scholarly journals Substance P suppresses GABAA receptor function via protein kinase C in primary sensory neurones of bullfrogs.

1996 ◽  
Vol 496 (2) ◽  
pp. 439-449 ◽  
Author(s):  
K Yamada ◽  
T Akasu
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Substance P ◽  
Gabaa Receptor ◽  
Receptor Function ◽  
Sensory Neurones ◽  
Kinase C

Regulation of GABAA receptor function by protein kinase C phosphorylation

Neuron ◽  
1994 ◽  
Vol 12 (5) ◽  
pp. 1081-1095 ◽  
Author(s):  
Belinda J. Krishek ◽  
Xinmin Xie ◽  
Craig Blackstone ◽  
Richard L. Huganir ◽  
Stephen J. Moss ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Gabaa Receptor ◽  
Receptor Function ◽  
Kinase C

scholarly journals Distinct Roles for Protein Kinase C Isoforms in Regulating Platelet Purinergic Receptor Function

2006 ◽  
Vol 70 (3) ◽  
pp. 1132-1142 ◽  
Author(s):  
Stuart J. Mundell ◽  
Matthew L. Jones ◽  
Adam R. Hardy ◽  
Johanna F. Barton ◽  
Stephanie M. Beaucourt ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Purinergic Receptor ◽  
Receptor Function ◽  
Kinase C ◽  
Protein Kinase C Isoforms

scholarly journals Protein kinase C-dependent and -independent mechanisms regulating the parotid substance P receptor as revealed by differential effects of protein kinase C inhibitors

1988 ◽  
Vol 256 (2) ◽  
pp. 677-680 ◽  
Author(s):  
H Sugiya ◽  
J W Putney
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Substance P ◽  
Time Course ◽  
Phorbol Esters ◽  
Inhibitory Effect ◽  
Protein Kinase C Inhibitors ◽  
Kinase C ◽  
Substance P Receptor ◽  
Rat Parotid

Substance P-induced inositol trisphosphate (InsP3) formation was inhibited by 1 microM-4 beta-phorbol 12,13-dibutyrate (PDBu) in rat parotid acinar cells. The inhibitory effect of PDBu was reversed by the protein kinase C inhibitors H-7 or K252a. Substance P also elicits a persistent desensitization of subsequent substance P-stimulated InsP3 formation. However, this desensitization was not inhibited by H-7. In addition, H-7 had no effect on the time course of substance P-induced InsP3 formation. These results suggest that, although activation of protein kinase C by phorbol esters can inhibit the substance P receptor-linked phospholipase C pathway, this mechanism apparently plays little, if any, role in regulating this system after activation by substance P.

scholarly journals Neurokinin-1 Receptor Antagonist Treatment in Polymicrobial Sepsis: Molecular Insights

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Akhil Hegde ◽  
Yung-Hua Koh ◽  
Shabbir M. Moochhala ◽  
Madhav Bhatia
Keyword(s):  
Transcription Factors ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Substance P ◽  
Receptor Antagonist ◽  
Polymicrobial Sepsis ◽  
Neurokinin 1 Receptor ◽  
Post Surgery ◽  
Kinase C ◽  
Neurokinin 1

Neurokinin-1 receptor blocking has been shown to be beneficial against lung injury in polymicrobial sepsis. In this paper, we evaluated the possible mediators and the mechanism involved. Mice were subjected to cecal ligation and puncture (CLP-) induced sepsis or sham surgery. Vehicle or SR140333 [1 mg/kg; subcutaneous (s.c.)] was administered to septic mice either 30 min before or 1 h after the surgery. Lung tissue was collected 8 h after surgery and further analyzed. CLP alone caused a significant increase in the activation of the transcription factors, protein kinase C-α, extracellular signal regulated kinases, neurokinin receptors, and substance P levels in lung when compared to sham-operated mice. SR140333 injected pre- and post surgery significantly attenuated the activation of transcription factors and protein kinase C-αand the plasma levels of substance P compared to CLP-operated mice injected with the vehicle. In addition, GR159897 (0.12 mg/kg; s.c.), a neurokinin-2 receptor antagonist, failed to show beneficial effects. We conclude that substance P acting via neurokinin-1 receptor in sepsis initiated signaling cascade mediated mainly by protein kinase C-α,led to NF-κB and activator protein-1 activation, and further modulated proinflammatory mediators.

Substance P inhibits pancreatic ductal HCO3-secretion via activation of protein kinase C in guinea pig

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
B Ozsvari ◽  
Z Rakonczay ◽  
L Tiszlavicz ◽  
T Takacs ◽  
G Papp ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Substance P ◽  
Guinea Pig ◽  
Kinase C
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