ReviewCellular and molecular life sciences : CMLS2013
Polycystins and cellular Ca2+ signaling.
Review in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanobiology and Primary Cilium in the Pathophysiology of Bone Marrow Myeloproliferative Diseases.International journal of molecular sciences · 2024Review
- Cross-Species Insights into Autosomal Dominant Polycystic Kidney Disease: Provide an Alternative View on Research Advancement.International journal of molecular sciences · 2024Review
- TRPV4 functional status in cystic cells regulates cystogenesis in autosomal recessive polycystic kidney disease during variations in dietary potassium.Physiological reports · 2023Article
- Endoplasmic Reticulum Calcium Homeostasis in Kidney Disease: Pathogenesis and Therapeutic Targets.The American journal of pathology · 2021Review
- Novel Potential Application of Chitosan Oligosaccharide for Attenuation of Renal Cyst Growth in the Treatment of Polycystic Kidney Disease.Molecules (Basel, Switzerland) · 2020Article
- An Overview of In Vivo and In Vitro Models for Autosomal Dominant Polycystic Kidney Disease: A Journey from 3D-Cysts to Mini-Pigs.International journal of molecular sciences · 2020Review
- TMEM16A drives renal cyst growth by augmenting CaJournal of molecular medicine (Berlin, Germany) · 2020Article
- Fundamental insights into autosomal dominant polycystic kidney disease from human-based cell models.Pediatric nephrology (Berlin, Germany) · 2019Article
- Primary Cilia as Signaling Hubs in Health and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Review
- Deficient transient receptor potential vanilloid type 4 function contributes to compromised [CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Role of Bicaudal C1 in renal gluconeogenesis and its novel interaction with the CTLH complex.PLoS genetics · 2018Article
- Liver involvement in kidney disease and vice versa.Pediatric nephrology (Berlin, Germany) · 2018Review
- Activation of Calcium-Sensing Receptor increases intracellular calcium and decreases cAMP and mTOR in PKD1 deficient cells.Scientific reports · 2018Article
- Expanding the role of vasopressin antagonism in polycystic kidney diseases: From adults to children?Pediatric nephrology (Berlin, Germany) · 2018Review
- Transcriptome analysis reveals manifold mechanisms of cyst development in ADPKD.Human genomics · 2016Article
- Virtual-tissue computer simulations define the roles of cell adhesion and proliferation in the onset of kidney cystic disease.Molecular biology of the cell · 2016Article
- Autophagy in renal diseases.Pediatric nephrology (Berlin, Germany) · 2016Review
- Role of calcium in polycystic kidney disease: From signaling to pathology.World journal of nephrology · 2016Review
- Deciphering physiological role of the mechanosensitive TRPV4 channel in the distal nephron.American journal of physiology. Renal physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca(2+) signaling seems to be a primary event and is clearly involved in many pathways that may lead to both types of cellular responses. In this review, we summarize the current knowledge about the molecular and functional interactions between polycystins and multiple components of the cellular Ca(2+)-signaling machinery. In addition, we discuss the relevant downstream responses of the changed Ca(2+) signaling that ultimately lead to increased proliferation and increased apoptosis as observed in many cystic cell types.
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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.