The NIMA-related kinase NEK1 cycles through the nucleus

Mutations in NEK1 in mice are causal for cystic kidneys, and model the ciliopathy polycystic kidney disease caused by abnormal ciliary structure or signaling. NEK1 has previously been shown to localize near centrosomes and to play a role in centrosomal stability and ciliogenesis. Recent data suggest...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-11, Vol.389 (1), p.52-56
Main Authors: Hilton, Laura K., White, Mark C., Quarmby, Lynne M.
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell Line
Cell Nucleus - enzymology
Cell Nucleus - genetics
Cilia
Cilia - enzymology
Cystic kidneys
CYSTS
ENDOCRINE DISEASES
ETIOLOGY
Gene Expression Regulation
GENE REGULATION
Kidney Diseases, Cystic - enzymology
Kidney Diseases, Cystic - genetics
Kidney Medulla - enzymology
KIDNEYS
Kinases
MICE
MUTATIONS
Nek
NEK1
NIMA-Related Kinase 1
Nuclear export signal
Nuclear localization signal
Nuclear Localization Signals - genetics
Nuclear Localization Signals - metabolism
Nucleus
PHOSPHOTRANSFERASES
PKD
Polycystic kidney disease
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
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Summary:Mutations in NEK1 in mice are causal for cystic kidneys, and model the ciliopathy polycystic kidney disease caused by abnormal ciliary structure or signaling. NEK1 has previously been shown to localize near centrosomes and to play a role in centrosomal stability and ciliogenesis. Recent data suggest that the etiology of kidney cysts involves aberrant signaling from the primary cilium to the nucleus. Here we demonstrate that NEK1 contains functional nuclear localization signals, is exported from the nucleus via a nuclear export signal-dependent pathway and that the protein cycles through the nucleus. Our data suggest that NEK1 is a candidate to transduce messages from the ciliary-basal body region to the regulation of nuclear gene expression.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.08.086