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Finally, mTOR-mediated regulation of mitochondrial oxidative function occurs through regulation of a transcription factor termed YY1 [9].
Among the effects of mTOR signaling, regulation of gene expression and transcription is well characterized for several specific genes, including DNA polymerase I (Pol I), Insulin Growth Factor II (IGF II), ribosomal DNA [6] [8] and regulators of mitochondrial oxidative function [9].
This protocol has been shown to robustly measure mitochondrial oxidative function during recovery from exercise [ 34, 53].
98, 101 Estrogen-related receptor alpha expression may also favor mitochondrial oxidative respiration in breast cancer cells through its regulation of genes involved in mitochondrial oxidative function.
34 Indeed, improved muscle mitochondrial oxidative function 38 as well as muscle energy metabolism 39 following vitamin D treatment may provide mechanistic explanations for improved strength and endurance.
6. Measurement of mitochondrial oxidative function We will use custom-built exercise apparatus to allow each participant to perform a standardised exercise protocol as previously described by members of our group [ 34, 53, 54], consisting of plantar flexion against fixed resistance during which time 31 P-MRS will be used to assess mitochondrial oxidative function (see Figure 2.
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The change of mitochondrial oxidative respiratory function by CSD under hypoxic conditions can partly be attenuated by flunarizine.
A Clark oxygen electrode system (OxygraphTM, Hansatech Instruments, King's Lynn, UK) was used to test the mitochondrial oxidative phosphorylation function.
Similarly, X-rays were shown to induce increase in mitochondrial mass and oxidative function under the cell-cycle control, whereas oncocytic relapses, tumours with an aberrant mitochondrial biogenesis, were observed to occur post-radiotherapy of colorectal cancers.
These changes seem to affect protein function, mitochondrial oxidative phosphorylation, excitation-contraction coupling, calcium kinetics, myofilament activation, matrix composition and regeneration, cell growth and size, and apoptosis process [ 14].
From the present study, we cannot deduce if the training-induced increase in mitochondrial content and enhanced oxidative function is responsible for the improved insulin sensitivity as seen in type 2 diabetic patients and control individuals.
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