Abstract
Loss of function in either VHL or Nek1 leads to cyst formation in tissues, especially in kidneys. Whether there is a connection between pVHL and Nek1 regulation is unknown. Here, we report that the VHL protein (pVHL) may be a substrate of Nek1. While Nek1 can phosphorylate pVHL at multiple sites, the phosphorylation at serine-168 results in pVHL degradation. Nek1-mediated phosphorylation of pVHL does not significantly affect hypoxia-inducible factors (HIF), a known target of pVHL. However, non-phosphorylable pVHL reconstituted in VHL-deficient cells induces more stable cilia than wild-type VHL during serum stimulation and Nocodazole treatment. The results suggest a possible regulation of pVHL by Nek1 that may contribute to ciliary homeostasis and cystogenesis.
Original language | English (US) |
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Pages (from-to) | 166-171 |
Number of pages | 6 |
Journal | Cell Cycle |
Volume | 12 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2013 |
Keywords
- Cilium
- Hypoxia-inducible factor
- Nek1
- Phosphorylation
- VHL
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology