Journal
CELL RESEARCH
Volume 21, Issue 1, Pages 169-182Publisher
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2010.159
Keywords
osteoclast; osteoblast; chondrocyte; arthritis; osteoporosis
Categories
Funding
- NIH [AR052705, EB007568]
- Children's Discovery Institute
- Barnes-Jewish Hospital Foundation
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR052705] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [R21EB007568] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R21DK067689] Funding Source: NIH RePORTER
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Since the discovery that deletion of the NF-kappa B subunits p50 and p52 causes osteopetrosis in mice, there has been considerable interest in the role of NF-kappa B signaling in bone. NF-kappa B controls the differentiation or activity of the major skeletal cell types - osteoclasts, osteoblasts, osteocytes and chondrocytes. However, with five NF-kappa B subunits and two distinct activation pathways, not all NF-kappa B signals lead to the same physiologic responses. In this review, we will describe the roles of various NF-kappa B proteins in basal bone homeostasis and disease states, and explore how NF-kappa B inhibition might be utilized therapeutically.
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