ArticleJournal of cellular and molecular medicine2020
The carboxy-terminus of the human ARPKD protein fibrocystin can control STAT3 signalling by regulating SRC-activation.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Fibrocystin/polyductin (FPC): new functional insights into ARPKD pathogenesis revealed by informatics, comparative genomics, and model systems.Pediatric nephrology (Berlin, Germany) · 2026Review
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Novel compound heterozygousFrontiers in medicine · 2026Article
- Defects of renal tubular homeostasis and cystogenesis in theiScience · 2024Article
- Fibrocystin/Polyductin releases a C-terminal fragment that translocates into mitochondria and suppresses cystogenesis.Nature communications · 2023Article
- Pkhd1Journal of molecular medicine (Berlin, Germany) · 2023Article
- Differential regulation of MYC expression byFrontiers in cell and developmental biology · 2023Article
- Is There a Functional Role of Mitochondrial Dysfunction in the Pathogenesis of ARPKD?Frontiers in medicine · 2021Article
- The carboxy-terminus of the human ARPKD protein fibrocystin can control STAT3 signalling by regulating SRC-activation.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
12 authors.
Funding
Abstract
Autosomal recessive polycystic kidney disease (ARPKD) is mainly caused by variants in the PKHD1 gene, encoding fibrocystin (FC), a large transmembrane protein of incompletely understood cellular function. Here, we show that a C-terminal fragment of human FC can suppress a signalling module of the kinase SRC and signal transducer and activator of transcription 3 (STAT3). Consistently, we identified truncating genetic variants specifically affecting the cytoplasmic tail in ARPKD patients, found SRC and the cytoplasmic tail of fibrocystin in a joint dynamic protein complex and observed increased activation of both SRC and STAT3 in cyst-lining renal epithelial cells of ARPKD patients.
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