Gellerich 2009 PLoS One: Difference between revisions
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{{Publication | {{Publication | ||
|title=Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F (2009) | |title=Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F (2009) Extramitochondrial Ca2+ in the nanomolar range regulates glutamate-dependent oxidative phosphorylation on demand. PloS One 4:e8181. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20011041 PMID: 20011041 Open Access] | |||
|authors=Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F | |authors=Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F | ||
|year=2009 | |year=2009 | ||
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|abstract=We present unexpected and novel results revealing that glutamate-dependent oxidative phosphorylation (OXPHOS) of brain mitochondria is exclusively and efficiently activated by extramitochondrial Ca<sup>2+</sup> in physiological concentration ranges (S<sub>0.5</sub>= 360 nM Ca<sup>2+</sup>). This regulation was not affected by RR, an inhibitor of the mitochondrial Ca<sup>2+</sup> uniporter. Active respiration is regulated by glutamate supply to mitochondria via aralar, a mitochondrial glutamate/aspartate carrier with regulatory Ca<sup>2+</sup>-binding sites in the mitochondrial intermembrane space providing full access to cytosolic Ca<sup>2+</sup>. At micromolar concentrations, Ca<sup>2+</sup> can also enter the intramitochondrial matrix and activate specific dehydrogenases. However, the latter mechanism is less efficient than extramitochondrial Ca<sup>2+</sup> regulation of respiration/OXPHOS via aralar. These results imply a new mode of glutamate-dependent OXPHOS regulation as a demand-driven regulation of mitochondrial function. This regulation involves the mitochondrial glutamate/aspartate carrier aralar which controls mitochondrial substrate supply according to the level of extramitochondrial Ca<sup>2+</sup>. | |abstract=We present unexpected and novel results revealing that glutamate-dependent oxidative phosphorylation (OXPHOS) of brain mitochondria is exclusively and efficiently activated by extramitochondrial Ca<sup>2+</sup> in physiological concentration ranges (S<sub>0.5</sub>= 360 nM Ca<sup>2+</sup>). This regulation was not affected by RR, an inhibitor of the mitochondrial Ca<sup>2+</sup> uniporter. Active respiration is regulated by glutamate supply to mitochondria via aralar, a mitochondrial glutamate/aspartate carrier with regulatory Ca<sup>2+</sup>-binding sites in the mitochondrial intermembrane space providing full access to cytosolic Ca<sup>2+</sup>. At micromolar concentrations, Ca<sup>2+</sup> can also enter the intramitochondrial matrix and activate specific dehydrogenases. However, the latter mechanism is less efficient than extramitochondrial Ca<sup>2+</sup> regulation of respiration/OXPHOS via aralar. These results imply a new mode of glutamate-dependent OXPHOS regulation as a demand-driven regulation of mitochondrial function. This regulation involves the mitochondrial glutamate/aspartate carrier aralar which controls mitochondrial substrate supply according to the level of extramitochondrial Ca<sup>2+</sup>. | ||
|keywords=Glutamate/aspartate carrier aralar, Extramitochondrial Ca (2+), Brain mitochondria | |keywords=Glutamate/aspartate carrier aralar, Extramitochondrial Ca (2+), Brain mitochondria | ||
| | |mipnetlab=EE_Tartu Paju K, DE Magdeburg Gellerich FN | ||
|discipline=Mitochondrial Physiology, Biomedicine | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |||
|tissues=Nervous system | |||
|enzymes=Inner mt-membrane transporter | |||
|topics=Calcium, Inhibitor | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |||
|additional=Ca-list | |||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} |
Latest revision as of 09:28, 7 May 2020
Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F (2009) Extramitochondrial Ca2+ in the nanomolar range regulates glutamate-dependent oxidative phosphorylation on demand. PloS One 4:e8181. |
Gellerich FN, Gizatullina Z, Arandarcikaite O, Jerzembek D, Vielhaber S, Seppet E, Striggow F (2009) PLoS One
Abstract: We present unexpected and novel results revealing that glutamate-dependent oxidative phosphorylation (OXPHOS) of brain mitochondria is exclusively and efficiently activated by extramitochondrial Ca2+ in physiological concentration ranges (S0.5= 360 nM Ca2+). This regulation was not affected by RR, an inhibitor of the mitochondrial Ca2+ uniporter. Active respiration is regulated by glutamate supply to mitochondria via aralar, a mitochondrial glutamate/aspartate carrier with regulatory Ca2+-binding sites in the mitochondrial intermembrane space providing full access to cytosolic Ca2+. At micromolar concentrations, Ca2+ can also enter the intramitochondrial matrix and activate specific dehydrogenases. However, the latter mechanism is less efficient than extramitochondrial Ca2+ regulation of respiration/OXPHOS via aralar. These results imply a new mode of glutamate-dependent OXPHOS regulation as a demand-driven regulation of mitochondrial function. This regulation involves the mitochondrial glutamate/aspartate carrier aralar which controls mitochondrial substrate supply according to the level of extramitochondrial Ca2+. โข Keywords: Glutamate/aspartate carrier aralar, Extramitochondrial Ca (2+), Brain mitochondria
โข O2k-Network Lab: EE_Tartu Paju K, DE Magdeburg Gellerich FN
Labels: MiParea: Respiration
Tissue;cell: Nervous system
Enzyme: Inner mt-membrane transporter Regulation: Calcium, Inhibitor Coupling state: OXPHOS
HRR: Oxygraph-2k
Ca-list