The voltage-gated Cav1.2 calcium channels respond to membrane depolarization by increasing
the membrane permeability to Ca2+, a major signal for cardiac muscle contraction, regulation of
vascular tone and CREB-dependent transcriptional activation. CACNB2 is one of the four homologous
genes coding for the auxiliary Cavβ subunits, which are important modulators of the Ca2+ channel activity.
Five serious mental disorders - autism spectrum disorder, attention deficit-hyperactivity disorder,
bipolar disorder, major depressive disorder, and schizophrenia, - and three major cardiovascular
diseases - hypertension, heart failure and sudden cardiac death, - have recently been linked to the
CACNB2 gene coding for the Cavβ2 subunits. Here I will focus on the Cavβ2-specific molecular determinant β2-CED as an emerging pharmacological target.