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. 2004 Jun 1;142(4):635–646. doi: 10.1038/sj.bjp.0705851

Table 1.

JNK activation in response to EGF treatment and GPCRs of different coupling specificities

    JNK activity (fold induction)a cAMP level IP level
GPCR GPCR agonists Agonist EGF Agonist + EGF % increaseb % decreasec % increased
Gs-coupled              
D1R Dopamine (10 μM) 1.4±0.2 1.7±0.3 2.1±0.5 1156±78** NA 10±12
LHR Chorionic 1.5±0.1 1.8±0.2 2.2±0.4 367±63** NA 14±19
  Gonadotropin (1 μg ml−1)            
SecR Secretin (1 μM) 4.6±0.6 1.6±0.1 4.9±0.6 2897±121** NA 712±63**
V2R Vasopressin (100 nM) 2.3±0.2 1.8±0.2 2.8±0.4 1342±119** NA 246±59**
Gi-coupled              
ORL1R OFQ (100 nM) 2.5±0.4 2.0±0.3 6.3±1.1* NA 29±11*** 14±15
D2R Dopamine (10 μM) 2.3±0.3 2.0±0.1 6.0±1.0* NA 26±8*** 19±22
SSTR1 Somatostatin (100 nM) 2.5±0.6 1.9±0.2 5.9±0.5* NA 28±7*** 16±39
mt1R Melatonin (100 nM) 2.2±0.2 2.1±0.4 5.6±0.6* NA 30±8*** 23±21
Gq-coupled              
GRPR Bombesin (100 nM) 6.7±0.7 1.7±0.1 7.1±0.6 6±18 NA 1209±128**
BK2R Bradykinin (100 nM) 6.8±0.9 2.0±0.4 7.7±1.2 4±29 NA 468±77**
M1R Carbachol (200 μM) 5.9±0.9 1.6±0.1 6.6±1.0 523±74** NA 833±67**
H1R Histamine (100 μM) 6.2±0.5 1.8±0.1 7.0±0.7 356±52** NA 642±87**

Cos-7 cells were transfected with the cDNAs encoding different GPCRs in the absence (for cAMP and IP assays) or presence (for JNK assay) of JNK-HA. Assays were performed as described in Methods. The JNK activities were determined at 30 min after individual or co-treatment with specific GPCR agonists (as indicated) and EGF (100 ng ml−1). For cAMP assays, transfected cells were stimulated with the corresponding agonists in the absence (for Gs- and Gq-coupled receptors) or presence (for Gi-coupled receptors) of forskolin (10 μM) co-treatment for 30 min. For IP assays, agonists were administered to the transfected cells for 30 min.

a

Values shown represent the mean±s.e. from at least three separate experiments, with the basal JNK activity (in the absence of GPCR agonists) defined as one-fold induction.

b,d

Data represent the mean±s.e. of three separate experiments, with the basal level defined as 100%.

c

Data represent the mean±s.e. of three separate experiments, with the forskolin-enhanced cAMP level defined as 100%. Data analysis was performed by Bonferroni's corrected t-test.

*

Co-administration of GPCR agonists and EGF triggered the JNK activations synergistically as compared to their individual responses (two-way ANOVA, P<0.05).

**

Agonist treatment significantly increased cAMP or IP formation as compared to the basal levels (one-way ANOVA, P<0.05).

***

Agonist treatment significantly suppressed the forskolin-induced cAMP formation (one-way ANOVA, P<0.05). NA, not applicable.