UK London Duchen MR

UK London Duchen MR

O2k-Network Lab	Department of Physiology University College London
Address	,
City	London
State/Prov
Country	United Kingdom
Weblink	UCL Consortium for Mitochondrial Research
Contact	Duchen Michael R
Team	Briston Thomas, Kotiadis Will, Stanzani Giacomo
Team previous
Status	O2k 2012-
Oroboros Events	IOC128, organizer of MiPschool 2015, Bioblast 2012
Topics

O2k-Publications

	Published	Reference
Saura-Esteller 2021 Int J Mol Sci	2021	Saura-Esteller J, Sánchez-Vera I, Núñez-Vázquez S, Cosialls AM, Gama-Pérez P, Bhosale G, Mendive-Tapia L, Lavilla R, Pons G, Garcia-Roves PM, Duchen MR, Iglesias-Serret D, Gil J (2021) Activation of the integrated stress response and ER stress protect from fluorizoline-induced apoptosis in HEK293T and U2OS cell lines. Int J Mol Sci 22:6117.
Connolly 2018 Cell Death Differ	2018	Connolly NMC, Theurey P, Adam-Vizi V, Bazan NG, Bernardi P, Bolaños JP, Culmsee C, Dawson VL, Deshmukh M, Duchen MR, Düssmann H, Fiskum G, Galindo MF, Hardingham GE, Hardwick JM, Jekabsons MB, Jonas EA, Jordán J, Lipton SA, Manfredi G, Mattson MP, McLaughlin B, Methner A, Murphy AN, Murphy MP, Nicholls DG, Polster BM, Pozzan T, Rizzuto R, Satrústegui J, Slack RS, Swanson RA, Swerdlow RH, Will Y, Ying Z, Joselin A, Gioran A, Moreira Pinho C, Watters O, Salvucci M, Llorente-Folch I, Park DS, Bano D, Ankarcrona M, Pizzo P, Prehn JHM (2018) Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases. Cell Death Differ 25:542-72. https://doi.org/10.1038/s41418-017-0020-4
Corrochano 2018 Hum Mol Genet	2018	Corrochano S, Blanco G, Williams D, Wettstein J, Simon M, Kumar S, Moir L, Agnew T, Stewart M, Landman A, Kotiadis VN, Duchen MR, Wackerhage H, Rubinsztein DC, Brown SDM, Acevedo-Arozena A (2018) A genetic modifier suggests that endurance exercise exacerbates Huntington's disease. Hum Mol Genet 27:1723-31.
Briston 2017 Sci Rep	2017	Briston T, Roberts M, Lewis S, Powney B, M Staddon J, Szabadkai G, Duchen MR (2017) Mitochondrial permeability transition pore: sensitivity to opening and mechanistic dependence on substrate availability. Sci Rep 7:10492.
Selwood 2017 US Patent	2017	Selwood DL, Baker D, Szabadkai G, Duchen MR, Hill JM, Warne JND (2017) Quinolium conjugates of cyclosporin. US Patent US20170349632 A1.
Briston 2016 Sci Rep	2016	Briston T, Lewis S, Koglin M, Mistry K, Shen Y, Hartopp N, Katsumata R, Fukumoto H, Duchen MR, Szabadkai G, Staddon JM, Roberts M, Powney B (2016) Identification of ER-000444793, a Cyclophilin D-independent inhibitor of mitochondrial permeability transition, using a high-throughput screen in cryopreserved mitochondria. Sci Rep 6:37798.
MiPNet20.03 IOC101 London	2015-04-21	London UK, 2015 Apr 21-23. Oroboros O2k-Workshop on HRR and O2k-Fluorometry, IOC101.
Warne 2015 J Biol Chem	2015	Warne J, Pryce G, Hill JM, Shi X, Lennerås F, Puentes F, Kip M, Hilditch L, Walker P, Simone MI, Chan AWE, Towers GJ, Coker AR, Duchen MR, Szabadkai G, Baker D, Selwood DL (2015) Selective inhibition of the mitochondrial permeability transition pore protects against neuro-degeneration in experimental multiple sclerosis. J Biol Chem 291:4356-73.
Corona 2014 Exp Neurol	2014	Corona JC, de Souza SC, Duchen MR (2014) PPARγ activation rescues mitochondrial function from inhibition of 2 complex I and loss of PINK1. Exp Neurol 253:16-27.
Logan 2014 Nat Genet	2014	Logan CV, Szabadkai G, Sharpe JA, Parry DA, Torelli S, Childs AM, Kriek M, Phadke R, Johnson CA, Roberts NY, Bonthron DT, Pysden KA, Whyte T, Munteanu I, Foley AR, Wheway G, Szymanska K, Natarajan S, Abdelhamed ZA, Morgan JE, Roper H, Santen GW, Niks EH, van der Pol WL, Lindhout D, Raffaello A, De Stefani D, den Dunnen JT, Sun Y, Ginjaar I, Sewry CA, Hurles M, Rizzuto R. UK10K Consortium, Duchen MR, Muntoni F, Sheridan E (2014) Loss-of-function mutations in MICU1 cause a brain and muscle disorder linked to primary alterations in mitochondrial calcium signaling. Nat Genet 46:188-93.

O2k-Abstracts

	Published	Reference
Logan 2015 Abstract MiPschool London 2015	2015	Loss-of-function mutations in MICU1 cause a brain and muscle disorder linked to primary alterations in mitochondrial calcium signalling.