stem cell transcription factor, to promote basal MaSC differentiation and proliferation growing the basal mammary gland. This is compared to luminal expansion and differentiation, increasing the movement and differentiation of the basal MaSC cells to the luminal surface. Knockdowns in mice have resulted in reduced mammary gland growth during puberty and pregnancy. Inversely, overexpression has been noted in basal subtype breast cancers, furthering LBHs effect on stem cell regulation. Diseases The overexpression of LBH is one of the causal factors for birth defects seen in partial trisomy 2p syndrome, an autosomal disorder that causes multiple congenital defects. Partial trisomy 2p patients have a triplication of the p arm of chromosome 2. Transgenic overexpression in mice of the LBH ortholog, Lbh, causes the continued overexpression and downregulation of multiple targets downstream of Lbh, mimicking symptoms of congenital heart disease (CHD) and skeletal defects seen in partial trisomy 2p patients. In addition to this, Lbh overexpression leads to the repression of Nkx2.5 and Tbx5, important regulators in cardiogenesis in developing embryos. The importance of LBH in cardiogenesis is evident of LBHs multifunctionality despite being highly conserved and having no paralogs. LBH also has an important oncological role in the development of mammary gland tumors. LBH has been noted for its overexpression in aggressive “basal” subtype breast cancers. Studies examining the role of Lbh in tumorigenesis in MMTV-Wnt1 transgenic mice as a model for Wnt induced breast cancer development. Lbh was conditionally deactivated in these transgenic mice, significantly delaying tumor onset and resulted in decreased differentiation and proliferation while also increasing apoptosis. References Further reading