Isoform 3 may have a role in regulating the growth and differentiation of arterial smooth muscle cells. ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Interacts with MTM1 (By similarity). Isoform 3 is found as a monomer or homodimer. Isoform 1 is preferentially expressed in striated muscle. Non-kinase form such as isoform 3 is predominantly expressed in the aorta. Isoform 3 appears to be expressed only in highly differentiated ASMC in normal vessel walls and down-regulated in dedifferentiated ASMC in vivo. In response to vascular injuries ASMC dedifferentiate and change from a quiescent and contractile phenotype to a proliferative and synthetic phenotype. This proliferation of vascular smooth muscle cells is one of the most prominent features of atherosclerosis. Isoform 1 and isoform 4 are expressed in cardiomyocytes of the developing heart. Isoform 3 is quickly down-regulated in response to vascular injury, when ASMC cells change from a quiescent to a proliferative phenotype. May be autophosphorylated. Mice lacking SPEG demonstrate dilation of right and left atria and ventricles, cardiac hypertrophy, myofibril degeneration, and a marked decrease in cardiac function. Moreover, mutant mice exhibit significant neonatal mortality. Expression is under the tight control of the locus control region (LCRs). Produced by alternative promoter usage. Produced by alternative promoter usage. Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family.