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. Author manuscript; available in PMC: 2021 Jun 11.
Published in final edited form as: Cell. 2020 May 28;181(6):1364–1379.e14. doi: 10.1016/j.cell.2020.04.053

Figure 3. SBI-553 antagonizes NTS-induced, Gq-mediated pERK, but permits NTS-induced, β-arrestin-mediated pERK generation.

Figure 3.

Cells expressing NTSR1 were stimulated with NTSR1 ligands. Phosphorylated ERK (pERK) and total ERK expression were assessed in whole cell lysates by Western blot analysis.

(A-B) Time course for NTS-stimulated pERK in HEK293T cells. NTSR1-expressing cells were treated with NTS in the presence or absence of the NTSR1/2 antagonist SR142948A. Controls cells lacking NTSR1 were stimulated only with NTS.

(C-D) Time course for SBI-553-stimulated pERK in HEK293T cells. NTSR1-expressing cells were treated with SBI-553 or vehicle.

(E-F) Time course for NTS and Vehicle or SBI-553 co-treatment-stimulated pERK in HEK293T cells. NTSR1-expressing cells were treated concurrently with NTS and vehicle or SBI-553.

(G-H) Time course for NTS and Vehicle or SBI-553 co-treatment-stimulated pERK in Gq-null cells. HEK293 cells genetically engineered to lack the Gq protein were treated concurrently with NTS and vehicle or SBI-553.

(I-J) Time course for NTS and Vehicle or SBI-553 co-treatment-stimulated pERK in β-arrestin1/2-null cells. HEK293 cells genetically engineered to lack β-arrestin1 and β-arrestin2 were treated concurrently with NTS and vehicle or SBI-553.

For details on statistical comparisons, see Table S3.