ArticleJournal of the American Society of Nephrology : JASN2013
Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- Global adaptation to climate change in the twilight zone revealed by shared signals of selection in mesopelagic lanternfishes.bioRxiv : the preprint server for biology · 2026Article
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Inhibition of Hedgehog signaling does not mitigate polycystic kidney disease severity in a Pkd1 mutant mouse model.Journal of cell science · 2025Article
- NEK8, a NIMA-family protein kinase at the core of the ciliary INV complex.Cell communication and signaling : CCS · 2025Review
- Certain heterozygous variants in the kinase domain of the serine/threonine kinase NEK8 can cause an autosomal dominant form of polycystic kidney disease.Kidney international · 2023Article
- Pathological consequences of DNA damage in the kidney.Nature reviews. Nephrology · 2023Review
- NEK Family Review and Correlations with Patient Survival Outcomes in Various Cancer Types.Cancers · 2023Review
- Regulator of G protein signaling 12 drives inflammatory arthritis by activating synovial fibroblasts through MYCBP2/KIF2A signaling.Molecular therapy. Nucleic acids · 2023Article
- Non-classical functions of nuclear pore proteins in ciliopathy.Frontiers in molecular biosciences · 2023Review
- Variable phenotypes and penetrance between and within different zebrafish ciliary transition zone mutants.Disease models & mechanisms · 2022Article
- The genetic landscape of cardiovascular left-right patterning defects.Current opinion in genetics & development · 2022Review
- An unexpected role for the conserved ADAM-family metalloprotease ADM-2 in Caenorhabditis elegans molting.PLoS genetics · 2022Article
- In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022Review
- Whole-Exome Sequencing Identifies the VHL Mutation (c.262T > C, p.Try88Arg) in Non-Obstructive Azoospermia-Associated Cystic Renal Cell CarcinomaCurrent oncology (Toronto, Ont.) · 2022Article
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021Review
- Biallelic loss of function NEK3 mutations deacetylate α-tubulin and downregulate NUP205 that predispose individuals to cilia-related abnormal cardiac left-right patterning.Cell death & disease · 2020Article
- Ppargc1a Controls Ciliated Cell Development by Regulating Prostaglandin Biosynthesis.Cell reports · 2020Article
- Novel fibrillar structure in the inversin compartment of primary cilia revealed by 3D single-molecule superresolution microscopy.Molecular biology of the cell · 2020Article
- Control of clathrin-mediated endocytosis by NIMA family kinases.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
A missense mutation in mouse Nek8, which encodes a ciliary kinase, produces the juvenile cystic kidneys (jck) model of polycystic kidney disease, but the functions of Nek8 are incompletely understood. Here, we generated a Nek8-null allele and found that homozygous mutant mice die at birth and exhibit randomization of left-right asymmetry, cardiac anomalies, and glomerular kidney cysts. The requirement for Nek8 in left-right patterning is conserved, as knockdown of the zebrafish ortholog caused randomized heart looping. Ciliogenesis was intact in Nek8-deficient embryos and cells, but we observed misexpression of left-sided marker genes early in development, suggesting that nodal ciliary signaling was perturbed. We also generated jck/Nek8 compound heterozygotes; these mutants developed less severe cystic disease than jck homozygotes and provided genetic evidence that the jck allele may encode a gain-of-function protein. Notably, NEK8 and polycystin-2 (PC2) proteins interact, and we found that Nek8(-/-) and Pkd2(-/-) embryonic phenotypes are strikingly similar. Nek8-deficient embryos and cells did express PC2 normally, which localized properly to the cilia. However, similar to cells lacking PC2, NEK8-depleted inner medullary collecting duct cells exhibited a defective response to fluid shear, suggesting that NEK8 may play a role in mediating PC2-dependent signaling.
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Registered trials
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