Excessive osteoclast activation by osteoblast paracrine factor RANKL is a major cause of the abnormal long bone phenotype in Apert syndrome model mice-Reference-Cited by-同舟云学术

Excessive osteoclast activation by osteoblast paracrine factor RANKL is a major cause of the abnormal long bone phenotype in Apert syndrome model mice

Published:2022-01-20 Issue:4 Volume:237 Page:2155-2168
ISSN:0021-9541
Container-title:Journal of Cellular Physiology
language:en
Short-container-title:Journal Cellular Physiology

Author:

Shin Hye‐Rim¹,Kim Bong‐Soo¹,Kim Hyun‐Jung¹,Yoon Heein¹,Kim Woo‐Jin¹,Choi Je‐Yong²^ORCID,Ryoo Hyun‐Mo¹^ORCID

Affiliation:

1. Department of Molecular Genetics and Dental Pharmacology, School of Dentistry and Dental Research Institute Seoul National University Seoul South Korea

2. Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Skeletal Disease Analysis Center, Korea Mouse Phenotyping Center (KMPC), School of Medicine Kyungpook National University Daegu South Korea

Funder

National Research Foundation of Korea

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcp.30682

Reference66 articles.

1. Current advances in regulation of bone homeostasis

2. Apert syndrome mutations in fibroblast growth factor receptor 2 exhibit increased affinity for FGF ligand

3. Positive Regulation of Adult Bone Formation by Osteoblast-Specific Transcription Factor Osterix

4. From Genotype to Phenotype: The Differential Expression of FGF, FGFR, and TGFβ Genes Characterizes Human Cranioskeletal Development and Reflects Clinical Presentation in FGFR Syndromes

5. Osteoclasts: more than ‘bone eaters’

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