Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
 

Learn about the flu shot, COVID-19 vaccine, and our masking policy »

Stanford Health Care

ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis CELL REPORTS Izawa, T., Rohatgi, N., Fukunaga, T., Wang, Q., Silva, M. J., Gardner, M. J., McDaniel, M. L., Abumrad, N. A., Semenkovich, C. F., Teitelbaum, S. L., Zou, W. 2015; 11 (10): 1625-1637

Abstract

ASXL2 is an ETP family protein that interacts with PPAR?. 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?/c-Fos-dependent manner and is required for RANK ligand- and thiazolidinedione-induced bone resorption independent of PGC-1ß. ASXL2 also promotes osteoclast mitochondrial biogenesis in a process mediated by PGC-1ß but independent of c-Fos. Thus, ASXL2 is a master regulator of skeletal, lipid, and glucose homeostasis.

View details for DOI 10.1016/j.celrep.2015.05.019

View details for Web of Science ID 000356372100013

View details for PubMedID 26051940

View details for PubMedCentralID PMC4472564