ArticlePloS one2013
The ciliary protein cystin forms a regulatory complex with necdin to modulate Myc expression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Kidney disease in adults with Prader-Willi syndrome: international cohort study and systematic literature review.Frontiers in endocrinology · 2023Pooled it
- Fibrocystin/polyductin (FPC): new functional insights into ARPKD pathogenesis revealed by informatics, comparative genomics, and model systems.Pediatric nephrology (Berlin, Germany) · 2026Review
- Disruption of the human cystin-1 myristoyl-electrostatic switch causes polycystic kidney disease that phenocopies autosomal recessive polycystic kidney disease.Kidney international · 2026Article
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- 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
- Differential regulation of MYC expression byFrontiers in cell and developmental biology · 2023Article
- Transcription factor Ap2b regulates the mouse autosomal recessive polycystic kidney disease genes,Frontiers in molecular biosciences · 2022Article
- Cystin genetic variants cause autosomal recessive polycystic kidney disease associated with altered Myc expression.Scientific reports · 2021Article
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis.Molecular therapy. Methods & clinical development · 2019Review
- c-Myc is a regulator of the PKD1 gene and PC1-induced pathogenesis.Human molecular genetics · 2019Article
- Casein kinase 1ε and 1α as novel players in polycystic kidney disease and mechanistic targets for (R)-roscovitine and (S)-CR8.American journal of physiology. Renal physiology · 2018Article
- Necdin is a breast cancer metastasis suppressor that regulates the transcription of c-Myc.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cystin is a novel cilia-associated protein that is disrupted in the cpk mouse, a well-characterized mouse model of autosomal recessive polycystic kidney disease (ARPKD). Interestingly, overexpression of the Myc gene is evident in animal models of ARPKD and is thought to contribute to the renal cystic phenotype. Using a yeast two-hybrid approach, the growth suppressor protein necdin, known to modulate Myc expression, was found as an interacting partner of cystin. Deletion mapping demonstrated that the C-terminus of cystin and both termini of necdin are required for their mutual interaction. Speculating that these two proteins may function to regulate gene expression, we developed a luciferase reporter assay and observed that necdin strongly activated the Myc P1 promoter, and cystin did so more modestly. Interestingly, the necdin effect was significantly abrogated when cystin was co-transfected. Chromatin immunoprecipitation and electrophoretic mobility shift assays revealed a physical interaction with both necdin and cystin and the Myc P1 promoter, as well as between these proteins. The data suggest that these proteins likely function in a regulatory complex. Thus, we speculate that Myc overexpression in the cpk kidney results from the dysregulation of the cystin-necdin regulatory complex and c-Myc, in turn, contributes to cystogenesis in the cpk mouse.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.