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Neil E. Reiner

Researcher at University of British Columbia

Publications -  91
Citations -  6610

Neil E. Reiner is an academic researcher from University of British Columbia. The author has contributed to research in topics: Leishmania donovani & Kinase. The author has an hindex of 40, co-authored 90 publications receiving 6088 citations. Previous affiliations of Neil E. Reiner include Columbia University Medical Center & Vancouver Coastal Health.

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An exosome-based secretion pathway is responsible for protein export from Leishmania and communication with macrophages.

TL;DR: It is shown that exosome-based secretion as a general mechanism for protein secretion by Leishmania, and thatExosomes are involved in the delivery of proteins into host target cells, suggesting that, like mammalian exosomes, LeishMania exosomal proteins function in long-range communication and immune modulation.
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Proteomic analysis of the secretome of Leishmania donovani

TL;DR: This analysis shows that protein secretion by L. donovani is a heterogeneous process that is unlikely to be determined by a classical amino-terminal secretion signal, and as an alternative, L.Donovani appears to use multiple nonclassical secretion pathways, including the release of exosome-like microvesicles.
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Antibacterial activity, inflammatory response, coagulation and cytotoxicity effects of silver nanoparticles.

TL;DR: In this article, the effects of 24 nm silver nanoparticles (AgNPs) on a panel of bacteria isolated from medical devices used in a hospital intensive care unit were studied, and the authors demonstrated that 24 nm AgNPs were effective in suppressing the growth of clinically relevant bacteria with moderate to high levels of antibiotic resistance.
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Leishmania exosomes modulate innate and adaptive immune responses through effects on monocytes and dendritic cells.

TL;DR: It is demonstrated that leishmania exosomes are predominantly immunosuppressive, and the first evidence to suggest that changes in the protein cargo of exosome may influence the impact of these vesicles on myeloid cell function is suggested.
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The 19-kDa Mycobacterium tuberculosis protein induces macrophage apoptosis through Toll-like receptor-2.

TL;DR: It is concluded that it is the polypeptide component of p19 that is responsible for signaling through TLR-2 and that the lipid moiety is not required, and the viability of M. tuberculosis in cells undergoing apoptosis induced by p19 was significantly reduced suggesting the possibility that this may favor containment of infection.