Phosducin is a protein kinase A-regulated G-protein regulator

Nature ◽  
1992 ◽  
Vol 358 (6381) ◽  
pp. 73-76 ◽  
Author(s):  
Petra H. Bauer ◽  
Stefan Müller ◽  
Mechthild Puzicha ◽  
Susanne Pippig ◽  
Brigitte Obermaier ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
Kinase A

scholarly journals Protein Kinase A-mediated Phosphorylation of the Gα13Switch I Region Alters the Gαβγ13-G Protein-coupled Receptor Complex and Inhibits Rho Activation

2002 ◽  
Vol 278 (1) ◽  
pp. 124-130 ◽  
Author(s):  
Jeanne M. Manganello ◽  
Jin-Sheng Huang ◽  
Tohru Kozasa ◽  
Tatyana A. Voyno-Yasenetskaya ◽  
Guy C. Le Breton
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
Receptor Complex ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Kinase A

The heterotrimeric G‐protein beta subunit Gpb1 controls hyphal growth under low oxygen conditions through the protein kinase A pathway and is essential for virulence in the fungus Mucor circinelloides

2020 ◽  
Vol 22 (10) ◽  
Author(s):  
Marco Iván Valle‐Maldonado ◽  
José Alberto Patiño‐Medina ◽  
Carlos Pérez‐Arques ◽  
Nancy Yadira Reyes‐Mares ◽  
Irvin Eduardo Jácome‐Galarza ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
Hyphal Growth ◽  
Mucor Circinelloides ◽  
Beta Subunit ◽  
Low Oxygen ◽  
Heterotrimeric G Protein ◽  
Oxygen Conditions ◽  
Kinase A

Mechanisms of PTH-induced rise in cytosolic calcium in adult rat hepatocytes

1994 ◽  
Vol 267 (5) ◽  
pp. G754-G763 ◽  
Author(s):  
M. Klin ◽  
M. Smogorzewski ◽  
H. Khilnani ◽  
M. Michnowska ◽  
S. G. Massry
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
Cytosolic Calcium ◽  
Amino Terminal ◽  
Kinase C ◽  
Dose Dependent ◽  
Kinase A ◽  
Stimulation Of

Available data indicate that the liver is a target organ for parathyroid hormone (PTH) and that this effect is most likely mediated by PTH-induced calcium entry into hepatocytes. The present study examined the effects of both PTH-(1-84) and its amino-terminal fragment [PTH-(1-34)] on cytosolic calcium concentration ([Ca2+]i) of hepatocytes and explored the cellular pathways that mediate this potential action of PTH. Both moieties of PTH produced a dose-dependent rise in [Ca2+]i, but the effect of PTH-(1-84) was greater (P < 0.01) than an equimolar amount of PTH-(1-34). This effect required calcium in the medium and was totally [PTH-(1-34)] or partially [PTH-(1-84)] blocked by PTH antagonist ([Nle8,18,Tyr34]bPTH-(7-34)-NH2] and by verapamil or nifedipine. Sodium or chloride channel blockers did not modify this effect. 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C, dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), and G protein activator also produced a dose-dependent rise in [Ca2+]i. Staurosporine abolished the effect of TPA, and both staurosporine and calphostin C partially inhibited the effect of PTH. Staurosporine and verapamil together produced greater inhibition of PTH action than each alone. Rp-cAMP, a competitive inhibitor of cAMP binding to the R subunit of protein kinase A, and N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), a protein kinase A inhibitor, blocked the effect of both DBcAMP and PTH, but the effect of these agents was greater (P < 0.01) on DBcAMP action. G protein inhibitor and pertussis toxin partially blocked the action of PTH. The data indicate that 1) PTH increases [Ca2+]i of hepatocytes; 2) this action of the hormone is receptor mediated; 3) the predominant pathway for this PTH action is the stimulation of a G protein-adenylate cyclase-cAMP system, which then leads to stimulation of a calcium transport system inhibitable by verapamil or nifedipine or activation of L-type calcium channels; 4) activation of protein kinase C is also involved; and 5) the PTH-induced rise in [Ca2+]i is due, in major parts, to movement of extracellular calcium into the cell.

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