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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Biochem Pharmacol. 2017 Dec 7;151:201–213. doi: 10.1016/j.bcp.2017.12.003

Table 1.

Summary of A2BAR-induced signaling.

Activity Agonista Evidencea Figure
HEK293 kidney cells
Gs-mediated cAMP production NECA, Bay GsKO 2A–C
Gs-mediated ERK1/2 stimulation NECA GsKO, CTX 3A,B
Gs-mediated ERK1/2 via PKA, EPAC NECA H89, ESI 3E
ERK1/2 activity via PKC NECA GO 3A
Gi-mediated ERK1/2 stimulation NECA PTX 3A,D,F
Gq-mediated Ca2+ mobilization NECA UBO, Gq/11KO 4A,C
A2B-overexpressing HEK293 kidney cells
Gs-mediated cAMP production left-shifted NECA C/R curve 5C
T24 bladder cancer cells
Gs-mediated cAMP production NECA, Bay PTX/UBO (−) 6
ERK1/2 activity via PKC NECA GO 7A
Gi-mediated ERK1/2 stimulation NECA PTX 7C
Gs/PKA-suppressed ERK1/2 activity NECA, Bay CTX, H89 7A,C–E
ERK1/2 activity suppressed by EPAC2 NECA HJC0350 7D
ERK1/2 stimulation requires PKC NECA GO 7D
Gi-mediated Ca2+ mobilization NECA PTX 8
1321N1 astrocytoma cells
Gs-mediated cAMP production NECA UBO/PTX (−) 9
Gs-suppressed ERK1/2 activity NECA forsk, CTX 10A,B
Gs-suppression of ERK1/2 is PKC-depend. NECA GO 10C
ERK1/2 inhibition via EPAC1 NECA CE3F4 10C
Gi-stimulated ERK1/2 activity NECA PTX 10B
ERK1/2 inhibition (other agonists) Bay, MRS5911, MRS3997 10D
Lack of A2BAR-induced Ca2+ mobilization NECA Ca2+ dye 11
a

Bay, BAY60-6583; C/R, concentration-response; ESI, ESI-09; forsk, forskolin; GO, GO6983; UBO, UBO-QIC.