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Hannah E. J. Polson

Researcher at London Research Institute

Publications -  11
Citations -  1758

Hannah E. J. Polson is an academic researcher from London Research Institute. The author has contributed to research in topics: Autophagy & Plasmodium falciparum. The author has an hindex of 9, co-authored 10 publications receiving 1523 citations. Previous affiliations of Hannah E. J. Polson include National Institute for Medical Research & Pasteur Institute.

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WIPI2 Links LC3 Conjugation with PI3P, Autophagosome Formation, and Pathogen Clearance by Recruiting Atg12–5-16L1

TL;DR: Mutation experiments and ectopic localization of WIPI2b to plasma membrane show that WIPi2b is a PtdIns(3)P effector upstream of Atg16L1 and is required for LC3 conjugation and starvation-induced autophagy through recruitment of the Atg12–5- 16L1 complex.
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Mammalian Atg18 (WIPI2) localizes to omegasome-anchored phagophores and positively regulates LC3 lipidation

TL;DR: A role for WIPI2 in the progression of omegasomes into autophagosomes is proposed, which is thought to act as platforms forAutophagosome formation.
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PIKfyve Regulation of Endosome‐Linked Pathways

TL;DR: It is suggested that PIKfyve inhibition may render the late endosome/lysosome compartment refractory to fusion with both autophagosomes and with EGFR‐containing multivesicular bodies.
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Clinical protection from falciparum malaria correlates with neutrophil respiratory bursts induced by merozoites opsonized with human serum antibodies.

TL;DR: This work presents the first clearly demonstrated functional antibody immune correlate of clinical protection from Plasmodium falciparum malaria, and begs the question regarding the importance of ADRB by PMN for immune protection against malaria in vivo.
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Membrane trafficking events that partake in autophagy.

TL;DR: To obtain this peculiar topology, the early AV, the phagophore or isolation membrane (IM) must be either synthesised de novo or expanded by vesicle fusion, and recent work has implicated several different organelles as potential membrane sources during the initial stages of IM formation and expansion.