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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bone Formation by Endochondral Ossification01:24

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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Bone Formation by Intramembranous Ossification01:29

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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Hormones and Bone Tissue01:17

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Bone Remodeling01:40

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Related Experiment Video

Updated: Aug 4, 2025

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2.

Qiong Zhu1, Yesheng Fu1, Chun-Ping Cui1

  • 1State Key Laboratory of Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 100850, China.

Signal Transduction and Targeted Therapy
|April 6, 2023
PubMed
Summary
This summary is machine-generated.

Osteoblast-specific deubiquitinase OTUB1 (OTUB1) is crucial for bone health. Loss of OTUB1 impairs osteogenic differentiation and bone strength by destabilizing FGFR2, offering a potential osteoporosis therapy.

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Analysis of Minerals Produced by hFOB 1.19 and Saos-2 Cells Using Transmission Electron Microscopy with Energy Dispersive X-ray Microanalysis
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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Bone Biology

Background:

  • Bone homeostasis relies on balanced osteoblast and osteoclast activity.
  • Dysregulation leads to diseases like osteoporosis, with incompletely understood molecular drivers.
  • Deubiquitinases play critical roles in cellular processes, but their function in bone homeostasis is not fully elucidated.

Purpose of the Study:

  • To investigate the role of deubiquitinase OTUB1 in osteoblast function and bone homeostasis.
  • To elucidate the molecular mechanisms by which OTUB1 regulates osteogenesis.
  • To explore OTUB1 as a potential therapeutic target for osteoporosis.

Main Methods:

  • Generated global and osteoblast-specific Otub1 knockout mouse models.
  • Utilized techniques to assess osteogenic differentiation, mineralization, and bone strength.
  • Investigated the interaction between OTUB1, FGFR2, and the E3 ligase SMURF1 using biochemical assays.
  • Employed adeno-associated virus serotype 9 (AAV9) for gene delivery in vivo.
  • Analyzed Otub1 expression in mouse models of osteoporosis.

Main Results:

  • Osteoblast-specific knockout of Otub1 resulted in reduced bone mass and strength due to impaired osteogenic differentiation and mineralization.
  • OTUB1 stabilizes FGFR2 by inhibiting SMURF1-mediated ubiquitination, preventing FGFR2 lysosomal degradation.
  • AAV9-delivered FGFR2 rescued bone loss in Otub1-deficient mice.
  • Otub1 mRNA levels were decreased in osteoporotic mouse bones.
  • AAV9-mediated restoration of OTUB1 attenuated osteopenia in an ovariectomy-induced osteoporosis model.

Conclusions:

  • OTUB1 positively regulates osteogenic differentiation and mineralization by maintaining FGFR2 stability.
  • OTUB1's role in controlling FGFR2 stability is critical for bone homeostasis.
  • Targeting OTUB1 presents a promising therapeutic strategy for osteoporosis.