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Sailer, J.* ; Nagel, J.* ; Akdogan, B. ; Jauch, A.T.* ; Engler, J.B.* ; Knolle, P.A.* ; Zischka, H.

Deadly excess copper.

Redox Biol. 75:103256 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Higher eukaryotes' life is impossible without copper redox activity and, literally, every breath we take biochemically demonstrates this. However, this dependence comes at a considerable price to ensure target-oriented copper action. Thereto its uptake, distribution but also excretion are executed by specialized proteins with high affinity for the transition metal. Consequently, malfunction of copper enzymes/transporters, as is the case in hereditary Wilson disease that affects the intracellular copper transporter ATP7B, comes with serious cellular damage. One hallmark of this disease is the progressive copper accumulation, primarily in liver but also brain that becomes deadly if left untreated. Such excess copper toxicity may also result from accidental ingestion or attempted suicide. Recent research has shed new light into the cell-toxic mechanisms and primarily affected intracellular targets and processes of such excess copper that may even be exploited with respect to cancer therapy. Moreover, new therapies are currently under development to fight against deadly toxic copper.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Acute Copper Toxicity ; Mitochondria ; Wilson Disease; Long-term Treatment; Wilsons-disease; Oxidative Stress; D-penicillamine; Intestinal Metallothionein; Dietary Copper; Amyloid-beta; Hepatocellular Mitochondria; Cellular Mechanisms; Oxidase Activity
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2213-2317
e-ISSN 2213-2317
Zeitschrift Redox Biology
Quellenangaben Band: 75, Heft: , Seiten: , Artikelnummer: 103256 Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOX)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-505200-003
Förderungen Bundesministerium fur Bildung und Forschung (BMBF)
Deutsche Forschungsgemeinschaft (DFG)
DOI 10.1016/j.redox.2024.103256
WOS ID 001264298100001
Scopus ID 85197243894
PubMed ID 38959622
Erfassungsdatum 2024-07-16
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