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Lee J. Sweetlove

Researcher at University of Oxford

Publications -  133
Citations -  13759

Lee J. Sweetlove is an academic researcher from University of Oxford. The author has contributed to research in topics: Mitochondrion & Metabolic network. The author has an hindex of 61, co-authored 128 publications receiving 12314 citations. Previous affiliations of Lee J. Sweetlove include University of Cambridge & University of St Andrews.

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Respiratory metabolism: glycolysis, the TCA cycle and mitochondrial electron transport.

TL;DR: A wide range of molecular and biochemical strategies have been adopted to elucidate the functional significance of these interactions between mitochondrial function in the photosynthetic and photorespiratory processes, amino-acid biosynthesis and the regulation of cellular redox.
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Not just a circle: flux modes in the plant TCA cycle

TL;DR: Alternative, non-cyclic flux modes occur in leaves in the light, in some developing oilseeds, and under specific physiological circumstances such as anoxia.
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The impact of oxidative stress on Arabidopsis mitochondria.

TL;DR: Using H2O2 as a model stress, further work revealed that this treatment induced a protease activity in isolated mitochondria, putatively responsible for the degradation of oxidatively damaged mitochondrial proteins and that O2 consumption by mitochondria was significantly decreased by H2 O2 treatment.
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Integrated Analysis of Metabolite and Transcript Levels Reveals the Metabolic Shifts That Underlie Tomato Fruit Development and Highlight Regulatory Aspects of Metabolic Network Behavior

TL;DR: Several aspects of the regulation of metabolism during fruit ripening were revealed, and it was apparent that transcript abundance was less strictly coordinated by functional group than metabolite abundance, suggesting that posttranslational mechanisms dominate metabolic regulation.
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Analysis of the Arabidopsis Mitochondrial Proteome

TL;DR: Analysis of full-length putative protein sequences using bioinformatic tools to predict subcellular targeting (TargetP, Psort, and MitoProt) revealed significant variation in predictions, and also a lack of mitochondrial targeting prediction for several characterized mitochondrial proteins.