scholarly journals Involvement of cyclic AMP-dependent protein kinases in the signal transduction pathway for interleukin-1.

1990 ◽  
Vol 10 (7) ◽  
pp. 3824-3827 ◽  
Author(s):  
M Chedid ◽  
S B Mizel
Keyword(s):  
Signal Transduction ◽  
Cyclic Amp ◽  
Protein Kinases ◽  
Gene Transcription ◽  
Interleukin 1 ◽  
Signal Transduction Pathway ◽  
Cell Types ◽  
Specific Protein ◽  
Transduction Pathway ◽  
Dependent Protein

Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat. This inhibitor did not affect protein kinase C-mediated gene transcription, suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of responsive cell types.

Involvement of cyclic AMP-dependent protein kinases in the signal transduction pathway for interleukin-1

1990 ◽  
Vol 10 (7) ◽  
pp. 3824-3827
Author(s):  
M Chedid ◽  
S B Mizel
Keyword(s):  
Signal Transduction ◽  
Cyclic Amp ◽  
Protein Kinases ◽  
Gene Transcription ◽  
Interleukin 1 ◽  
Signal Transduction Pathway ◽  
Cell Types ◽  
Specific Protein ◽  
Transduction Pathway ◽  
Dependent Protein

Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat. This inhibitor did not affect protein kinase C-mediated gene transcription, suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of responsive cell types.

Participation of cAMP in a signal-transduction pathway relating erythrocyte deformation to ATP release

2001 ◽  
Vol 281 (4) ◽  
pp. C1158-C1164 ◽  
Author(s):  
Randy S. Sprague ◽  
Mary L. Ellsworth ◽  
Alan H. Stephenson ◽  
Andrew J. Lonigro
Keyword(s):  
Signal Transduction ◽  
Adenylyl Cyclase ◽  
Atp Release ◽  
Signal Transduction Pathway ◽  
Intracellular Camp ◽  
Transmembrane Conductance Regulator ◽  
Transduction Pathway ◽  
Camp Analog ◽  
Dependent Protein ◽  
Erythrocyte Deformation

Previously, we reported that red blood cells (RBCs) of rabbits and humans release ATP in response to mechanical deformation and that this release of ATP requires the activity of the cystic fibrosis transmembrane conductance regulator (CFTR). It was reported that cAMP, acting through a cAMP-dependent protein kinase, PKA, is an activator of CFTR. Here we investigate the hypothesis that cAMP stimulates ATP release from RBCs. Incubation of human and rabbit RBCs with the direct activator of adenylyl cyclase, forskolin (10 or 100 μM), with IBMX (100 μM), resulted in ATP release and increases in intracellular cAMP. In addition, epinephrine (1 μM), a receptor-mediated activator of adenylyl cyclase, stimulated ATP release from rabbit RBCs. Moreover, incubation of human and rabbit RBCs with an active cAMP analog [adenosine 3′5′-cyclic monophosphorothioate Sp-isomer (Sp-cAMP, 100 μM)] resulted in ATP release. In contrast, forskolin and Sp-cAMP were without effect on dog RBCs, cells known not to release ATP in response to deformation. When rabbit RBCs were incubated with the inactive cAMP analog and inhibitor of PKA activity, adenosine 3′,5′-cyclic monophosphorothioate Rp-isomer (100 μM), deformation-induced ATP release was attenuated. These results are consistent with the hypothesis that adenylyl cyclase and cAMP are components of a signal-transduction pathway relating RBC deformation to ATP release from human and rabbit RBCs.

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