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

scholarly journals Compartmentalization of protein kinase A signaling by the heterotrimeric G protein Go

2006 ◽  
Vol 103 (50) ◽  
pp. 19158-19163 ◽  
Author(s):  
S. Ghil ◽  
J.-M. Choi ◽  
S.-S. Kim ◽  
Y.-D. Lee ◽  
Y. Liao ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
Heterotrimeric G Protein ◽  
Kinase A

Impaired G-protein-stimulated adenylyl cyclase activity in Alzheimer's disease brain is not accompanied by reduced cyclic-AMP-dependent protein kinase A activity

1996 ◽  
Vol 737 (1-2) ◽  
pp. 155-161 ◽  
Author(s):  
Willy L Bonkale ◽  
Johan Fastbom ◽  
Birgitta Wiehager ◽  
Rivka Ravid ◽  
Bengt Winblad ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cyclic Amp ◽  
Protein Kinase A ◽  
Adenylyl Cyclase ◽  
G Protein ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity ◽  
Dependent Protein Kinase ◽  
Dependent 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

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

High-Intensity Swimming Exercise Decreases Glutamate-Induced Nociception by Activation of G-Protein-Coupled Receptors Inhibiting Phosphorylated Protein Kinase A

2016 ◽  
Vol 54 (7) ◽  
pp. 5620-5631 ◽  
Author(s):  
Daniel F. Martins ◽  
Aline Siteneski ◽  
Daniela D. Ludtke ◽  
Daniela Dal-Secco ◽  
Adair R. S. Santos
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
G Protein ◽  
High Intensity ◽  
G Protein Coupled Receptors ◽  
Swimming Exercise ◽  
Phosphorylated Protein ◽  
G Protein Coupled ◽  
Kinase A

scholarly journals Pannexin 1 is the conduit for low oxygen tension-induced ATP release from human erythrocytes

2010 ◽  
Vol 299 (4) ◽  
pp. H1146-H1152 ◽  
Author(s):  
Meera Sridharan ◽  
Shaquria P. Adderley ◽  
Elizabeth A. Bowles ◽  
Terrance M. Egan ◽  
Alan H. Stephenson ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Adenylyl Cyclase ◽  
Atp Release ◽  
Human Erythrocytes ◽  
Low Oxygen ◽  
Pannexin 1 ◽  
Prostacyclin Receptor ◽  
Low Oxygen Tension ◽  
Kinase A

Erythrocytes release ATP in response to exposure to the physiological stimulus of lowered oxygen (O2) tension as well as pharmacological activation of the prostacyclin receptor (IPR). ATP release in response to these stimuli requires activation of adenylyl cyclase, accumulation of cAMP, and activation of protein kinase A. The mechanism by which ATP, a highly charged anion, exits the erythrocyte in response to lowered O2 tension or receptor-mediated IPR activation by iloprost is unknown. It was demonstrated previously that inhibiting pannexin 1 with carbenoxolone inhibits hypotonically induced ATP release from human erythrocytes. Here we demonstrate that three structurally dissimilar compounds known to inhibit pannexin 1 prevent ATP release in response to lowered O2 tension but not to iloprost-induced ATP release. These results suggest that pannexin 1 is the conduit for ATP release from erythrocytes in response to lowered O2 tension. However, the identity of the conduit for iloprost-induced ATP release remains unknown.

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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