Activation of extracellular signal regulated protein kinase by neuropeptide Y and pancreatic polypeptide in CHO cells expressing the NPY Y1, Y2, Y4 and Y5 receptor subtypes
In: Regulatory peptides, Jg. 105 (2002), Heft 1, S. 65-73
academicJournal
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Zugriff:
Neuropeptide Y (NPY), 36-amino acid amidated peptide expressed in central and peripheral neurons, regulates a variety of physiological activities, including food intake, energy expenditure, vasoconstriction, anxiolysis, nociception and ethanol consumption. NPY binds to a family of G-protein coupled receptors whose activation results in inhibition of adenylyl cyclase activity. To more fully characterize the signal transduction pathways utilized by the NPY receptor subtypes, the pathways leading to phosphorylation of the extracellular signal regulated protein kinases 1 and 2 (ERK) have been compared in CHO cells expressing each of the four cloned human NPY receptor subtypes, Y1 Y2, Y4 and Y5. NPY Y1, Y2, Y4 and Y5 receptor-mediated ERK phosphorylation was blocked by pertussis toxin (PTX) exposure, indicating that all four receptors are coupled to inhibitory Gi/o proteins. Exposure to the protein kinase C (PKC) inhibitor GF109203X diminished Y1, Y2 and Y4 receptor-mediated ERK phosphorylation but completely blocked Y5 receptor-mediated ERK phosphorylation. Additionally, Y5 receptor-mediated ERK phosphorylation was inhibited by the phosphatidylinositol 3-kinase inhibitors LY294002 and wortmannin to a greater extent than was Y1-mediated ERK phosphorylation. These results demonstrate that in CHO cells, the Y5 receptor and the Y1 Y2 and Y4 receptors utilize different pathways to activate ERK.
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Activation of extracellular signal regulated protein kinase by neuropeptide Y and pancreatic polypeptide in CHO cells expressing the NPY Y1, Y2, Y4 and Y5 receptor subtypes
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Autor/in / Beteiligte Person: | MULLINS, Deborra E ; XIAOPING, ZHANG ; HAWES, Brian E |
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Zeitschrift: | Regulatory peptides, Jg. 105 (2002), Heft 1, S. 65-73 |
Veröffentlichung: | Amsterdam; Shannon: Elsevier, 2002 |
Medientyp: | academicJournal |
Umfang: | print, 30 ref |
ISSN: | 0167-0115 (print) |
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