SAG (Smoothened Agonist) HCl

SAG regulates Smo activity by binding directly to the Smo heptahelical bundle. ^[1]

SAG induces Smo-dependent signaling through Gli in a GRK2-dependent way. ^[2]

SAG also (1 nM) induces proliferation of neuronal and glial precursors without affecting the differentiation pattern of newly produced cells. ^[3]

In the adult rat hippocampus, the intracerebroventricular administration of SAG (2.5 nM) significantly increases the number of newly generated cells and extends survival of hippocampal cells. ^[3]

In mice, SAG (20 μg/g, i.p.) effectively prevents GC-induced neonatal cerebellar developmental abnormalities. ^[4]

• Cell-Based Assays for Hh Pathway Activation

  Assays for Hh pathway activation in Shh-LIGHT2 cells, a clonal NIH 3T3 cell line stably incorporating Gli-dependent firefly luciferase and constitutive Renilla luciferase reporters, are conducted. For studies of SAG (a chlorobenzothiophene-containing Hh pathway agonist) and PA-SAG, Shh-LIGHT2 cells are cultured to confluency in 96-well plates and then treated with various concentrations of these compounds in DMEM containing 0.5% (vol/vol) bovine calf serum.

• Cell lines

  Shh-LIGHT2 cells

• Concentrations

  3 nM

• Incubation Time

  30 h

• Method

  Cells were treated with various concentrations of SAG in DMEM containing 0.5% (vol/vol) bovine calf serum.

• Animal Models

  Rat

• Dosages

  2.5 nM

• Administration

  Intracerebroventricular administration