ArticleJournal of the American Society of Nephrology : JASN2016
Phosphoinositide 3-Kinase-C2α Regulates Polycystin-2 Ciliary Entry and Protects against Kidney Cyst Formation.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 52 citations in OpenAlex.
- Extra-ciliary role for polycystins in regulation of Ezrin and renal tubular morphology.bioRxiv : the preprint server for biology · 2025Article
- Role of lipids in the control of autophagy and primary cilium signaling in neurons.Neural regeneration research · 2024Review
- GPRC5C regulates the composition of cilia in the olfactory system.BMC biology · 2023Article
- Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023Review
- The Role of Primary Cilia-Associated Phosphoinositide Signaling in Development.Journal of developmental biology · 2022Review
- Phosphoinositide Conversion Inactivates R-RAS and Drives Metastases in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling.Frontiers in molecular biosciences · 2022Review
- An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022Article
- The ATG5 interactome links clathrin-mediated vesicular trafficking with the autophagosome assembly machinery.Autophagy reports · 2022Article
- The Role of Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3 in the Pathogenesis of Human Cancer.International journal of molecular sciences · 2021Review
- Review
- Review
- Phosphoinositide lipids in primary cilia biology.The Biochemical journal · 2020Review
- Regulation of polycystin expression, maturation and trafficking.Cellular signalling · 2020Review
- Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model.Nature communications · 2019Article
- Ciliotherapy: Remote Control of Primary Cilia Movement and Function by Magnetic Nanoparticles.ACS nano · 2019Article
- Class II PI3Ks at the Intersection between Signal Transduction and Membrane Trafficking.Biomolecules · 2019Review
- Rab11 activity and PtdIns(3)P turnover removes recycling cargo from endosomes.Nature chemical biology · 2018Article
- Motile Ciliary Disorders in Chronic Airway Inflammatory Diseases: Critical Target for Interventions.Current allergy and asthma reports · 2018Review
- Myosin-Va is required for preciliary vesicle transportation to the mother centriole during ciliogenesis.Nature cell biology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
Abstract
Signaling from the primary cilium regulates kidney tubule development and cyst formation. However, the mechanism controlling targeting of ciliary components necessary for cilium morphogenesis and signaling is largely unknown. Here, we studied the function of class II phosphoinositide 3-kinase-C2α (PI3K-C2α) in renal tubule-derived inner medullary collecting duct 3 cells and show that PI3K-C2α resides at the recycling endosome compartment in proximity to the primary cilium base. In this subcellular location, PI3K-C2α controlled the activation of Rab8, a key mediator of cargo protein targeting to the primary cilium. Consistently, partial reduction of PI3K-C2α was sufficient to impair elongation of the cilium and the ciliary transport of polycystin-2, as well as to alter proliferation signals linked to polycystin activity. In agreement, heterozygous deletion of PI3K-C2α in mice induced cilium elongation defects in kidney tubules and predisposed animals to cyst development, either in genetic models of polycystin-1/2 reduction or in response to ischemia/reperfusion-induced renal damage. These results indicate that PI3K-C2α is required for the transport of ciliary components such as polycystin-2, and partial loss of this enzyme is sufficient to exacerbate the pathogenesis of cystic kidney disease.
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.