ArticleProceedings of the National Academy of Sciences of the United States of America1997
Homo- and heterodimeric interactions between the gene products of PKD1 and PKD2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 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.
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Who cites it
193 citing papers in PubMed, 476 citations in OpenAlex.
- Polycystin-1 suppresses apoptotic signalling in endothelial cells and protects from atherosclerosis.Cardiovascular research · 2026Article
- Deep learning-supported image quantification of epithelial cell shapes and its application to polycystic kidney disease.PLoS computational biology · 2026Article
- Pathophysiological significance of cholesterol in ciliopathies.Fujita medical journal · 2026Article
- Advances in the Treatment of Autosomal Dominant Polycystic Kidney Disease and Novel Therapeutic Targets.Current issues in molecular biology · 2026Review
- A heteromeric TRP channel that functions as a WNT-activated G protein-coupled receptor.Nature communications · 2026Article
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Ion channel function of polycystin-2/polycystin-1 heteromer revealed by structure-guided mutagenesis.FEBS letters · 2025Article
- Cholesterol ensures ciliary polycystin-2 localization to prevent polycystic kidney disease.Life science alliance · 2025Article
- The spectrum of diseases, genetic landscape and new mutation sites of hereditary cystic kidney disease.Clinical kidney journal · 2025Article
- Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.Pflugers Archiv : European journal of physiology · 2025Article
- Vascular polycystin proteins in health and disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Molecular and structural basis of the dual regulation of the polycystin-2 ion channel by small-molecule ligands.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Autosomal Dominant Polycystic Kidney Disease: Extrarenal Involvement.International journal of molecular sciences · 2024Review
- Bone health in autosomal dominant polycystic kidney disease (ADPKD) patients after kidney transplantation.Bone reports · 2023Article
- Crosstalk between the mTOR pathway and primary cilia in human diseases.Current topics in developmental biology · 2023Review
- PKD1 and PKD2 mRNA cis-inhibition drives polycystic kidney disease progression.Nature communications · 2022Article
- Restoration of atypical protein kinase C ζ function in autosomal dominant polycystic kidney disease ameliorates disease progression.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A plasma membrane-localized polycystin-1/polycystin-2 complex in endothelial cells elicits vasodilation.eLife · 2022Article
- The GPCR properties of polycystin-1- A new paradigm.Frontiers in molecular biosciences · 2022Review
133 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
PKD1 and PKD2 are two recently identified genes that are responsible for the vast majority of autosomal polycystic kidney disease, a common inherited disease that causes progressive renal failure. PKD1 encodes polycystin, a large glycoprotein that contains several extracellular motifs indicative of a role in cell-cell or cell-matrix interactions, and the PKD2 encodes a protein with homology to a voltage-activated calcium channel and to PKD1. It is currently unknown how mutations of either protein functionally cause autosomal polycystic kidney disease. We show that PKD1 and PKD2 interact through their C-terminal cytoplasmic tails. This interaction resulted in an up-regulation of PKD1 but not PKD2. Furthermore, the cytoplasmic tail of PKD2 but not PKD1 formed homodimers through a coiled-coil domain distinct from the region required for interaction with PKD1. These interactions suggest that PKD1 and PKD2 may function through a common signaling pathway that is necessary for normal tubulogenesis and that PKD1 may require the presence of PKD2 for stable expression.
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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.