ArticleThe Journal of cell biology2013
Vps35 loss promotes hyperresorptive osteoclastogenesis and osteoporosis via sustained RANKL signaling.
Article in The Journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Brain neuron-derived WDFY1 induces bone loss.Nature aging · 2026Article
- Exploring the role of mitochondrial dysfunction-related genes in osteoporosis using weighted gene co-expression network analysis and machine learning.European journal of medical research · 2025Article
- Leucine-Rich Repeat Kinase 1 Signaling Targets Proteins Critical for Endosome/Lysosome Sorting and Trafficking in Osteoclasts.Biology · 2025Article
- Interconnected Pathways of Alzheimer's Disease and Osteoporosis: A Review of Genetic, Hormonal, and Environmental Influences.Aging and disease · 2025Review
- Cuproptosis related genes in immune infiltration and treatment of osteoporosis by bioinformatic analysis and machine learning methods.Frontiers in physiology · 2025Article
- Identification of potential cell death-related biomarkers for diagnosis and treatment of osteoporosis.BMC musculoskeletal disorders · 2024Article
- Exploration of the Shared Hub Genes and Biological Mechanism in Osteoporosis and Type 2 Diabetes Mellitus based on Machine Learning.Biochemical genetics · 2023Article
- Alzheimer's Disease and Impaired Bone Microarchitecture, Regeneration and Potential Genetic Links.Life (Basel, Switzerland) · 2023Review
- Exploring the shared gene signatures of smoking-related osteoporosis and chronic obstructive pulmonary disease using machine learning algorithms.Frontiers in molecular biosciences · 2023Article
- Article
- Parkinson's in the bone.Cell & bioscience · 2021Review
- Expression of Low Level of VPS35-mCherry Fusion Protein Diminishes Vps35 Depletion Induced Neuron Terminal Differentiation Deficits and Neurodegenerative Pathology, and Prevents Neonatal Death.International journal of molecular sciences · 2021Article
- Osteocytes regulate neutrophil development through IL-19: a potent cytokine for neutropenia treatment.Blood · 2021Article
- RANKL and RANK in extracellular vesicles: surprising new players in bone remodeling.Extracellular vesicles and circulating nucleic acids · 2021Article
- Protective Effects of Vitamin K Compounds on the Proteomic Profile of Osteoblasts under Oxidative Stress Conditions.Molecules (Basel, Switzerland) · 2020Article
- Up-regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF-κB pathway.Journal of cellular and molecular medicine · 2019Article
- Lack of Myosin X Enhances Osteoclastogenesis and Increases Cell Surface Unc5b in Osteoclast-Lineage Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- APP promotes osteoblast survival and bone formation by regulating mitochondrial function and preventing oxidative stress.Cell death & disease · 2018Article
- The endosomal trafficking factors CORVET and ESCRT suppress plasma membrane residence of the renal outer medullary potassium channel (ROMK).The Journal of biological chemistry · 2018Article
- Identification of potential pathogenic genes associated with osteoporosis.Bone & joint research · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
Receptor activator of NF-κB (RANK) plays a critical role in osteoclastogenesis, an essential process for the initiation of bone remodeling to maintain healthy bone mass and structure. Although the signaling and function of RANK have been investigated extensively, much less is known about the negative regulatory mechanisms of its signaling. We demonstrate in this paper that RANK trafficking, signaling, and function are regulated by VPS35, a major component of the retromer essential for selective endosome to Golgi retrieval of membrane proteins. VPS35 loss of function altered RANK ligand (RANKL)-induced RANK distribution, enhanced RANKL sensitivity, sustained RANKL signaling, and increased hyperresorptive osteoclast (OC) formation. Hemizygous deletion of the Vps35 gene in mice promoted hyperresorptive osteoclastogenesis, decreased bone formation, and caused a subsequent osteoporotic deficit, including decreased trabecular bone volumes and reduced trabecular thickness and density in long bones. These results indicate that VPS35 critically deregulates RANK signaling, thus restraining increased formation of hyperresorptive OCs and preventing osteoporotic deficits.
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Registered trials
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.