ArticleJournal of biomedical science2014
Expression of Nek1 during kidney development and cyst formation in multiple nephron segments in the Nek1-deficient kat2J mouse model of polycystic kidney disease.
Article in Journal of biomedical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Pml loss worsens NEK1-linked ALS and Pml induction drives NEK1 degradation, precluding disease onset.The FEBS journal · 2026Article
- Review
- 7-azaindole as privileged scaffold: Advances in drug design and structural modification.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- NEK Family Kinases: Structure, Function, and Role in Disease.Biomolecules · 2025Review
- Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease.JCI insight · 2024Article
- Functional characterization of C21ORF2 association with the NEK1 kinase mutated in human in diseases.Life science alliance · 2023Article
- The role of primary cilia in thyroid diseases.Frontiers in endocrinology · 2023Review
- Centrosome amplification disrupts renal development and causes cystogenesis.The Journal of cell biology · 2018Article
- Aberrant DNA damage response and DNA repair pathway in high glucose conditions.Journal of cancer research updates · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNeks, mammalian orthologs of the fungal protein kinase never-in-mitosis A, have been implicated in the pathogenesis of polycystic kidney disease. Among them, Nek1 is the primary protein inactivated in kat2J mouse models of PKD.
resultWe report the expression pattern of Nek1 and characterize the renal cysts that develop in kat2J mice. Nek1 is detectable in all murine tissues but its expression in wild type and kat2J heterozygous kidneys decrease as the kidneys mature, especially in tubular epithelial cells. In the embryonic kidney, Nek1 expression is most prominent in cells that will become podocytes and proximal tubules. Kidney development in kat2J homozygous mice is aberrant early, before the appearance of gross cysts: developing cortical zones are thin, populated by immature glomeruli, and characterized by excessive apoptosis of several cell types. Cysts in kat2J homozygous mice form postnatally in Bowman's space as well as different tubular subtypes. Late in life, kat2J heterozygous mice form renal cysts and the cells lining these cysts lack staining for Nek1. The primary cilia of cells lining cysts in kat2J homozygous mice are morphologically diverse: in some cells they are unusually long and in others there are multiple cilia of varying lengths.
conclusionOur studies indicate that Nek1 deficiency leads to disordered kidney maturation, and cysts throughout the nephron.
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