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Facilitative glucose transporter. Additionally we are shipping SLC2A3 Antibodies (92) and SLC2A3 Kits (47) and many more products for this protein.
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GLUT3-mediated glucose utilization and glycogenolysis in platelets promotes alpha-granule release, platelet activation, and postactivation functions.
Studies suggest that a combination of glucose transporter s (GLUTs) 1 and 3 might help predict malignancy of cancers and direct effective cancer therapy.
We found that insulin (show INS Proteins) increases the cytotoxic effect of 5-fluorouracil and cyclophosphamide in vitro up to two-fold. The effect was linked to enhancement of apoptosis, activation of apoptotic and autophagic pathways, and overexpression of glucose transporters 1 and 3 as well as inhibition of cell proliferation and motility
effects of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4 (show SLC2A4 Proteins) and GLUT3. The anionic phospholipids, phosphatidic acid, phosphatidylserine, phosphatidylglycerol, and phosphatidylinositol, were found to be essential for transporter function by activating it and stabilizing its structure.
High Glut3 expression is associated with gastric cancer.
Both Glut1 (show SLC2A1 Proteins) and GLUT3 are strongly expressed by papillary thyroid carcinomas, and their expressions were significantly associated with the presence of the BRAF (show BRAF Proteins) V600E mutation.
GLUT3 and OCT4 (show POU5F1 Proteins) expression were correlated suggesting that Human embryonic stem cells self-renewal is regulated by the rate of glucose uptake.
Using lipidic cubic phase crystallization and microfocus X-ray diffraction, we determined the structure of human GLUT3 in complex with D-glucose at 1.5 A resolution in an outward-occluded conformation
We observed a strong relationship between characteristics of adaptive change to hypoxia, GLUT3 expression among birth weight-discordant twin
Leptin (show LEP Proteins) at concentrations used in the study does not change glucose transport into lymphocytes and seems to have no influence on the expression of GLUT1 (show SLC2A1 Proteins), GLUT3, GLUT4 (show SLC2A4 Proteins) and and leptin (show LEP Proteins) receptors
Morphological changes and GLUT1 (show SLC2A1 Proteins), GLUT3, and GLUT4 (show SLC2A4 Proteins) 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
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
Glut3 is a downstream target of mTORC1, and it is critical for oncogenic mTORC1-mediated aerobic glycolysis and tumorigenesis.
GLUT3 levels in the brains of scrapie-infected animals was significantly downregulated.
Placental endoplasmic reticulum stress by administration of Tun causes downregulation of Slc2a1(GLUT1 (show SLC2A1 Proteins)) and upregulation of Slc2a3(GLUT3) mRNA expression.
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
Data suggest that co-activation of CREST (calcium-responsive transactivator (show SS18L1 Proteins)) and CBP (CREB-binding protein (show CREBBP Proteins)) enhances signaling between p-Creb (show CREB1 Proteins)/AP-1 (show JUN Proteins) and p-HIF-1 (show HIF1A Proteins)/HRE resulting in up-regulation of Glut3 gene; here, stimulus was cell hypoxia.
Recruitment of Creb1 (show CREB1 Proteins)-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.
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.
These findings indicated that heat shock (HS)-induced autophagy regulates lactate secretion by inhibiting apoptosis and increasing mRNA transcript and protein levels of SLC2A3, LDHA (show LDHA Proteins), and SLC16A1 (show SLC16A1 Proteins), which suggests that HS-induced autophagy may enhance lactate secretion by sertoli cells.
Anti-GLUT3 predominantly labels axonal bundles. TEM (show TNMD Proteins) immunolabeling with colloidal gold displays a very specific distribution of GLUT-1 (show SLC2A1 Proteins) in the membranes of vascular endothelial cells and in periaxonal astrocyte expansions
Low GLUT1 (show SLC2A1 Proteins) and GLUT3 expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 (show SLC2A4 Proteins) mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin (show INS Proteins) responsive.
GLUT3 gene expression increased during late lactation.
Facilitative glucose transporter. Probably a neuronal glucose transporter.
solute carrier family 2 (facilitated glucose transporter), member 3
, solute carrier family 2, facilitated glucose transporter member 3
, glucose transporter type 3, brain
, Solute carrier family 2 A3 (neuron glucose transporter)
, solute carrier family 2, member 2
, solute carrier family 2, member 3
, glucose transporter type 3
, neuron glucose transporter 3
, Solute carrier family 2, facilitated glucose transporter member 3
, glucose transporter 3