Results 201 to 210 of about 43,964 (292)

Disruption of iron metabolism resulting from Dmt1/Slc11a2 deficiency compromises Notch protein degradation and transcriptional activation

open access: yesThe FEBS Journal, EarlyView.
Divalent metal transporter 1 (Dmt1) maintains iron homeostasis and lysosomal proteostasis required for physiological Notch receptor–ligand signaling. Dmt1 loss lowers iron storage capacity (ferritin), increasing intracellular Fe2+, driving ROS and lipid peroxidation, and leading to lysosomal/mitochondrial dysfunction.
Rui Zhang   +5 more
wiley   +1 more source

Hsp70 diversification and repurposing across the tree of life: Lessons from the evolutionary and mechanistic trajectory of the Hsp70–Hsp110 chaperone system

open access: yesThe FEBS Journal, EarlyView.
Evolutionary and mechanistic divergence in the Hsp70–Hsp110 chaperone system. Prokaryotic Hsp70s probably diversified into multiple orthologues that cooperated with co‐chaperones such as JDPs and NEF, forming increasingly complex proteostasis networks.
Pierre Goloubinoff   +2 more
wiley   +1 more source

Biogenesis of TNF‐α‐insights into proteostasis and inflammation

open access: yesThe FEBS Journal, EarlyView.
TNF‐α biogenesis, trafficking, and signalling are tightly and reciprocally coupled to cellular proteostasis systems, including ER chaperones and endoplasmic reticulum‐associated degradation. This bidirectional crosstalk determines whether TNF‐α responses are adaptive or proteotoxic.
Bailasan Haidar   +3 more
wiley   +1 more source

Arsenite methyltransferase 3 is required for mitochondrial function and hepatic lipid metabolism

open access: yesThe FEBS Journal, EarlyView.
AS3MT is a protein that helps the body process arsenic, a naturally occurring toxin found in water and soil. We discovered it also helps cells make and use energy properly. Without AS3MT, cells' mitochondria do not work well, leading to fatty liver and reduced activity. Increasing AS3MT in liver cells restores energy and protects against arsenic damage,
Patrice Delaney   +10 more
wiley   +1 more source

Iloperidone treatment mitigates the Juvenile Huntington's Disease phenotype possibly via Sigma‐1 Receptor Modulation

open access: yesThe FEBS Journal, EarlyView.
We investigated the potential of iloperidone as an activator of Sigma‐1 receptor (S1R) neuroprotective function in juvenile Huntington's disease (jHD). We tested iloperidone on cortical neurons differentiated from patient‐derived iPSCs, demonstrating that it acts as a S1R agonist, decreasing apoptosis, huntingtin aggregation, and oxidative stress ...
Ersilia Fornetti   +11 more
wiley   +1 more source

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