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Lack of Glut3 during early postnatal life, results in a reduction in dendritic spines and brain size, along with a shortened lifespan.
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1) that decrease of GLUT3 is associated with the reduction of protein O-GlcNAcylation in Alzheimer's disease (AD)brain, 2) that GLUT3 level is negatively correlated with calpain I activation in human brain, 3) that calpain I proteolyzes GLUT3 at the N-terminus in vitro, and 4) that activation of calpain I is negatively correlated with protein O-GlcNAcylation in AD brain.
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Study found no differences in mRNA or protein levels of neuronal monocarboxylate transporters (MCTs). Functional analyses revealed that neuronal MCT2 had high catalytic efficiency in Huntington's disease (HD) cells. Ascorbic acid did not stimulate lactate uptake in HD cells; and was unable to inhibit glucose transport in HD cells because they exhibit decreased expression of the neuronal glucose transporter GLUT3.
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Neonatal hypothyroridism downregulates the expressions of GLUT3 and GLUT8 in the testis of perpubertal mice.
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GLUT3-mediated glucose utilization and glycogenolysis in platelets promotes alpha-granule release, platelet activation, and postactivation functions.
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Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy
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Results define Glut3 to be a rab11-dependent trafficking cargo and suggest that impaired Glut3 trafficking arising from rab11 dysfunction underlies the glucose hypometabolism observed in Huntington's disease
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Glut3 is a downstream target of mTORC1, and it is critical for oncogenic mTORC1-mediated aerobic glycolysis and tumorigenesis.
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GLUT3 levels in the brains of scrapie-infected animals was significantly downregulated.
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Placental endoplasmic reticulum stress by administration of Tun causes downregulation of Slc2a1(GLUT1) and upregulation of Slc2a3(GLUT3) mRNA expression.
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knock-down of glucose transporter 3 in embryonic stem cells impaired the beating function of ESC-derived cardiomyocytes, suggesting its potential role in mediating stem cell differentiation
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Data suggest that co-activation of CREST (calcium-responsive transactivator) and CBP (CREB-binding protein) enhances signaling between p-Creb/AP-1 and p-HIF-1/HRE resulting in up-regulation of Glut3 gene; here, stimulus was cell hypoxia.
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Recruitment of Creb1-Mecp2 by glut3-(m)CpG contributes towards transactivation, formulating an escape from (m)CpG-induced gene suppression, and thereby promoting developmental neuronal glut3 gene transcription and expression.
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These observations collectively support a temporal contribution by transcription toward ensuring adequate tissue-specific, developmental (placenta and embryonic brain), and postnatal hypoxic brain GLUT3 expression.
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In glut3(+/-) mice, a key role of placental Glut3 in mediating transplacental and intraplacental glucose transport was established.
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Hesperetin and hesperidin downregulate Akt, GLUT3, and GLUT4 of the insulin signaling pathway in Abeta1-42-induced Neuro-2A cells.
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This study demonistrated that Glut3 haploinsufficiency does not impair brain glucose uptake or utilization.
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This is the first description of GLUT3 deficiency that forms a possible novel genetic mechanism for pervasive developmental disorders, such as the neuropsychiatric autism spectrum disorders
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phosphorylated CREB and Sp3 induce GLUT 3 expression in response to development/cell differentiation and neurotransmission
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crosstalk between an imprinted growth demand gene (Igf2) and placental supply transporter genes (Slc38a4, Slc38a2, and Slc2a3) may be a component of the genetic control of nutrient supply and demand during mammalian development