Plows, Louise D., Cook, Richard T., Davies, Angela J. and Walker, Anthony J. (2004) Activation of extracellular-signal regulated kinase is required for phagocytosis by Lymnaea stagnalis Haemocytes. BBA - Molecular Cell Research, 1692(1), pp. 25-33. ISSN (print) 0167-4889
Full text not available from this archive.Abstract
Haemocytes are the primary defence cells of molluscs. In the present study, extracellular-signal regulated kinase (ERK) 1/2-like proteins were identified within Lymnaea stagnalis haemocytes, with apparent molecular weights of 44 and 43 kDa, respectively. Mitogen-activated protein kinase (MAPK) activity assays have confirmed that the L. stagnalis ERK possesses kinase activity towards Elk-1. Challenge of haemocytes with bacterial lipopolysaccharide (LPS) resulted in a transient activation of ERK, and immunocytochemistry revealed that phospho-ERK was present in both the perinuclear region and the nucleus following challenge. MAPK/ERK kinase (MEK) inhibitors blocked ERK activation confirming that MEK lies upstream of ERK in haemocytes. Moreover, phagocytosis assays, using various inhibitors, showed that ERK activity was vital for efficient phagocytosis and that ERK may be activated by both Ras-dependent and Ras-independent mechanisms. Overall, this study has furthered knowledge of ERK signalling in molluscan immunity and has shown that the ERK pathway regulates the phagocytic activity of molluscan haemocytes.
| Item Type: | Article |
|---|---|
| Additional Information: | This work was supported by the Royal Society. |
| Research Area: | Allied health professions and studies Biological sciences |
| Faculty, School or Research Centre: | Faculty of Science (until 2011) > School of Life Sciences Faculty of Science (until 2011) > School of Pharmacy and Chemistry Faculty of Science (until 2011) |
| Related URLs: | |
| Depositing User: | Ban Talal |
| Date Deposited: | 20 Jun 2007 |
| Last Modified: | 30 Sep 2010 10:41 |
| URI: | http://eprints.kingston.ac.uk/id/eprint/1472 |
Actions (Repository Editors)
![]() |
Item Control Page |
