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- Publisher Website: 10.1016/j.mce.2008.12.006
- Scopus: eid_2-s2.0-58649097003
- PMID: 19135127
- WOS: WOS:000263662500012
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Article: The constitutive activity of the ghrelin receptor attenuates apoptosis via a protein kinase C-dependent pathway
Title | The constitutive activity of the ghrelin receptor attenuates apoptosis via a protein kinase C-dependent pathway |
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Authors | |
Keywords | Constitutive activity Apoptosis Ghrelin receptors |
Issue Date | 2009 |
Citation | Molecular and Cellular Endocrinology, 2009, v. 299, n. 2, p. 232-239 How to Cite? |
Abstract | The ghrelin receptor (GHS-R1a) displays a high level of constitutive signaling through a phospholipase C/protein kinase C-dependent pathway. Therefore, we have investigated the role of agonist-dependent and agonist-independent signaling of GHS-R1a in apoptosis using the seabream GHS-R1a stably expressed in human embryonic kidney 293 cells (HEK-sbGHS-R1a cells). Cadmium-induced activation of caspase-3 was significantly attenuated in HEK-sbGHS-R1a cells compared to wild-type HEK293 cells, while the apoptotic responses to the protein kinase C inhibitor staurosporine were similar. GHS-R1a ligands had no effect on caspase-3 activation or on cell proliferation. Concentrations of the inverse agonist [d-Arg1,d-Phe5,d-Trp7,9,Leu11]-substance P sufficient to inhibit constitutive inositol phosphate generation did not enhance caspase-3 activity, suggesting a possible role of phosphatidylcholine-specific phospholipase C in the anti-apoptotic activity of GHS-R1a. In conclusion, our data suggests that the constitutive activity of sbGHS-R1a may be sufficient alone to attenuate apoptosis via a protein kinase C-dependent pathway. © 2008 Elsevier Ireland Ltd. All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/225047 |
ISSN | 2023 Impact Factor: 3.8 2023 SCImago Journal Rankings: 1.130 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Lau, Pui Ngan | - |
dc.contributor.author | Chow, Kevin B S | - |
dc.contributor.author | Chan, Chi Bun | - |
dc.contributor.author | Cheng, Christopher H K | - |
dc.contributor.author | Wise, Helen | - |
dc.date.accessioned | 2016-04-18T11:16:37Z | - |
dc.date.available | 2016-04-18T11:16:37Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | Molecular and Cellular Endocrinology, 2009, v. 299, n. 2, p. 232-239 | - |
dc.identifier.issn | 0303-7207 | - |
dc.identifier.uri | http://hdl.handle.net/10722/225047 | - |
dc.description.abstract | The ghrelin receptor (GHS-R1a) displays a high level of constitutive signaling through a phospholipase C/protein kinase C-dependent pathway. Therefore, we have investigated the role of agonist-dependent and agonist-independent signaling of GHS-R1a in apoptosis using the seabream GHS-R1a stably expressed in human embryonic kidney 293 cells (HEK-sbGHS-R1a cells). Cadmium-induced activation of caspase-3 was significantly attenuated in HEK-sbGHS-R1a cells compared to wild-type HEK293 cells, while the apoptotic responses to the protein kinase C inhibitor staurosporine were similar. GHS-R1a ligands had no effect on caspase-3 activation or on cell proliferation. Concentrations of the inverse agonist [d-Arg1,d-Phe5,d-Trp7,9,Leu11]-substance P sufficient to inhibit constitutive inositol phosphate generation did not enhance caspase-3 activity, suggesting a possible role of phosphatidylcholine-specific phospholipase C in the anti-apoptotic activity of GHS-R1a. In conclusion, our data suggests that the constitutive activity of sbGHS-R1a may be sufficient alone to attenuate apoptosis via a protein kinase C-dependent pathway. © 2008 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | eng | - |
dc.relation.ispartof | Molecular and Cellular Endocrinology | - |
dc.subject | Constitutive activity | - |
dc.subject | Apoptosis | - |
dc.subject | Ghrelin receptors | - |
dc.title | The constitutive activity of the ghrelin receptor attenuates apoptosis via a protein kinase C-dependent pathway | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.mce.2008.12.006 | - |
dc.identifier.pmid | 19135127 | - |
dc.identifier.scopus | eid_2-s2.0-58649097003 | - |
dc.identifier.volume | 299 | - |
dc.identifier.issue | 2 | - |
dc.identifier.spage | 232 | - |
dc.identifier.epage | 239 | - |
dc.identifier.isi | WOS:000263662500012 | - |
dc.identifier.issnl | 0303-7207 | - |