Journal
CELL REPORTS
Volume 11, Issue 10, Pages 1625-1637Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.05.019
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Funding
- NIH [DK076729, DK56341, DK20579, 5R01AR050211, 5R01AR03278828, 5R01AR05703705, 5R37AR04652315, P30AR057235, P30DK056341]
- Shriners Hospitals for Children grant [85400-STL]
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ASXL2 is an ETP family protein that interacts with PPAR gamma. We find that ASXL2-/- mice are insulin resistant, lipodystrophic, and fail to respond to a high-fat diet. Consistent with genetic variation at the ASXL2 locus and human bone mineral density, ASXL2-/- mice are also severely osteopetrotic because of failed osteoclast differentiation attended by normal bone formation. ASXL2 regulates the osteoclast via two distinct signaling pathways. It induces osteoclast formation in a PPAR gamma/c-Fos-dependent manner and is required for RANK ligand-and thiazolidinedione-induced bone resorption independent of PGC-1 beta. ASXL2 also promotes osteoclast mitochondrial biogenesis in a process mediated by PGC-1 beta but independent of c-Fos. Thus, ASXL2 is a master regulator of skeletal, lipid, and glucose homeostasis.
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