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Publication : ESET histone methyltransferase regulates osteoblastic differentiation of mesenchymal stem cells during postnatal bone development.

First Author  Lawson KA Year  2013
Journal  FEBS Lett Volume  587
Issue  24 Pages  3961-7
PubMed ID  24188826 Mgi Jnum  J:202988
Mgi Id  MGI:5523735 Doi  10.1016/j.febslet.2013.10.028
Citation  Lawson KA, et al. (2013) ESET histone methyltransferase regulates osteoblastic differentiation of mesenchymal stem cells during postnatal bone development. FEBS Lett 587(24):3961-7
abstractText  To investigate the effects of histone methyltransferase ESET (also known as SETDB1) on bone metabolism, we analyzed osteoblasts and osteoclasts in ESET knockout animals, and performed osteogenesis assays using ESET-null mesenchymal stem cells. We found that ESET deletion severely impairs osteoblast differentiation but has no effect on osteoclastogenesis, that co-transfection of ESET represses Runx2-mediated luciferase reporter while siRNA knockdown of ESET activates the luciferase reporter in mesenchymal cells, and that ESET is required for postnatal expression of Indian hedgehog protein in the growth plate. As the bone phenotype in ESET-null mice is 100% penetrant, these results support ESET as a critical regulator of osteoblast differentiation during bone development.
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