Mediates pre-mRNA alternative splicing regulation. Acts either as activator or repressor of splicing on specific pre-mRNA targets. Inhibits cardiac troponin-T (TNNT2) pre-mRNA exon inclusion but induces insulin receptor (IR) pre-mRNA exon inclusion in muscle. Antagonizes the alternative splicing activity pattern of CELF proteins. May play a role in myotonic dystrophy pathophysiology (DM). Could inhibit terminal muscle differentiation, acting at approximately the time of myogenin induction.
Highly expressed in the placenta.
Belongs to the muscleblind family. Contains 4 C3H1-type zinc fingers.
Nucleus. Cytoplasm. Greater concentration in the nucleus. In both DM1 and DM2 patients, colocalizes with nuclear foci of retained expanded-repeat transcripts.