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Difference between revisions of "Template:SUIT text D050"

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SUIT-003 O2 ce D050 protocol is designed to study CI-deficiency in [[living cells]]. Plasma membrane-permeable succinate ([[MitoKit-CII/Succinate-nv]], Snv), which is added in [[ROUTINE]] stimulates mitochondrial respiration in CI-deficient human blood cells, fibroblasts and heart fibres, acting on Complex II of the electron transfer system. Moreover, the SUIT-003 O2 ce D050 protocol allows to evaluate the [[coupling control state |coupling control]] of living cells. Respiratory capacities are tested in a sequence of coupling states: [[ROUTINE]] and [[Electron transfer pathway]]. Optionally, to study [[LEAK respiration]], the [[phosphorylation system]] is inhibited by [[oligomycin]]. The final concentration of [[oligomycin]] has to be carefully optimized for various cell types, to minimize the inhibitory effect on the [[Electron transfer pathway|electron transfer system]] which would lead to an underestimation of [[ET-capacity]].
SUIT-003 O2 ce D050 protocol is designed to study CI-deficiency in [[living cells]]. Plasma membrane-permeable succinate ([[MitoKit-CII/Succinate-nv]], Snv), which is added in [[ROUTINE]] stimulates mitochondrial respiration in CI-deficient human blood cells, fibroblasts and heart fibres, acting on Complex II of the electron transfer system. Moreover, the SUIT-003 O2 ce D050 protocol allows to evaluate the [[coupling control state |coupling control]] of living cells. Respiratory capacities are tested in a sequence of coupling states: [[ROUTINE]] and [[Electron transfer pathway]]. Optionally, to study [[LEAK respiration]], the [[phosphorylation system]] is inhibited by [[oligomycin]]. The final concentration of [[oligomycin]] has to be carefully optimized for various cell types, to minimize the inhibitory effect on the [[Electron transfer pathway|electron transfer system]] which would lead to an underestimation of [[ET capacity]].

Revision as of 16:10, 8 June 2020

SUIT-003 O2 ce D050 protocol is designed to study CI-deficiency in living cells. Plasma membrane-permeable succinate (MitoKit-CII/Succinate-nv, Snv), which is added in ROUTINE stimulates mitochondrial respiration in CI-deficient human blood cells, fibroblasts and heart fibres, acting on Complex II of the electron transfer system. Moreover, the SUIT-003 O2 ce D050 protocol allows to evaluate the coupling control of living cells. Respiratory capacities are tested in a sequence of coupling states: ROUTINE and Electron transfer pathway. Optionally, to study LEAK respiration, the phosphorylation system is inhibited by oligomycin. The final concentration of oligomycin has to be carefully optimized for various cell types, to minimize the inhibitory effect on the electron transfer system which would lead to an underestimation of ET capacity.