@article{MTMT:1133064,
	title = {Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels.},
	url = {https://m2.mtmt.hu/api/publication/1133064},
	author = {Szabadkai, G and Bianchi, K and Várnai, Péter and De Stefani, D and Wieckowski, MR and Cavagna, D and Nagy, Anikó Ilona and Balla, Tamás and Rizzuto, R},
	doi = {10.1083/jcb.200608073},
	journal-iso = {J CELL BIOL},
	journal = {JOURNAL OF CELL BIOLOGY},
	volume = {175},
	unique-id = {1133064},
	issn = {0021-9525},
	abstract = {The voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane
		mediates metabolic flow, Ca(2+), and cell death signaling between the endoplasmic
		reticulum (ER) and mitochondrial networks. We demonstrate that VDAC1 is
		physically linked to the endoplasmic reticulum Ca(2+)-release channel inositol
		1,4,5-trisphosphate receptor (IP(3)R) through the molecular chaperone
		glucose-regulated protein 75 (grp75). Functional interaction between the channels
		was shown by the recombinant expression of the ligand-binding domain of the
		IP(3)R on the ER or mitochondrial surface, which directly enhanced Ca(2+)
		accumulation in mitochondria. Knockdown of grp75 abolished the stimulatory
		effect, highlighting chaperone-mediated conformational coupling between the
		IP(3)R and the mitochondrial Ca(2+) uptake machinery. Because organelle Ca(2+)
		homeostasis influences fundamentally cellular functions and death signaling, the 
		central location of grp75 may represent an important control point of cell fate
		and pathogenesis.},
	year = {2006},
	eissn = {1540-8140},
	pages = {901-911},
	orcid-numbers = {Várnai, Péter/0000-0002-7777-806X; Nagy, Anikó Ilona/0000-0002-0519-5172}
}

@article{MTMT:1486705,
	title = {Mitochondrial calcium and oxidative stress as mediators of ischemic brain injury},
	url = {https://m2.mtmt.hu/api/publication/1486705},
	author = {Starkov, AA and Chinopoulos, Christos and Fiskum, G},
	doi = {10.1016/j.ceca.2004.02.012},
	journal-iso = {CELL CALCIUM},
	journal = {CELL CALCIUM},
	volume = {36},
	unique-id = {1486705},
	issn = {0143-4160},
	year = {2004},
	eissn = {1532-1991},
	pages = {257-264},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149}
}

@article{MTMT:1030897,
	title = {Generation of reactive oxygen species in the reaction catalyzed by alpha-ketoglutarate dehydrogenase},
	url = {https://m2.mtmt.hu/api/publication/1030897},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1523/JNEUROSCI.1842-04.2004},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {24},
	unique-id = {1030897},
	issn = {0270-6474},
	year = {2004},
	eissn = {1529-2401},
	pages = {7771-7778},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1688418,
	title = {Quasi-synaptic calcium signal transmission between endoplasmic reticulum and mitochondria},
	url = {https://m2.mtmt.hu/api/publication/1688418},
	author = {Csordas, G and Thomas, AP and Hajnóczky, György},
	doi = {10.1093/emboj/18.1.96},
	journal-iso = {EMBO J},
	journal = {EMBO JOURNAL},
	volume = {18},
	unique-id = {1688418},
	issn = {0261-4189},
	abstract = {Transmission of cytosolic [Ca2+] ([Ca2+](c)) oscillations into the mitochondrial matrix is thought to be supported by local calcium control between IP3 receptor Ca2+ channels (IP3R) and mitochondria, but study of the coupling mechanisms has been difficult. We established a permeabilized cell model in which the Ca2+ coupling between endoplasmic reticulum (ER) and mitochondria is retained, and mitochondrial [Ca2+] ([Ca2+](m)) can be monitored by fluorescence imaging. We demonstrate that maximal activation of mitochondrial Ca2+ uptake is evoked by IP3-induced perimitochondrial [Ca2+] elevations, which appear to reach values >20-fold higher than the global increases of [Ca2+](c), Incremental doses of IP3 elicited [Ca2+](m) elevations that followed the quantal pattern of Ca2+ mobilization, even at the level of individual mitochondria, In contrast, gradual increases of IP3 evoked relatively small [Ca2+](m) responses despite eliciting similar [Ca2+](c) increases. We conclude that each mitochondrial Ca2+ uptake site faces multiple IP3R, a concurrent activation of which is required for optimal activation of mitochondrial Ca2+ uptake. This architecture explains why calcium oscillations evoked by synchronized periodic activation of IP3R are particularly effective in establishing dynamic control over mitochondrial metabolism. Furthermore, our data reveal fundamental functional similarities between ER-mitochondrial Ca2+ coupling and synaptic transmission.},
	year = {1999},
	eissn = {1460-2075},
	pages = {96-108}
}

@article{MTMT:1690267,
	title = {DECODING OF CYTOSOLIC CALCIUM OSCILLATIONS IN THE MITOCHONDRIA},
	url = {https://m2.mtmt.hu/api/publication/1690267},
	author = {Hajnóczky, György and ROBBGASPERS, LD and SEITZ, MB and THOMAS, AP},
	doi = {10.1016/0092-8674(95)90430-1},
	journal-iso = {CELL},
	journal = {CELL},
	volume = {82},
	unique-id = {1690267},
	issn = {0092-8674},
	abstract = {Frequency-modulated oscillations of cytosolic Ca2+ ([Ca2+](c)) are believed to be important in signal transduction, but it has been difficult to correlate [Ca2+](c) oscillations directly with the activity of Ca2+-regulated targets. We have studied the control of Ca2+-sensitive mitochondrial dehydrogenases (CSMDHs) by monitoring mitochondrial Ca2+ ([Ca2+](m)) and the redox state of flavoproteins and pyridine nucleotides simultaneously with [Ca2+](c) in single hepatocytes. Oscillations of [Ca2+](c) induced by IP3-dependent hormones were efficiently transmitted to the mitochondria as [Ca2+](m) oscillations. Each [Ca2+](m) spike was sufficient to cause a maximal transient activation of the CSMDHs and [Ca2+](m) oscillations at frequencies above 0.5 per minute caused a sustained activation of mitochondrial metabolism. By contrast, sustained [Ca2+](c) increases yielded only transient CSMDH activation, and slow or partial [Ca2+](c) elevations were ineffective in increasing [Ca2+](m) or stimulating CSMDHs. We conclude that the mitochondria are tuned to oscillating [Ca2+](c) signals, the frequency of which can control the CSMDHs over the full range of potential activities.},
	year = {1995},
	eissn = {1097-4172},
	pages = {415-424}
}

@article{MTMT:11010306,
	title = {MEASUREMENT OF THE MATRIX FREE CA-2+ CONCENTRATION IN HEART- MITOCHONDRIA BY ENTRAPPED FURA-2 AND QUIN2},
	url = {https://m2.mtmt.hu/api/publication/11010306},
	author = {Lukács, Gergely and Kapus, A},
	doi = {10.1042/bj2480609},
	journal-iso = {BIOCHEM J},
	journal = {BIOCHEMICAL JOURNAL},
	volume = {248},
	unique-id = {11010306},
	issn = {0264-6021},
	year = {1987},
	eissn = {1470-8728},
	pages = {609-613}
}