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| http://dx.doi.org/10.1016/j.bbagen.2021.130082 | DOI Listing |
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BackgroundWhile mutation impacts normal myelination through disruptions of iron and lipid homeostasis, the (homeostatic iron regulatory gene) polymorphism directly participates in white matter (WM) myelination and neuroinflammations processes via modulating iron homeostasis.ObjectiveThis study investigated effects of polymorphism in gene carriers in the context of WM degeneration and neuroinflammation in Alzheimer's disease (AD).MethodsWM degeneration in AD subjects of carriers with and without polymorphism was evaluated and compared with age- and sex-matched cognitive normal (CN) groups using diffusion tensor imaging (DTI) data from the Alzheimer's Disease Neuroimaging Initiative database.
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Institut für Physikalische Biologie, Heinrich-Heine-Universität, Düsseldorf, Germany.
Directed evolution leverages the principles of natural selection to engineer biomolecules with desired properties. Microbead-based approaches within water-in-oil emulsions have proven invaluable for high-throughput selections. However, highly aggregation-prone microbeads present significant challenges, including clustering, inconsistent distribution, and droplet instability.
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Osteoarthritis (OA) is a prevalent degenerative joint disease affecting over 530 million individuals worldwide. Recent studies suggest a potential link between iron overload, a condition characterised by the excessive accumulation of iron in the body, and the onset of OA. Iron is essential for various biological processes, and any disruption in its homeostasis can trigger significant health effects, including OA.
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is a commensal of the human upper respiratory tract that can infect diverse host niches due, at least in part, to its ability to withstand both endogenous and host-mediated oxidative stresses. Here, we show that , a gene previously linked to iron import, is essential for manganese recruitment the HfeBCD transporter. Structural analyses show that metal binding in HfeA uses a unique mechanism that involves substantial rotation of the C-terminal lobe of the protein.
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Background: Glioblastoma (GBM) displays alterations in iron that drive proliferation and tumor growth. Iron regulation is complex and involves many regulatory mechanisms, including the homeostatic iron regulator () gene, which encodes the homeostatic iron regulatory protein. While is upregulated in GBM and correlates with poor survival outcomes, the function of HFE in GBM remains unclear.
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