Knockdown of Mns1 increases susceptibility to craniofacial defects following gastrulation-stage alcohol exposure in mice.

CONCLUSIONS: These data demonstrate that a partial or complete knockdown of Mns1 interacts with PAE to increases susceptibility to ocular defects and correlating craniofacial and brain anomalies, likely though interaction of alcohol with motile cilia function. These results further our understanding of genetic risk factors that may underlie susceptibility to teratogenic exposures. This article is protected by copyright. All rights reserved.
PMID: 30129265 [PubMed - as supplied by publisher]

Source: Alcoholism, Clinical and Experimental Research - August 20, 2018 Category: Addiction Authors: Boschen KE, Gong H, Murdaugh LB, Parnell SE Tags: Alcohol Clin Exp Res Source Type: research