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SAG is a potent, selective, and cell-permeable small-molecule agonist of the Hedgehog pathway. It modulates the coupling of Smo with its downstream effector by interacting with the Smo heptahelical domain (KD = 59 nM). SAG induces Hedgehog pathway activation with an EC₅₀ of ~3 nM in NIH 3T3-derived Shh-LIGHT2 cells and counteracts Cyclopamine-KAAD inhibition of Smo. It was reported that SAG acts as an activator at low concentrations and as an inhibitor at high concentrations (>1 µM). In recent studies, SAG was shown to prevent glucocorticoid-induced neonatal cerebellar injury, and trigger rapid metabolic rewiring via AMPK.

How to Use:

• In vitro: SAG was used at 200 nM to induce Hh pathway activation.
• In vivo: n/a

Reference:

1. 1. Frank-Kamenetsky M, et al. Small-molecule modulators of Hedgehog signaling: identification and characterization of Smoothened agonists and antagonists. (2002) Journal of Biology (1): 10.2-10.19.
2. 2. Chen JK, et al. Small molecule modulation of Smoothened activity.(2002) Proc Natl Acad Sci U S A. 99(22):14071-6.
3. 3. Chen W, et al. Activity-dependent internalization of smoothened mediated by beta-arrestin 2 and GRK2. (2004) Science. 306(5705):2257-60.
4. 4. Dyer LA, et al. BMP signaling modulates hedgehog-induced secondary heart field proliferation. (2010) Dev Biol. 348(2):167-76.
5. 5. Heine VM, et al. A small-molecule smoothened agonist prevents glucocorticoid-induced neonatal cerebellar injury. (2011) Sci Transl Med. 3(105).
6. 6. Teperino R, et al. Hedgehog partial agonism drives Warburg-like metabolism in muscle and brown fat. (2012) Cell. 151(2):414-26.

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