ArticleEndocrinology2011
Mutant p62P392L stimulation of osteoclast differentiation in Paget's disease of bone.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture.Nature genetics · 2012Pooled it
- Paget's Disease of the Bone and Lynch Syndrome: An Exceptional Finding.Diagnostics (Basel, Switzerland) · 2023Article
- Update on the pathogenesis and genetics of Paget's disease of bone.Frontiers in cell and developmental biology · 2022Review
- Immunoexpression pattern of autophagy mediators in alveolar bone osteoclasts following estrogen withdrawal in female rats.Journal of molecular histology · 2021Article
- Global deletion of Optineurin results in altered type I IFN signaling and abnormal bone remodeling in a model of Paget's disease.Cell death and differentiation · 2020Article
- Paget's Disease of Bone.Calcified tissue international · 2019Review
- p62/sequestosome 1 deficiency accelerates osteoclastogenesisThe Journal of biological chemistry · 2018Article
- Measles virus nucleocapsid protein modulates the Signal Regulatory Protein-β1 (SIRPβ1) to enhance osteoclast differentiation in Paget's disease of bone.Bone reports · 2017Article
- Diverse ubiquitin linkages regulate RIP kinases-mediated inflammatory and cell death signaling.Cell death and differentiation · 2017Review
- P62: An emerging oncotarget for osteolytic metastasis.Journal of bone oncology · 2016Review
- RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-κB-dependent inflammation.The Journal of investigative dermatology · 2015Article
- CYLD-mediated signaling and diseases.Current drug targets · 2015Review
- Genetics of Paget's disease of bone.Current osteoporosis reports · 2014Review
- Alternative splicing in osteoclasts and Paget's disease of bone.BMC medical genetics · 2014Article
- Article
- Increased IL-6 expression in osteoclasts is necessary but not sufficient for the development of Paget's disease of bone.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- Pathobiology of Paget's Disease of Bone.Journal of bone metabolism · 2014Review
- The adaptor protein p62/SQSTM1 in osteoclast signaling pathways.Journal of molecular signaling · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paget's disease of the bone (PDB) is an autosomal dominant trait with genetic heterogeneity, characterized by abnormal osteoclastogenesis. Sequestosome 1 (p62) is a scaffold protein that plays an important role in receptor activator of nuclear factor κB (RANK) signaling essential for osteoclast (OCL) differentiation. p62P392L mutation in the ubiquitin-associated (UBA) domain is widely associated with PDB; however, the mechanisms by which p62P392L stimulate OCL differentiation in PDB are not completely understood. Deubiquitinating enzyme cylindromatosis (CYLD) has been shown to negatively regulate RANK ligand-RANK signaling essential for OCL differentiation. Here, we report that CYLD binds with the p62 wild-type (p62WT), non-UBA mutant (p62A381V) but not with the UBA mutant (p62P392L) in OCL progenitor cells. Also, p62P392L induces expression of c-Fos (2.8-fold) and nuclear factor of activated T cells c1 (6.0-fold) transcription factors critical for OCL differentiation. Furthermore, p62P392L expression results in accumulation of polyubiquitinated TNF receptor-associated factor (TRAF)6 and elevated levels of phospho-IκB during OCL differentiation. Retroviral transduction of p62P392L/CYLD short hairpin RNA significantly increased TRAP positive multinucleated OCL formation/bone resorption activity in mouse bone marrow cultures. Thus, the p62P392L mutation abolished CYLD interaction and enhanced OCL development/bone resorption activity in PDB.
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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.