Detalhes bibliográficos
| Resumo: | Neutrophil migration is vital for immunity and precedes effector functions such as pathogen killing. Here, we report that this process is regulated by the Rab27a GTPase, a protein known to control granule exocytosis. Rab27a-deficient (Rab27a KO) neutrophils exhibit migration defects in vitro and in vivo, and live-cell microscopy suggests that delayed uropod detachment causes the migratory defect. Surface expression of CD11b, a key adhesion molecule, is increased in chemokine-stimulated Rab27a KO neutrophils compared with the control, suggesting a turnover delay caused by a defect in elastase secretion from azurophilic granules at the rear of bone marrow polymorphonuclear leukocytes (BM-PMNs). We suggest that Rab27a-dependent protease secretion regulates neutrophil migration through proteolysis-dependent de-adhesion of uropods, a mechanism that could be conserved in cell migration and invasion. |
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| Autores principais: | Singh, Rajesh K. |
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| Outros Autores: | Liao, Wenjia; Tracey-White, Dhani; Recchi, Chiara; Tolmachova, Tanya; Rankin, Sara M.; Hume, Alistair N.; Seabra, Miguel C.; C Seabra, Miguel |
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| Assunto: | Cell migration Chemotaxis Neutrophil Rab27a Uropod Cell Biology |
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| Ano: | 2012 |
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| País: | Portugal |
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| Tipo de documento: | artigo |
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| Tipo de acesso: | acesso aberto |
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| Instituição associada: | Universidade Nova de Lisboa |
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| Idioma: | inglês |
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| Origem: | Repositório Institucional da UNL |
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