Extended Data Fig. 2 | Glucagon-stimulated glucose production requires
activation of the PLC and PKA pathways, converging to activate INSP3
signalling. a–p, In vitro glucose production and VPC in isolated hepatocytes
with and without ET-18-OCH 3 (n = 3) (a, b), U-73122 (n = 3, except for
knockout − glucagon-U-73122 in d (n = 2)) (c, d), H-89 (n = 6) (e, f), vasopressin
(n = 3) (g, h), 2-APB (n = 3) (i, j), caffeine (n = 3) (k, l), KN-93 (n = 6) (m, n) and
thapsigargin (n = 3) (o, p). In all panels, *P < 0.05, **P < 0.01 and ***P < 0.001
versus wild type − glucagon − drug; §P < 0.05, §§P < 0.01 and §§§P < 0.001 versus
wild type + glucagon − drug by two-tailed unpaired Student’s t-test. If no
statistical comparison is denoted, the groups were not significantly different.
Mean ± s.e.m. is shown.