The beta-adrenergic signaling cascade regulating L-type Ca2+ channels becomes functionally active late in murine embryonic development, with early-stage insensitivity driven by low expression of cA-PK holoenzyme and upstream uncoupling.
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Delineates timing of beta-adrenergic maturation in embryonic myocytes; extends developmental mechanisms but leaves open human fetal translation.
An et al. (1996) studied this question.
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