ArticleEBioMedicine2016
Retromer in Osteoblasts Interacts With Protein Phosphatase 1 Regulator Subunit 14C, Terminates Parathyroid Hormone's Signaling, and Promotes Its Catabolic Response.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Lysosomal down-regulation of the mu opioid receptor is opposed by the Retromer complex.Science advances · 2026Article
- Brain neuron-derived WDFY1 induces bone loss.Nature aging · 2026Article
- Proteomic analysis of the quality deterioration of pork: a comparative study of fresh and six-month frozen storage.Food chemistry: X · 2025Article
- Leucine-Rich Repeat Kinase 1 Signaling Targets Proteins Critical for Endosome/Lysosome Sorting and Trafficking in Osteoclasts.Biology · 2025Article
- ATP6AP2, a regulator of LRP6/β-catenin protein trafficking, promotes Wnt/β-catenin signaling and bone formation in a cell type dependent manner.Bone research · 2024Article
- Review
- Attenuation of Alzheimer's brain pathology in 5XFAD mice by PTHAlzheimer's research & therapy · 2023Article
- Differential Expression of MED12-Associated Coding RNA Transcripts in Uterine Leiomyomas.International journal of molecular sciences · 2023Article
- Retromer dependent changes in cellular homeostasis and Parkinson's disease.Essays in biochemistry · 2021Review
- Parkinson's in the bone.Cell & bioscience · 2021Review
- Anabolic actions of PTH in murine models: two decades of insights.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Linking skeletal muscle aging with osteoporosis by lamin A/C deficiency.PLoS biology · 2020Article
- To degrade or not to degrade: mechanisms and significance of endocytic recycling.Nature reviews. Molecular cell biology · 2018Review
- Identification of potential pathogenic genes associated with osteoporosis.Bone & joint research · 2017Article
- Updated Insight into the Physiological and Pathological Roles of the Retromer Complex.International journal of molecular sciences · 2017Review
- GPCR Signaling and Trafficking: The Long and Short of It.Trends in endocrinology and metabolism: TEM · 2017Review
- Article
- VPS35: Two Ways to Recycle the Parathyroid Hormone Receptor (PTH1R) in Osteoblasts.EBioMedicine · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Parathyroid hormone (PTH) plays critical, but distinct, roles in bone remodeling, including bone formation (anabolic response) and resorption (catabolic response). Although its signaling and function have been extensively investigated, it just began to be understood how distinct functions are induced by PTH activating a common receptor, the PTH type 1 receptor (PTH1R), and how PTH1R signaling is terminated. Here, we provide evidence for vacuolar protein sorting 35 (VPS35), a major component of retromer, in regulating PTH1R trafficking, turning off PTH signaling, and promoting its catabolic function. VPS35 is expressed in osteoblast (OB)-lineage cells. VPS35-deficiency in OBs impaired PTH(1-34)-promoted PTH1R translocation to the trans-Golgi network, enhanced PTH(1-34)-driven signaling, and reduced PTH(1-34)'s catabolic response in culture and in mice. Further mechanical studies revealed that VPS35 interacts with not only PTH1R, but also protein phosphatase 1 regulatory subunit 14C (PPP1R14C), an inhibitory subunit of PP1 phosphatase. PPP1R14C also interacts with PTH1R, which is necessary for the increased endosomal PTH1R signaling and decreased PTH(1-34)'s catabolic response in VPS35-deficient OB-lineage cells. Taken together, these results suggest that VPS35 deregulates PTH1R-signaling likely by its interaction with PTH1R and PPP1R14C. This event is critical for the control of PTH(1-34)-signaling dynamics, which may underlie PTH-induced catabolic response and adequate bone remodeling.
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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.