@article{MTMT:30317831,
	title = {Copper signalling: causes and consequences},
	url = {https://m2.mtmt.hu/api/publication/30317831},
	author = {Kardos, Julianna and Héja, László and Simon, Ágnes and Jablonkai, István and Kovács, Richárd and Jemnitz, Katalin},
	doi = {10.1186/s12964-018-0277-3},
	journal-iso = {CELL COMM SIGN},
	journal = {CELL COMMUNICATION AND SIGNALING},
	volume = {16},
	unique-id = {30317831},
	issn = {1478-811X},
	abstract = {Copper-containing enzymes perform fundamental functions by activating dioxygen (O-2) and therefore allowing chemical energy-transfer for aerobic metabolism. The copper-dependence of O-2 transport, metabolism and production of signalling molecules are supported by molecular systems that regulate and preserve tightly-bound static and weakly-bound dynamic cellular copper pools. Disruption of the reducing intracellular environment, characterized by glutathione shortage and ambient Cu(II) abundance drives oxidative stress and interferes with the bidirectional, copper-dependent communication between neurons and astrocytes, eventually leading to various brain disease forms. A deeper understanding of of the regulatory effects of copper on neuro-glia coupling via polyamine metabolism may reveal novel copper signalling functions and new directions for therapeutic intervention in brain disorders associated with aberrant copper metabolism.},
	keywords = {GSH; Redox disproportionation and speciation of copper; Dynamic copper pool; Copper-rich aggregates; GSSG ratio; Copper chelate therapy; Neuro-glia coupling},
	year = {2018},
	eissn = {1478-811X}
}