The Splicing Factor hnRNPA1 Regulates Alternate Splicing of the MYLK Gene.

ABSTRACT: Profound lung vascular permeability is a cardinal feature of acute respiratory distress syndrome (ARDS) and ventilator-induced lung injury (VILI), two syndromes known to centrally involve the nonmuscle isoform of myosin light chain kinase (nmMLCK) in vascular barrier dysregulation. Two main splice variants, nmMLCK1 and nmMLCK2, are well represented in human lung endothelial cells and encoded by MYLK, and they differ only in the presence of exon 11 in nmMLCK1, which contains critical phosphorylation sites (Y⁴⁶⁴ and Y⁴⁷¹) that influence nmMLCK enzymatic activity, cellular translocation, and localization in response to vascular agonists. We recently demonstrated the functional role of SNPs in altering MYLK splicing, and in the present study we sought to identify the role

SUBMITTER: Mascarenhas JB 

PROVIDER: S-EPMC5946327 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature