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1. -inositol (MI) is an essential metabolite for cell function in animals and humans. The aim of this study was to characterise the transport mechanism of MI in the small intestine of laying hens as there is a lack of knowledge about the MI uptake mechanisms.

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Gene switch for l-glucose-induced biopharmaceutical production in mammalian cells.

Biotechnol Bioeng

June 2021

Department of Biosystems, Science and Engineering, ETH Zurich, Basel, Switzerland.

In this study, we designed and built a gene switch that employs metabolically inert l-glucose to regulate transgene expression in mammalian cells via d-idonate-mediated control of the bacterial regulator LgnR. To this end, we engineered a metabolic cascade in mammalian cells to produce the inducer molecule d-idonate from its precursor l-glucose by ectopically expressing the Paracoccus species 43P-derived catabolic enzymes LgdA, LgnH, and LgnI. To obtain ON- and OFF-switches, we fused LgnR to the human transcriptional silencer domain Krüppel associated box (KRAB) and the viral trans-activator domain VP16, respectively.

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Glucose transporters in cardiovascular system in health and disease.

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Institut de Recherche Expérimentale et Clinique, Pole of Cardiovascular Research, Université catholique de Louvain, Avenue Hippocrate 55, B1.55.05, B-1200, Brussels, Belgium.

Glucose transporters are essential for the heart to sustain its function. Due to its nature as a high energy-consuming organ, the heart needs to catabolize a huge quantity of metabolic substrates. For optimized energy production, the healthy heart constantly switches between various metabolites in accordance with substrate availability and hormonal status.

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SMIT (Sodium-Myo-Inositol Transporter) 1 Regulates Arterial Contractility Through the Modulation of Vascular Kv7 Channels.

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October 2020

Vascular Research Centre, Institute of Molecular & Clinical Sciences, St George's, University of London, United Kingdom (V.B., J.B.S., S.N.B., I.A.G.).

Objective: The SMIT1 (sodium:myo-inositol transporter 1) regulates myo-inositol movement into cells and responses to hypertonic stimuli. Alteration of myo-inositol levels has been associated with several diseases, including hypertension, but there is no evidence of a functional role of SMIT1 in the vasculature. Recent evidence showed that in the nervous system SMIT1 interacted and modulated the function of members of the Kv7 family of voltage-gated potassium channels, which are also expressed in the vasculature where they regulate arterial contractility.

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