Scientific background:

Summary: The protein product plays an important role in inactivation of the aldosterone-sensitive sodium channel. Dysfunction is associated with Liddle syndrome.

Gene: The locus of this gene is 18q21. It spans about 400kb and consists of at least 40 exons. Several different splice variants are expressed in a tissue specific manner.

Pathology: The protein contains a WW domain, which binds with the PP.Y domain of the gamma and beta subunits of the aldosterone-sensitive sodium channel (ENaC). This interaction leads to ubiquitylation, internalization, and finally inactivation of the channel.

Methodology:

Literature: 

Rossier BC et al. (2004) The epithelial sodium channel: activation by membrane-bound serine proteases.
Warnock DG et al. (2001) Liddle syndrome: genetics and mechanisms of Na+ channel defects.
Umemura M et al. (2006) Transcriptional diversity and expression of NEDD4L gene in distal nephron.