Arrest defective-1 controls tumor cell behavior by acetylating myosin light chain kinase.

ABSTRACT:

Background

The enhancement of cell motility is a critical event during tumor cell spreading. Since myosin light chain kinase (MLCK) regulates cell behavior, it is regarded as a promising target in terms of preventing tumor invasion and metastasis. Since MLCK was identified to be associated with human arrest defective-1 (hARD1) through yeast two-hybrid screening, we here tested the possibility that hARD1 acts as a regulator of MLCK and by so doing controls tumor cell motility.

Methodology/principal findings

The physical interaction between MLCK and hARD1 was confirmed both in vivo and in vitro by immunoprecipitation assay and affinity chromatography. hARD1, which is known to have the activity of protein lysine epsilon-acetylation, bound to and acetylated MLCK activated by Ca(

SUBMITTER: Shin DH 

PROVIDER: S-EPMC2758594 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature