dc.contributor.author | Killock, DJ | |
dc.contributor.author | Parsons, M | |
dc.contributor.author | Zarrouk, M | |
dc.contributor.author | Ameer-Beg, SM | |
dc.contributor.author | Ridley, AJ | |
dc.contributor.author | Haskard, DO | |
dc.contributor.author | Zvelebil, M | |
dc.contributor.author | Ivetic, A | |
dc.date.accessioned | 2018-08-30T08:16:33Z | |
dc.date.issued | 2009-03 | |
dc.identifier.citation | The Journal of biological chemistry, 2009, 284 (13), pp. 8833 - 8845 | |
dc.identifier.issn | 0021-9258 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/2415 | |
dc.identifier.eissn | 1083-351X | |
dc.identifier.doi | 10.1074/jbc.m806983200 | |
dc.description.abstract | L-selectin is a cell adhesion molecule that tethers leukocytes to the luminal walls of venules during inflammation and enables them to roll under the force of blood flow. Clustering of L-selectin during rolling is thought to promote outside-in signals that lead to integrin activation and chemokine receptor expression, ultimately contributing to leukocyte arrest. Several studies have underscored the importance of the L-selectin cytoplasmic tail in functionally regulating adhesion and signaling. Interestingly, the L-selectin tail comprises only 17 amino acids, and yet it is thought to bind simultaneously to several proteins. For example, constitutive association of calmodulin (CaM) and ezrin/radixin/moesin (ERM) to L-selectin confers resistance to proteolysis and microvillar positioning, respectively. In this report we found that recombinant purified CaM and ERM bound non-competitively to the same tail of L-selectin. Furthermore, molecular modeling supported the possibility that CaM, L-selectin, and moesin could form a heterotrimeric complex. Finally, using fluorescence lifetime imaging microscopy to measure fluorescence resonance energy transfer, it was shown that CaM, L-selectin, and ERM could interact simultaneously in vivo. Moreover, L-selectin clustering promoted CaM/ERM interaction in cis (i.e. derived from neighboring L-selectin tails). These results highlight a novel intracellular event that occurs as a consequence of L-selectin clustering, which could participate in transducing signals that promote the transition from rolling to arrest. | |
dc.format | Print-Electronic | |
dc.format.extent | 8833 - 8845 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc/4.0 | |
dc.subject | COS Cells | |
dc.subject | U937 Cells | |
dc.subject | Animals | |
dc.subject | Humans | |
dc.subject | Multiprotein Complexes | |
dc.subject | Microfilament Proteins | |
dc.subject | Calmodulin | |
dc.subject | Cytoskeletal Proteins | |
dc.subject | L-Selectin | |
dc.subject | Membrane Proteins | |
dc.subject | Recombinant Proteins | |
dc.subject | Signal Transduction | |
dc.subject | Leukocyte Rolling | |
dc.subject | Protein Binding | |
dc.subject | Chlorocebus aethiops | |
dc.title | In Vitro and in Vivo Characterization of Molecular Interactions between Calmodulin, Ezrin/Radixin/Moesin, and L-selectin. | |
dc.type | Journal Article | |
rioxxterms.versionofrecord | 10.1074/jbc.m806983200 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by-nc/4.0 | |
rioxxterms.licenseref.startdate | 2009-03 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | The Journal of biological chemistry | |
pubs.issue | 13 | |
pubs.notes | Not known | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Closed research teams | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Closed research teams/Cancer Informatics | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Closed research teams | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Closed research teams/Cancer Informatics | |
pubs.publication-status | Published | |
pubs.volume | 284 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Cancer Informatics | en_US |
dc.contributor.icrauthor | Zvelebil, Marketa Juditha | en |