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Ali Shawki

Researcher at University of California, Riverside

Publications -  44
Citations -  1308

Ali Shawki is an academic researcher from University of California, Riverside. The author has contributed to research in topics: DMT1 & Medicine. The author has an hindex of 12, co-authored 33 publications receiving 1025 citations. Previous affiliations of Ali Shawki include University of Cincinnati & University of Cincinnati Academic Health Center.

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ZIP8 Is an Iron and Zinc Transporter Whose Cell-surface Expression Is Up-regulated by Cellular Iron Loading

TL;DR: Analysis of 20 different human tissues revealed abundant ZIP8 expression in lung and placenta and showed that its expression profile differs markedly from ZIP14, suggesting nonredundant functions, and identifies ZIP8 as an iron transport protein that may function in iron metabolism.
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Substrate Profile and Metal-ion Selectivity of Human Divalent Metal-ion Transporter-1

TL;DR: The data reveal that D MT1 selects Fe2+ over its other physiological substrates and provides a basis for predicting the contribution of DMT1 to intestinal, nasal, and pulmonary absorption of metal ions and their cellular uptake in other tissues.
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Zip14 is a complex broad-scope metal-ion transporter whose functional properties support roles in the cellular uptake of zinc and nontransferrin-bound iron

TL;DR: Whereas zinc appears to be a preferred substrate under normal conditions, it is found that Zip14 is capable of mediating cellular uptake of NTBI characteristic of iron-overload conditions and proposes a model to account for these observations.
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Functional properties of human ferroportin, a cellular iron exporter reactive also with cobalt and zinc

TL;DR: It is concluded that ferroportin is an iron-preferring cellular metal-efflux transporter with a narrow substrate profile that includes cobalt and zinc.
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Mechanisms of Intestinal Epithelial Barrier Dysfunction by Adherent-Invasive Escherichia coli.

TL;DR: Current evidence suggests that AIEC may selectively target protein components of tight junctions, leading to increased barrier permeability, which may represent one mechanism by which AIEC could contribute to the development of inflammatory bowel disease.