Store operated Ca²⁺ entry in neural crest cells and their derivatives

Neural crest cells (NCCs) are multipotent stem cells that migrate extensively during embryogenesis and give rise to a broad spectrum of derivatives, including melanocytes, Schwann cells, chromaffin cells, and neurons of the enteric nervous system. NCC proliferation, migration, or differentiation defects lead to a group of disorders collectively known as neurocristopathies. Understanding the signaling pathways that govern NCC behavior is therefore crucial for elucidating the origins of these conditions. Store-Operated Calcium Entry (SOCE) is recognized as the principal calcium influx mechanism in non-excitable cells and regulates key cellular processes such as proliferation, migration, and differentiation. Accumulating evidence indicates a significant role for Ca²⁺ signaling and SOCE in multiple NCC-derived cell types. This review examines current knowledge on Ca²⁺ signaling mediated by SOCE in NCCs and their derivatives, and discusses how dysregulated SOCE signaling may influence the pathogenesis of neurocristopathies.