Figure 1. Schematic diagram for proposed functional role of cAMP in glaucoma. The differential effects of cAMP generated by tmACs or sAC are shown in terms of IOP regulation and RGCs and ONH astrocytes protection. Black arrows with solid or dotted lines are experimentally confirmed or inferred from other types of astrocytes, respectively (see more detail in the text). Question marks represent what should be experimentally confirmed in future studies. Definitions: cAMP, cyclic adenosine 3′,5′-monophosphate; IOP, intraocular pressure; RGCs, retinal ganglion cells; ONH, optic nerve head; sAC, soluble adenylyl cyclase; tmACs, transmembrane adenylyl cyclases.
Figure 1. Regulation of the Hippo-YAP
pathway by extracellular biophysical cues. Mechanical stress inhibits Lats1/2
kinase activity via Rho GTPase and the actin cytoskeleton. GPCR signaling can
either activate or inhibit YAP/TAZ activity through the coupled Ga protein.
Cellular junction and cell polarity modulate the Hippo pathway. Nutrient
signaling modulates the core Hippo kinase and YAP activity through AMPK.
YAP/TAZ activity is involved in amino-acid induced mTORC1 activation.
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