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Exogenous GLUT1 expression after AAV-GLUT1 injection approximated that of physiological human GLUT1 expression. Local central nervous system administration of AAV-GLUT1 improved CSF glucose levels and motor function of GLUT1-deficient mice and minimized off-target effects.
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AQP7 and GLUT1 mRNA and protein have a higher expression in T1DM mice, but the levels of AQP9 mRNA and protein are not changed in the lung difference between normal and T1DM mice. T1DM may increase the expression of transporters of trivalent inorganic arsenic.
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Corticotropin releasing hormone and 8-Br-cAMP led to robust GLUT1 upregulation and increased membrane translocation.
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Biochemical studies identify a Bmp-mTORC1-Hif1a signaling cascade resulting in upregulation of Glut1 in chondrocytes that is essential for murine skeletal development.
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Adequate Glut1 protein is indispensable for the proper development and maintenance of the capillary network of the brain.
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Immunoreactivity of vGluT1 in continuous theta-burst stimulation (iTBS; cTBS) repeated session (RS) decreased, while GLT-1 increased in cTBS SS and cTBS RS, compared to control
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Expression of GLUT1 is stimulated by hyperglycemia and low oxygen supply, and this overexpression was associated with increased activity of GLUT1 in the cell membrane that contributes to the impairment of the RPE secretory function of PEDF.
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GLUT1 may play an important role in Prostate Cancer progression via mediating glycolysis and proliferation. There is potential crosstalk between GLUT1-mediated glycolysis and androgen sensitivity in Prostate Cancer.
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ARAP2 knockdown did not affect fatty acid uptake but reduced basal glucose uptake, total levels of the glucose transporter GLUT1, and GLUT1 levels in the plasma membrane and the lipid micro-domain fraction.
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TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retromer-dependent GLUT1 trafficking.
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inhibition of GLUT1 activity and/or expression is shown to impair TGF-beta-driven fibrogenic processes, including cell proliferation and production of profibrotic mediators
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B cell leukemia-induced inhibition of T cell Akt/mTORC1 signaling and glucose metabolism drives T cell dysfunction; metabolic defects included reduced Akt/mammalian target of rapamycin complex 1 (mTORC1) signaling, decreased expression of the glucose transporter Glut1 and hexokinase 2, and reduced glucose uptake
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This study demonstrates a strict requirement for GLUT1 in the early stages of mammary tumorigenesis in vitro and in vivo.
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GLUT1-dependent glycolysis regulates fibrogenesis in aged lung.
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Data (including data from studies using transgenic mice) suggest that Glut1 (glucose transporter type 1) is a critical downstream target of Hif1a (hypoxia-inducible factor 1, alpha subunit) mediating hyperglycemia-induced extracellular matrix accumulation in kidney via regulation of Nox4 (NADPH oxidase type 4) expression in nephropathy due to diabetes type 1.
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CRISPR/Cas9-mediated disruption of the Hdac2 gene increased Slc2a1 expression, suggesting that it is one of the responsible histone deacetylases (HDACs). These results confirm that b-OHB is a HDAC inhibitor and show that b-OHB plays an important role in fasting-induced epigenetic activation of a glucose transporter gene in the brain.
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Taken together, the data suggest that curcumin binds directly to GLUT1 at a site that overlaps with the cytochalasin B binding site and thereby inhibits glucose transport.
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overnutrition during early life induces short-term metabolic disturbances, impairment in heart insulin signaling, up-regulates GLUT-1 and switch cardiac fuel preference in juvenile mice
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alpha(1)-AR activation is anti-apoptotic and protective during cardiac ischemia due to glucose deprivation and not hypoxia by enhancing glucose uptake into the heart via PKCdelta-mediated GLUT translocation that may be specific to the alpha(1A)-AR subtype.
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Glut1 connects the enhanced glucose uptake in atheromatous plaques of ApoE(-/-) mice with their myelopoiesis through regulation of hematopoietic stem and multipotential progenitor cell maintenance and myelomonocytic fate.
