CHIP regulates skeletal development and postnatal bone growth.
CHIP
NF-κB signaling
bone formation
conditional knockout
skeletal development
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
11
06
2019
accepted:
19
12
2019
pubmed:
4
1
2020
medline:
10
3
2021
entrez:
4
1
2020
Statut:
ppublish
Résumé
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
Identifiants
pubmed: 31898815
doi: 10.1002/jcp.29424
pmc: PMC7056513
mid: NIHMS1065647
doi:
Substances chimiques
NF-kappa B
0
Stub1 protein, mouse
EC 2.3.2.27
Ubiquitin-Protein Ligases
EC 2.3.2.27
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5378-5385Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR070222
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR054465
Pays : United States
Informations de copyright
© 2020 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.
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