Three cell lines derived from TS patients demonstrated a consistent and highly significant deficit in ATP-evoked Ca 2+ signals as compared with matched controls ( Figures 2a–c ), but without any appreciable difference in intracellular Ca 2+ store content as assessed by ionomycin application ( Figure 2a , lower panel).
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Shared functional defect in IP₃R-mediated calcium signaling in diverse monogenic autism syndromes.
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