Overexpression of LINCR in the developing mouse lung epithelium inhibits distal differentiation and induces cystic changes.

Background: Lung maturation can be disrupted through pro-inflammatory processes including intra-uterine amniotic infection, mechanical ventilation, or oxidative stress. Lincr, originally identified as a gene induced in the lung by lipopolysaccharide (LPS), is also expressed in the developing lung. The Lung-inducible Neuralized-related C3HC4 RING domain (LINCR) protein is structurally related to Drosophila Neuralized, a regulator of the developmentally important Notch signaling pathway.