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Related Experiment Video

Updated: Jun 3, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Decreased SH3BP2 inhibits osteoclast differentiation and function.

Teruya Kawamoto¹, Chun Fan, Robert J Gaivin

¹Department of Anatomic Pathology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society

|March 31, 2011

Summary

Decreasing SH3BP2 levels inhibits osteoclast differentiation and function, crucial for bone remodeling. This finding highlights SH3BP2 as a potential target for managing excessive bone resorption disorders.

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Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

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Last Updated: Jun 3, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

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Published on: July 3, 2020

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Area of Science:

Biochemistry
Cell Biology
Skeletal Biology

Background:

Germline mutations in the SH3BP2 gene are linked to cherubism, a skeletal disorder.
Cherubism involves excessive osteoclastic bone resorption in the jawbone.
Previous work showed SH3BP2 overexpression enhances osteoclast formation.

Purpose of the Study:

To investigate the impact of reduced SH3BP2 levels on osteoclastogenesis.
To determine the role of SH3BP2 in regulating osteoclast differentiation and function.

Main Methods:

Utilized shRNA to knock down SH3BP2 expression in cells.
Examined downstream signaling pathways, including PLCγ2 phosphorylation and NFATc1 expression.
Assessed osteoclast differentiation, multinucleation, and bone resorptive activity in vitro.
Analyzed osteoclast formation in Sh3bp2(-/-) deficient mice.

Main Results:

SH3BP2 knockdown reduced PLCγ2 phosphorylation and NFATc1 expression.
Knockdown led to decreased expression of osteoclast-specific genes.
Fewer and smaller TRAP-positive multinucleated osteoclasts were formed upon SH3BP2 reduction.
Bone resorption activity was significantly inhibited by SH3BP2 knockdown.
Osteoclasts from Sh3bp2(-/-) mice were smaller and stained less intensely for TRAP.

Conclusions:

SH3BP2 plays a critical role in promoting osteoclast differentiation and function.
Reduced SH3BP2 levels significantly impair osteoclastogenesis.
SH3BP2 is a potential therapeutic target for suppressing pathological bone resorption.