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COST Action CA15203 (2016-2021): MitoEAGLE
Evolution-Age-Gender-Lifestyle-Environment: mitochondrial fitness mapping
Tuncay Erkan
MitoPedia topics: EAGLE
COST: Member
COST WG2: WG2 COST WG3: WG3 COST WG4: WG4
Name | Tuncay Erkan, Dr. |
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Institution | Department of Biophysics,
Faculty of Medicine, Ankara University, TR |
Address | Morfoloji Binasi, Sihhiye, 06100 |
City | Ankara |
State/Province | |
Country | Turkey |
[email protected] | |
Weblink | |
O2k-Network Lab |
Labels:
Publications
Published | Reference | |
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BEC 2020.1 doi10.26124bec2020-0001.v1 | 2020 | Gnaiger E et al β MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1. https://doi.org/10.26124/bec:2020-0001.v1 |
Makrecka-Kuka 2019 Acta Physiol (Oxf) | 2019 | Makrecka-Kuka M, Liepinsh E, Murray AJ, Lemieux H, Dambrova M, Tepp K, Puurand M, KÀÀmbre T, Han WH, de Goede P, O'Brien KA, Turan B, Tuncay E, Olgar Y, Rolo AP, Palmeira CM, Boardman NT, Wüst RCI, Larsen TS (2019) Altered mitochondrial metabolism in the insulin-resistant heart. Acta Physiol (Oxf) 228:e13430. |
Billur 2016 Biol Trace Elem Res | 2016 | Billur D, Tuncay E, Okatan EN, Olgar Y, Durak AT, Degirmenci S, Can B, Turan B (2016) Interplay between cytosolic free Zn2+ and mitochondrion morphological changes in rat ventricular cardiomyocytes. Biol Trace Elem Res 174:177-188. |
Abstracts
Published | Reference | |
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Tuncay 2020 MiP2020 | 2020 | |
Tuncay 2020 MiPschool Obergurgl | 2020 | |
Lemieux 2019b MiP2019 | 2019 | Altered mitochondrial metabolism in the diabetic heart. |
Tuncay 2018 MiP2018 | 2018 | Regulation of mitochondrial Zn2+ transporter ZIP7 effects sarco(endo)plasmic reticulum S(E)R-mitochondria coupling in hyperglycemia. |
Tuncay 2018 MiPschool Tromso C2 | 2018 | MitoTEMPO ameliorates hyperglycemia induced mitochondrial damage in cardiomyocytes. |
Durak 2017 MiP2017 | 2017 | Role of Zn2+-transporters on mitochondrial function in cardiomyocytes under pathological condition. |
Olgar 2017 MiP2017 | 2017 | Impaired mitochondrial function seems to be contributing to aging-associated abnormal heart function via increased production of reactive oxygen species. |