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It was found that SLC2A5, which encodes solute carrier family 2 member 5 (SLC2A5, previously termed GLUT5) facilitates cell fructose uptake and was up-regulated in Philadelphia chromosome-positive ALL.
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High expression of SLC2A5 in SUP-B15/R acute lymphoblastic leukemia cells leads to increased fructose absorption, and further activates PI3K/AKT pathway which cause the SUP-B15 cell resistance to imatinib.
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Besides GLUT1, GLUT5 seems to be regulated under hypoxia.
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identified amino acid residues of GLUT5 that define its substrate specificity for glucose transporter 5 (GLUT5)-mediated fructose transport.
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fructose can be used by glioma cells, and restrict the fructose intake or targeting GLUT5 could be efficacious strategies in glioma.
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SLC2A5-inhibits the human normal adjacent lung adenocarcinoma cytoplasmic pro-B cell development mechanism network.
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SGLT1 and GLUT5 expression in the plasma membrane is regulated by TNFalpha, leading to alteration on sugar transport, suggesting that TNFalpha could be a physiological local regulator of nutrient absorption in response to an intestinal inflammatory status.
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This study determined if single nucleotide polymorphisms in genes involved in fructose transport,SLC2A2 and SLC2A5 and metabolism, etohexokinase affect inter-individual variability in metabolic phenotypes.
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[(99m)Tc]GLA uptake is related to GLUT-5 transporter expression and transport
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In high grade prostatic intraepithelial neoplasia, Glut-1 was immunohistochemically undetectable and Glut-5 localized to the apical portion of the plasma membrane of the hyper-proliferative cells
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A role for the GLUT5 isoform in fructose uptake that takes place in clear renal cell carcinoma cells and which subsequently leads to the malignant progression.
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these results suggest that methylation of histone H3 at K4 and acetylation of histones H3 and H4 are involved in SLC2A5 gene induction associated with intestinal differentiation of Caco-2 cells.
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Fructose modulation of GLUT5 mRNA stability via cyclic AMP-signalling pathway and PABP (polyadenylated-binding protein)-interacting protein (Paip) 2.
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Differentiation of THP-1 monocytes into macrophages was associated with marked induction of GLUT 3 and GLUT 5 protein expression, and high levels of GLUT 1, GLUT 3, and GLUT 5 were maintained after transformation to foam cells.
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GLUT4 and GLUT12 were predominantly expressed in type I oxidative fibers; however, GLUT5 was expressed predominantly in type II (white) fibers
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GLUT5 expression is dramatically increased in diabetic muscle and pioglitazone treatment reverses this overexpression.
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These results suggest that inactivation of p44/42 MAPK enhances T(3)-induced GLUT5 gene expression in Caco-2 cells through increasing TRalpha-1 transactivity and binding activity to the GLUT5-TRE, probably due to de-phosphorylation of TRalpha-1.
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De-phosphorylation of GR at Ser203 in nuclei associates with GR nuclear translocation and GLUT5 gene expression in Caco-2 cells.
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These results suggest that the histone H3 di-methylation at lysine 9, as well as acetylation at lysine 9/14, may be indispensable for coordinated induction of the GLUT5 gene by p44/42 MAP kinase inhibition and the glucocorticoid hormone.
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Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose-induced hypertension.