ReviewTrends in molecular medicine2014
Polycystin-1: a master regulator of intersecting cystic pathways.
Review in Trends in molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Use of mammalian target of rapamycin inhibitors in patient with autosomal dominant polycystic kidney disease: an updated meta-analysis.International urology and nephrology · 2019Pooled it
- Broadening horizons: Pathogenesis and therapeutics of renal ciliopathies.Journal of cell communication and signaling · 2026Review
- Primary and motile cilia in the efferent ductules: a role for IFT88 in maintaining male fertility.Cellular and molecular life sciences : CMLS · 2026Article
- Whole Exome Sequencing Reveals Promising Genes Associated with Congenital Renal Parenchymal Anomalies in Greek Children.Children (Basel, Switzerland) · 2026Article
- Genomic and epigenomic landscape of ADPKD: towards precision diagnostics and tailored treatments.Frontiers in epigenetics and epigenomics · 2026Review
- Autosomal dominant polycystic kidney disease: an overview of recent genetic and clinical advances.Renal failure · 2025Review
- Breaking Left-Right Symmetry by the Interplay of Planar Cell Polarity, Calcium Signaling and Cilia.Cells · 2024Review
- Multiomics profiling of mouse polycystic kidney disease progression at a single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The role ofbioRxiv : the preprint server for biology · 2024Article
- Multi-omics profiling of mouse polycystic kidney disease progression at a single cell resolution.bioRxiv : the preprint server for biology · 2024Article
- How Does ADPKD Severity Differ Between Family Members?Kidney international reports · 2024Review
- A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Role ofIntegrative organismal biology (Oxford, England) · 2024Article
- Editorial: Molecular mechanisms underlying polycystic kidney disease: from the smallest bricks to the big scenario.Frontiers in molecular biosciences · 2024Article
- Article
- Fibrocystin/Polyductin releases a C-terminal fragment that translocates into mitochondria and suppresses cystogenesis.Nature communications · 2023Article
- CFTR and PC2, partners in the primary cilia in autosomal dominant polycystic kidney disease.American journal of physiology. Cell physiology · 2023Article
- Individuals heterozygous for ALG8 protein-truncating variants are at increased risk of a mild cystic kidney disease.Kidney international · 2023Article
- Primary cilia and actin regulatory pathways in renal ciliopathies.Frontiers in nephrology · 2023Review
- Autosomal dominant and autosomal recessive polycystic kidney disease: hypertension and secondary cardiovascular effect in children.Frontiers in molecular biosciences · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common potentially lethal monogenic disorder, with more than 12 million cases worldwide. The two causative genes for ADPKD, PKD1 and PKD2, encode protein products polycystin-1 (PC1) and polycystin-2 (PC2 or TRPP2), respectively. Recent data have shed light on the role of PC1 in regulating the severity of the cystic phenotypes in ADPKD, autosomal recessive polycystic kidney disease (ARPKD), and isolated autosomal dominant polycystic liver disease (ADPLD). These studies showed that the rate for cyst growth was a regulated trait, a process that can be either sped up or slowed down by alterations in functional PC1. These findings redefine the previous understanding that cyst formation occurs as an 'on-off' process. Here, we review these and other related studies with an emphasis on their translational implications for polycystic diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.