CHIP regulates skeletal development and postnatal bone growth. Issue 6 (3rd January 2020)

• Record Type: Journal Article
• Authors: Wang, Wenbo; Li, Jun; Ko, Frank C.; Zhao, Xia; Qiao, Yusen; Lu, Ronald S.; Sumner, D. Rick; Wang, Tingyu; Chen, Di
• Is Part Of: Journal of cellular physiology. Volume 235:Issue 6(2020:Jun.)
• Page Start: 5378
• Page End: 5385
• Publication Date: 2020-01-03
• Subjects: bone formation -- CHIP -- conditional knockout -- NF‐κB signaling -- skeletal development; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29424
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: C terminus of Hsc70‐interacting protein (CHIP) is a chaperone‐dependent and U‐box containing E3 ubiquitin ligase. In previous studies, we found that CHIP regulates the stability of multiple tumor necrosis factor receptor‐associated factor proteins in bone cells. In Chip global knockout (KO) mice, nuclear factor‐κB signaling is activated, osteoclast formation is increased, osteoblast differentiation is inhibited, and bone mass is decreased in postnatal Chip KO mice. To determine the role of Chip in different cell types at different developmental stages, we created Chip flox/flox mice. We then generated Chip conditional KO mice Chip CMV and Chip OsxER and demonstrated defects in skeletal development and postnatal bone growth in Chip conditional KO mice. Our findings indicate that Chip conditional KO mice could serve as a critical reagent for further investigations of functions of CHIP in bone cells and in other cell types. Abstract : In this study, we observed defects in skeletal development and postnatal bone growth in C terminus of Hsc70‐interacting protein (CHIP) conditional knockout mice.