ArticleHuman molecular genetics2019
c-Myc is a regulator of the PKD1 gene and PC1-induced pathogenesis.
Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Disruption of a six-nucleotide miRNA motif improves PKD1 dosage and ameliorates polycystic kidney disease.Nucleic acids research · 2026Article
- Disruption of a six-nucleotide miRNA motif improvesbioRxiv : the preprint server for biology · 2025Article
- Kcnn4/KCa3.1 inhibition blunts polycystic kidney disease progression in mouse models.JCI insight · 2025Article
- Metabolic Reprogramming in Autosomal Dominant Polycystic Kidney Disease: Role in Cystogenesis and Novel Therapeutic Approaches.Biomedicines · 2025Review
- Amino acid metabolism in kidney health and disease.Nature reviews. Nephrology · 2024Review
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- Co-Inheritance of Pathogenic Variants inGenes · 2023Article
- Cystin is required for maintaining fibrocystin (FPC) levels and safeguarding proteome integrity in mouse renal epithelial cells: A mechanistic connection between the kidney defects in cpk mice and human ARPKD.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- ModelingMolecular therapy. Methods & clinical development · 2023Article
- Mechanisms of Cyst Development in Polycystic Kidney Disease.Advances in kidney disease and health · 2023Review
- Differential regulation of MYC expression byFrontiers in cell and developmental biology · 2023Article
- Small hairpin inhibitory RNA delivery in the metanephric organ culture identifies long noncoding RNAAmerican journal of physiology. Renal physiology · 2022Article
- c-Jun N-terminal kinase (JNK) signaling contributes to cystic burden in polycystic kidney disease.PLoS genetics · 2021Article
- PKD1 alleviates oxidative stress-inhibited osteogenesis of rat bone marrow-derived mesenchymal stem cells through TAZ activation.Journal of cellular biochemistry · 2021Article
- Cystin genetic variants cause autosomal recessive polycystic kidney disease associated with altered Myc expression.Scientific reports · 2021Article
- H3K14 hyperacetylation‑mediated c‑Myc binding to the miR‑30a‑5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury.Molecular medicine reports · 2021Article
- Pathway identification through transcriptome analysis.Cellular signalling · 2020Review
- Rapamycin and dexamethasone during pregnancy prevent tuberous sclerosis complex-associated cystic kidney disease.JCI insight · 2020Article
- Hippo signaling-a central player in cystic kidney disease?Pediatric nephrology (Berlin, Germany) · 2020Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is among the most common monogenic disorders mainly associated with PKD1/PC1 mutations. We show herein that renal regulation in Pc1 dosage-reduced and -increased mouse models converge toward stimulation of c-Myc expression along with β-catenin, delineating c-Myc as a key Pkd1 node in cystogenesis. Enhanced renal c-Myc-induced ADPKD in SBM transgenic mice lead conversely to striking upregulation of Pkd1/Pc1 expression and β-catenin activation, lending credence for reciprocal crosstalk between c-Myc and Pc1. In adult SBM kidneys, c-Myc is strongly enriched on Pkd1 promoter with RNA pol II, consistent with Pkd1 upregulation during cystogenesis. Similar c-Myc direct binding at birth uncovers an equivalent role on Pkd1 regulation during renal developmental program. Concurrent with enriched c-Myc binding, recruitment of active chromatin modifying co-factors by c-Myc at the Pkd1 regulatory region probably opens chromatin to stimulate transcription. A similar transcriptional activation by c-Myc is also likely operant on endogenous human PKD1 gene from our transactivation analysis in response to human c-MYC upregulation. Genetic ablation of c-Myc in Pc1-reduced and -increased mouse models significantly attenuates cyst growth, proliferation and PKD progression. Our study determined a dual role for c-Myc, as a major contributor in Pc1-induced cystogenesis and in a feed-forward regulatory Pkd1-c-Myc loop mechanism that may also prevail in human ADPKD.
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