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NIMA-Related Kinases Defective in Murine Models of Polycystic Kidney Diseases Localize to Primary Cilia and Centrosomes

Moe R. Mahjoub, Melissa L. Trapp and Lynne M. Quarmby
JASN December 2005, 16 (12) 3485-3489; DOI: https://doi.org/10.1681/ASN.2005080824
Moe R. Mahjoub
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Melissa L. Trapp
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Lynne M. Quarmby
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Abstract

A key feature of the polycystic kidney diseases is aberrant cell proliferation, a consequence of dysfunctional ciliary signaling. The NIMA-related kinases (Nek) Nek1 and Nek8 carry the causal mutations of two of the eight established mouse models of polycystic kidneys. Nek proteins have roles in cell cycle and may contribute to coordinate regulation of cilia and cell-cycle progression. Herein is reported that in a mouse kidney epithelial cell line, mNek1 localizes to centrosomes in interphase and remains associated with the mitotic spindle pole during mitosis. In contrast, mNek8 localizes to the proximal region of the primary cilium and is not observed in dividing cells. Knockdown of mNek8 by siRNA does not affect ciliary assembly. Taken together with the phenotypes of the mutant mice, these data suggest that mNek1 and mNek8 provide links between cilia, centrosomes, and cell-cycle regulation.

  • © 2005 American Society of Nephrology
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Journal of the American Society of Nephrology: 16 (12)
Journal of the American Society of Nephrology
Vol. 16, Issue 12
1 Dec 2005
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NIMA-Related Kinases Defective in Murine Models of Polycystic Kidney Diseases Localize to Primary Cilia and Centrosomes
Moe R. Mahjoub, Melissa L. Trapp, Lynne M. Quarmby
JASN Dec 2005, 16 (12) 3485-3489; DOI: 10.1681/ASN.2005080824

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NIMA-Related Kinases Defective in Murine Models of Polycystic Kidney Diseases Localize to Primary Cilia and Centrosomes
Moe R. Mahjoub, Melissa L. Trapp, Lynne M. Quarmby
JASN Dec 2005, 16 (12) 3485-3489; DOI: 10.1681/ASN.2005080824
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More in this TOC Section

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  • Prorenin and Angiotensin-Dependent Renal Vasoconstriction in Type 1 and Type 2 Diabetes
  • Cyst Number but Not the Rate of Cystic Growth Is Associated with the Mutated Gene in Autosomal Dominant Polycystic Kidney Disease
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Cited By...

  • Control of clathrin-mediated endocytosis by NIMA family kinases
  • In depth analysis of kinase cross screening data to identify chemical starting points for inhibition of the nek family of kinases
  • Conserved Ankyrin Repeat Proteins and Their NIMA Kinase Partners Regulate Extracellular Matrix Remodeling and Intracellular Trafficking in Caenorhabditis elegans
  • A NIMA-related kinase, CNK4, regulates ciliary stability and length
  • The cAMP Signaling Pathway and Direct Protein Kinase A Phosphorylation Regulate Polycystin-2 (TRPP2) Channel Function
  • Tubulin transport by IFT is upregulated during ciliary growth by a cilium-autonomous mechanism
  • The Tumor Suppressor pVHL Down-regulates Never-in-Mitosis A-related Kinase 8 via Hypoxia-inducible Factors to Maintain Cilia in Human Renal Cancer Cells
  • Nek1 kinase associates with ATR-ATRIP and primes ATR for efficient DNA damage signaling
  • Loss of the Ciliary Kinase Nek8 Causes Left-Right Asymmetry Defects
  • Nek1 and TAZ Interact to Maintain Normal Levels of Polycystin 2
  • Rare copy number variations in congenital heart disease patients identify unique genes in left-right patterning
  • The NIMA-family kinase Nek3 regulates microtubule acetylation in neurons
  • Pancreatic Cancer and Precursor Pancreatic Intraepithelial Neoplasia Lesions Are Devoid of Primary Cilia
  • NEK8 Mutations Affect Ciliary and Centrosomal Localization and May Cause Nephronophthisis
  • Nek8 Regulates the Expression and Localization of Polycystin-1 and Polycystin-2
  • Too Much of a Good Thing: Does Nek8 Link Polycystic Kidney Disease and Nephronophthisis?
  • von Hippel-Lindau: A Tumor Suppressor Links Microtubules to Ciliogenesis and Cancer Development
  • GSK-3{beta}-regulated interaction of BICD with dynein is involved in microtubule anchorage at centrosome
  • The roles of cilia in developmental disorders and disease
  • Development of Polycystic Kidney Disease in Juvenile Cystic Kidney Mice: Insights into Pathogenesis, Ciliary Abnormalities, and Common Features with Human Disease
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