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10.1152/jn.00363.2021 J

Supplementary material The Supplementary Material for this article can be found online at: References 1 BaoY

A proposed mechanism of these beneficial outcomes is the inhibition of endoplasmic reticulum stress-induced apoptosis through extracellular signal-regulated kinase (ERK1/2) and the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in combination with the inhibition of adenylyl cyclase activity via Gi of the m2AChR, thereby reducing cAMP production and further attenuation of ER-stress and apoptosis (Fig

Plant Signaling & Behavior 7, 16211633

However, studies to date have documented almost no adverse effects when Selank was administered to either human or animal subjects