Relationship between Fc.gamma.2b receptor and adenylate cyclase of a murine macrophagelike cell line, P388D1

Biochemistry ◽  
1987 ◽  
Vol 26 (14) ◽  
pp. 4183-4192 ◽  
Author(s):  
Yasuhiko Hirata ◽  
Rafael Fernandez-Botran ◽  
Tsuneo Suzuki
Keyword(s):  
Adenylate Cyclase ◽  
Cell Line ◽  
Macrophagelike Cell

Antibody-mediated growth of influenza A NWS virus in macrophagelike cell line P388D1.

1988 ◽  
Vol 62 (1) ◽  
pp. 20-26 ◽  
Author(s):  
H Ochiai ◽  
M Kurokawa ◽  
K Hayashi ◽  
S Niwayama
Keyword(s):  
Cell Line ◽  
Influenza A ◽  
Macrophagelike Cell

scholarly journals Heavy isotope labeling study of the turnover of forskolin-stimulated adenylate cyclase in BC3H1 cell line.

1987 ◽  
Vol 262 (18) ◽  
pp. 8470-8475
Author(s):  
R Bouhelal ◽  
J Bockaert ◽  
R Mermet-Bouvier ◽  
G Guillon ◽  
V Homburger
Keyword(s):  
Adenylate Cyclase ◽  
Cell Line ◽  
Isotope Labeling ◽  
Heavy Isotope

Activation of protein kinase C attenuates prostaglandin E2 responses in a colonic cell line

1988 ◽  
Vol 255 (1) ◽  
pp. G27-G32 ◽  
Author(s):  
G. Warhurst ◽  
N. B. Higgs ◽  
M. Lees ◽  
A. Tonge ◽  
L. A. Turnberg
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adenylate Cyclase ◽  
Prostaglandin E2 ◽  
Cell Line ◽  
Cellular Response ◽  
Short Circuit ◽  
Regulatory Subunit ◽  
Epithelial Cell Line ◽  
Kinase C

We examined the possibility that the protein kinase C pathway may interact with the adenosine 3',5'-cyclic monophosphate (cAMP) pathway in intestinal epithelium by studying the influence of phorbol esters on the response to prostaglandin E2 (PGE2) in a colonic epithelial cell line. Pretreatment of T84 cells with 4 beta-phorbol 12,13-dibutyrate (PDB) markedly attenuated the rise in short-circuit current provoked by PGE2, a receptor-mediated cAMP agonist. The EC50 of this effect was 52 nM PDB with a half time of 4-6 min. The responses to nonreceptor-mediated agonists, forskolin and dibutyryl cAMP, were unaffected by phorbol ester. PDB also reduced the ability of PGE2 to stimulate adenylate cyclase activity in these cells. The accumulation of cAMP in response to PGE2 was inhibited by PDB (EC50 38 nM), an effect mimicked by the diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol. In addition, PGE2 stimulation of adenylate cyclase in membranes from PDB-treated cells was reduced by 30-40%. Inhibition was not mediated via the catalytic or regulatory subunit of the adenylate cyclase, implying an action involving desensitization of PGE2 receptors. These results provide evidence of a complex interrelationship between protein kinase C- and cAMP-mediated pathways that might be important in regulating the cellular response to secretagogues.

scholarly journals Nobiletin Stimulates Chloride Secretion in Human Bronchial Epithelia via a cAMP/PKA-Dependent Pathway

2015 ◽  
Vol 37 (1) ◽  
pp. 306-320 ◽  
Author(s):  
Yuan Hao ◽  
Cindy S.T. Cheung ◽  
Wallace C.Y. Yip ◽  
Wing-hung Ko
Keyword(s):  
Cystic Fibrosis ◽  
Adenylate Cyclase ◽  
Cell Line ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Epithelial Cell Line ◽  
Electrical Measurements ◽  
Cl Secretion ◽  
Bronchial Epithelia

Background/Aims: Nobiletin, a citrus flavonoid isolated from tangerines, alters ion transport functions in intestinal epithelia, and has antagonistic effects on eosinophilic airway inflammation of asthmatic rats. The present study examined the effects of nobiletin on basal short-circuit current (ISC) in a human bronchial epithelial cell line (16HBE14o-), and characterized the signal transduction pathways that allowed nobiletin to regulate electrolyte transport. Methods: The ISC measurement technique was used for transepithelial electrical measurements. Intracellular calcium ([Ca2+]i) and cAMP were also quantified. Results: Nobiletin stimulated a concentration-dependent increase in ISC, which was due to Cl- secretion. The increase in ISC was inhibited by a cystic fibrosis transmembrane conductance regulator inhibitor (CFTRinh-172), but not by 4,4'-diisothiocyano-stilbene-2,2'-disulphonic acid (DIDS), Chromanol 293B, clotrimazole, or TRAM-34. Nobiletin-stimulated ISC was also sensitive to a protein kinase A (PKA) inhibitor, H89, and an adenylate cyclase inhibitor, MDL-12330A. Nobiletin could not stimulate any increase in ISC in a cystic fibrosis (CF) cell line, CFBE41o-, which lacked a functional CFTR. Nobiletin stimulated a real-time increase in cAMP, but not [Ca2+]i. Conclusion: Nobiletin stimulated transepithelial Cl- secretion across human bronchial epithelia. The mechanisms involved activation of adenylate cyclase- and cAMP/PKA-dependent pathways, leading to activation of apical CFTR Cl- channels.

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