G
Gabriela Cosío
Researcher at University of Toronto
Publications - 6
Citations - 1186
Gabriela Cosío is an academic researcher from University of Toronto. The author has contributed to research in topics: Phagocytosis & Internalization. The author has an hindex of 5, co-authored 6 publications receiving 1083 citations.
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Journal ArticleDOI
Antimicrobial mechanisms of phagocytes and bacterial evasion strategies
TL;DR: An overview of the antimicrobial defences of the host cell is presented, with emphasis on macrophages, for which phagocytosis has been studied most extensively and some of the evasive strategies used by bacteria are described.
Journal ArticleDOI
Multimolecular Signaling Complexes Enable Syk-Mediated Signaling of CD36 Internalization
Bryan Heit,Hani Kim,Gabriela Cosío,Diana Castaño,Richard F. Collins,Clifford A. Lowell,Kevin C. Kain,William S. Trimble,Sergio Grinstein +8 more
TL;DR: Using a combination of phosphoprotein isolation, mass spectrometry, superresolution imaging, and gene silencing, it is determined that the receptor induces ligand internalization through a heteromeric complex consisting of CD36, β1 and/or β2 integrins, and the tetraspanins CD9 and/ or CD81.
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CD36 and TLR Interactions in Inflammation and Phagocytosis: Implications for Malaria
Laura K. Erdman,Gabriela Cosío,Andrew Helmers,D. Channe Gowda,Sergio Grinstein,Kevin C. Kain,Kevin C. Kain +6 more
TL;DR: It is shown that selective engagement and internalization of this receptor did not lead to proinflammatory cytokine production by primary human and murine macrophages, and that CD36 must cooperate with other receptors such as TLRs to participate in cytokine responses.
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Class I and class III phosphoinositide 3-kinases are required for actin polymerization that propels phagosomes
TL;DR: Phagosomes formed by engagement of complement receptors (CR3) are moved within macrophages by PI3K-driven formation of actin “comet tails” on the phagosomal membrane.
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Role of CrkII in Fcγ Receptor-mediated Phagocytosis
TL;DR: The finding that CrkII-DOCK180 is also responsible, at least in part, for the effects of Fcγ receptors implies that additional, parallel pathways must account for the associated pro-inflammatory effect.