |
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Project description:Background Congenital anomalies of the kidney and urinary tract (CAKUT) refer to a diverse group of developmental malformations, which are the leading cause of chronic kidney disease and end-stage renal disease in children. The etiology and pathogenesis of CAKUT are complex. In recent years, the relationship between long noncoding RNAs and renal development and disease has attracted much attention. Our previous study established a long noncoding RNA 4933425B07Rik (Rik) overexpression mouse model by inserting the PB transposon and found that overexpression of Rik led to renal hypoplasia. This study aimed to explore the molecular mechanism of renal hypoplasia induced by Rik overexpression in vitro. Results In this study, by constructing Rik overexpression cell models and a Rik knockout cell model to accompany previously developed RikPB/PB;Hoxb7 mice and by applying RNA-seq, RT‒PCR and other experimental methods, it was found that when Rik was highly expressed, the expression of Wnt10b, Fzd8 and β-catenin decreased, while Rik was knock down, the expression of these genes increased. Conclusions The findings suggest that overexpression of Rik leads to renal hypoplasia by inactivating the Wnt/β-catenin signaling pathway. This research perspective may provide a basis for exploring new causes and mechanisms of CAKUT and provide new targets for the prevention and treatment of CAKUT.
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Project description:Molecular Characterization of Clinical Renal Tumors
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