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Last Updated: 08/11/2024

Exploring the role of Decay-accelerating factor and tight junction formation during erythrocyte invasion by Plasmodium falciparum

Objectives

This project aims to further understand the role of Decay-accelerating factor (CD55), a lipid anchored protein that is known to be important for the invasion process between the parasite and RBCs.

Principal Investigators / Focal Persons

Emmaline Stotter

Rationale and Abstract

Malaria is a serious disease caused by species of Plasmodium. This research will focus on P. falciparum, which causes the most severe form of malaria. The parasite’s complex life cycle involves both mosquito and human hosts, but it is during the human blood stage that symptoms arise. Here, parasites rapidly invade human red blood cells (RBCs) and develop into 32 parasite daughter cells. The process of invasion involves multiple interactions between the parasite and RBC; parasite proteins specifically recognise and engage with receptor proteins on the host cell. The role played by specific individual host receptor proteins in the invasion process is not well understood, but likely involves the context of the local environment, characteristics and properties of the protein. This is a protein that is reported to be highly mobile and can interact with other membrane proteins under certain conditions. To further current understanding behind the molecular mechanism of invasion, this project will also aim to identify other host proteins recruited to the local site of invasion and explore the reason behind their selection.

Thematic Categories

Basic Science

Date

Sep 2022 — Sep 2025

Funding Details
Wellcome Trust, United Kingdom

Grant ID: 227196/Z/23/Z
Project Site

United Kingdom

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