Dental enamel formation is an intricate process tightly regulated by ameloblast cells. The correct spatiotemporal patterning of enamel matrix protein (EMP) expression is fundamental to orchestrate the formation of enamel crystals, which depend on a robust supply of Ca²⁺. In the extracellular milieu, Ca²⁺-EMP interactions occur at different levels. Despite its recognized role in enamel development, the molecular machinery involved in Ca²⁺ homeostasis in ameloblasts remains poorly understood. A common mechanism for Ca²⁺ influx is store-operated Ca²⁺ entry (SOCE). We evaluated the possibility that Ca²⁺ influx in enamel cells might be mediated by SOCE and the Ca²⁺ release-activated Ca²⁺ (CRAC) channel, the prototypical SOCE channel. Using ameloblast-like LS8 cells, we demonstrate that these cells express Ca²⁺-handling molecules and mediate Ca²⁺ influx through SOCE. As a rise in the cytosolic Ca²⁺ concentration is a versatile signal that can modulate gene expression, we assessed whether SOCE in enamel cells had any effect on the expression of EMPs. Our results demonstrate that stimulating LS8 cells or murine primary enamel organ cells with thapsigargin to activate SOCE leads to increased expression of Amelx, Ambn, Enam, Mmp20. This effect is reversed when cells are treated with a CRAC channel inhibitor. These data indicate that Ca²⁺ influx in LS8 cells and enamel organ cells is mediated by CRAC channels and that Ca²⁺ signals enhance the expression of EMPs. Ca²⁺ plays an important role not only in mineralizing dental enamel but also in regulating the expression of EMPs.