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Examining how GHS-R1a-driven calcium mobilisation potentiates GHRH-induced cAMP-PKA signalling exclusively in somatotrophs without off-target lactotroph and corticotroph co-stimulation, enabling attribution of all observed downstream biological effects to the GH secretory response rather than to co-secreted prolactin or cortisol
The first step is the metabolism of overall ROS, and the second is the quality control of proteins and organelles injured by H 2 O 2
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Self-regulatory role of 4-hydroxynonenal in signaling for stress-induced programmed cell death
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