ArticleThe EMBO journal2015
Cell cycle-dependent ubiquitylation and destruction of NDE1 by CDK5-FBW7 regulates ciliary length.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 78 citations in OpenAlex.
- Multifaceted role of primary cilia and ciliary proteins: A potential nexus for hedgehog signaling and prostate cancer.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
- Hedgehog pathway, cell cycle, and primary cilium.Cell death discovery · 2025Review
- Non-canonical CDK6 activity promotes cilia disassembly by suppressing axoneme polyglutamylation.The Journal of cell biology · 2025Article
- LncRNA GClnc1 promotes osteosarcoma progression by stabilizing NONO and blocking FBXW7-mediated ubiquitination.BMC cancer · 2024Article
- Structure, function, and research progress of primary cilia in reproductive physiology and reproductive diseases.Frontiers in cell and developmental biology · 2024Review
- MAST4 promotes primary ciliary resorption through phosphorylation of Tctex-1.Life science alliance · 2023Article
- Regulation of the length of neuronal primary cilia and its potential effects on signalling.Trends in cell biology · 2023Review
- Functional analysis reveals driver cooperativity and novel mechanisms in endometrial carcinogenesis.EMBO molecular medicine · 2023Article
- Clinical significance of FBXW7 loss of function in human cancers.Molecular cancer · 2022Review
- Systematic Discovery of FBXW7-Binding Phosphodegrons Highlights Mitogen-Activated Protein Kinases as Important Regulators of Intracellular Protein Levels.International journal of molecular sciences · 2022Article
- CDK1/FBXW7 facilitates degradation and ubiquitination of MLST8 to inhibit progression of renal cell carcinoma.Cancer science · 2022Article
- Nde1 and Ndel1: Outstanding Mysteries in Dynein-Mediated Transport.Frontiers in cell and developmental biology · 2022Review
- Tfh Exosomes Derived from Allergic Rhinitis Promote DC Maturation Through miR-142-5p/CDK5/STAT3 Pathway.Journal of inflammation research · 2022Article
- SCFThe EMBO journal · 2021Article
- FBW7 couples structural integrity with functional output of primary cilia.Communications biology · 2021Article
- Moonlighting of mitotic regulators in cilium disassembly.Cellular and molecular life sciences : CMLS · 2021Review
- Exploring the Spectrum of Kidney Ciliopathies.Diagnostics (Basel, Switzerland) · 2020Review
- Myeloid FBW7 deficiency disrupts redox homeostasis and aggravates dietary-induced insulin resistance.Redox biology · 2020Article
- Loss of polycystins suppresses deciliation via the activation of the centrosomal integrity pathway.Life science alliance · 2020Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Primary cilia start forming within the G1 phase of the cell cycle and continue to grow as cells exit the cell cycle (G0). They start resorbing when cells re-enter the cell cycle (S phase) and are practically invisible in mitosis. The mechanisms by which cilium biogenesis and disassembly are coupled to the cell cycle are complex and not well understood. We previously identified the centrosomal phosphoprotein NDE1 as a negative regulator of ciliary length and showed that its levels inversely correlate with ciliogenesis. Here, we identify the tumor suppressor FBW7 (also known as FBXW7, CDC4, AGO, or SEL-10) as the E3 ligase that mediates the destruction of NDE1 upon entry into G1. CDK5, a kinase active in G1/G0, primes NDE1 for FBW7-mediated recognition. Cells depleted of FBW7 or CDK5 show enhanced levels of NDE1 and a reduction in ciliary length, which is corrected in cells depleted of both FBW7 or CDK5 and NDE1. These data show that cell cycle-dependent mechanisms can control ciliary length through a CDK5-FBW7-NDE1 pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.