Figure 1.
Diagram showing canonical and non-canonical HH signaling in Wt, Ptch1-/- and Ptch2-/- cells. Depletion of Ptch1 causes canonical pathway activation driving Gli1 transcription but lacks activation of Erk. In contrast, depletion of Ptch2 induces canonical Gli transcription and also directs HH ligands towards Ptch1 increasing non-canonical Erk phosphorylation. B BM cells of Wt, Ptch1+/- and Ptch2-/- mice were checked for Gli1 and Ptch1 expression via qPCR (transcript levels are shown relative to Hprt or Gapdh) and for Erk phosphorylation via flow cytometry (n≥3 each genotype, t-test). C Western Blot of 293T cells transfected with siRNA against Ptch1 or Ptch2 and blotted with antibodies against Ptch1, Ptch2, pErk and total Erk.

Diagram showing canonical and non-canonical HH signaling in Wt, Ptch1-/- and Ptch2-/- cells. Depletion of Ptch1 causes canonical pathway activation driving Gli1 transcription but lacks activation of Erk. In contrast, depletion of Ptch2 induces canonical Gli transcription and also directs HH ligands towards Ptch1 increasing non-canonical Erk phosphorylation. B BM cells of Wt, Ptch1+/- and Ptch2-/- mice were checked for Gli1 and Ptch1 expression via qPCR (transcript levels are shown relative to Hprt or Gapdh) and for Erk phosphorylation via flow cytometry (n≥3 each genotype, t-test). C Western Blot of 293T cells transfected with siRNA against Ptch1 or Ptch2 and blotted with antibodies against Ptch1, Ptch2, pErk and total Erk.

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