Regulation of mAC isoforms

This table focuses on known direct regulators of AC, although there are indirect routes to altering AC activity. Some of the effects listed have been clearly demonstrated as “direct” using purified, cell free components, whereas others have only been shown in intact cells. In the case of the latter, one must consider indirect mechanisms as well as the requirement for other factors for the effect to be realized. This table is adapted and updated from that published by Ostrom et al. (2012).

RegulatorEffectAC IsoformReferences
FSK (no known physiologic ligand for FSK site)StimulationAll isoforms (except AC9)Premont et al. (1996); Yan et al. (1998); Onda et al. (2001); Cumbay and Watts (2004)
GαsStimulationAll isoformsIyengar (1993)
GαiInhibitionAC1, AC5, AC6; not AC2Federman et al. (1992); Chen and Iyengar (1993); Taussig et al. (1993a, 1994a)
GβγInhibitionAC1, AC3, AC8Taussig et al., (1993b); Diel et al. (2006)
Stimulation (conditional)AC2, AC4, AC5, AC6Tang and Gilman (1991); Gao and Gilman (1991); Thomas and Hoffman (1996); Gao et al. (2007); Brand et al. (2015)
Ca2+InhibitionAC5, AC6Yoshimura and Cooper (1992); Katsushika et al. (1992)
Ca2+/CaMStimulationAC1, AC3 (weak), AC8Tang et al. (1991);Choi et al. (1992); Cali et al. (1994)
CaM KinaseInhibitionAC1, AC3Wayman et al. (1996); Wei et al. (1996)
PKCStimulationAC1, AC2, AC3, AC5, AC7Jacobowitz et al. (1993); Jacobowitz and Iyengar (1994); Kawabe et al. (1994) ; Watson et al. (1994); Bol et al. (1997)
PKCInhibitionAC6Lai et al. (1997)
PKAInhibitionAC5, AC6, AC8Iwami et al. (1995); Chen et al. (1997); Willoughby et al. (2012)
NOInhibitionAC5, AC6McVey et al. (1999); Hill et al. (2000)
Raf kinaseStimulationAC2, AC5, AC6Ding et al. (2004)
RGS proteinsInhibitionAC3, AC5Sinnarajah et al. (2001); Xie et al. (2012)