Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 Proteins (SLC2A3)

Human Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) interaction partners

1. means of immunolabeled cells for GLUT-3 varied approximately from 19% to 73%

2. PPAR-gamma and Akt regulate GLUT1 and GLUT3 surface localization during Mycobacterium tuberculosis infection

3. miR-29c was down-regulated in Prostate cancer samples. SLC2A3, a regulator of glycolysis, was validated as a direct target of miR-29c. Moreover, functional studies showed miR-29c could inhibit cell growth, induce apoptosis and deceased the rate of glucose metabolism.

4. Both common and rare SLC2A3 variation impacting regulation of neuronal glucose utilization and energy homeostasis may result in neurocognitive deficits known to contribute to ADHD risk.

5. N-methyl-D aspartate (NMDA) receptor activity increases GLUT3 expression.

6. identify a subset of tumors within the "proneural" and "classical" subtypes that are addicted to aberrant signaling from integrin alphavbeta3, which activates a PAK4-YAP/TAZ signaling axis to enhance Glut3 expression

7. GLUT3-mediated glucose utilization and glycogenolysis in platelets promotes alpha-granule release, platelet activation, and postactivation functions.

8. Studies suggest that a combination of glucose transporter s (GLUTs) 1 and 3 might help predict malignancy of cancers and direct effective cancer therapy.

9. We found that insulin 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

10. effects of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4 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.

11. High Glut3 expression is associated with gastric cancer.

12. Both Glut1 and GLUT3 are strongly expressed by papillary thyroid carcinomas, and their expressions were significantly associated with the presence of the BRAF V600E mutation.

13. GLUT3 and OCT4 expression were correlated suggesting that Human embryonic stem cells self-renewal is regulated by the rate of glucose uptake.

14. 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

15. We observed a strong relationship between characteristics of adaptive change to hypoxia, GLUT3 expression among birth weight-discordant twin

16. Leptin at concentrations used in the study does not change glucose transport into lymphocytes and seems to have no influence on the expression of GLUT1, GLUT3, GLUT4 and and leptin receptors

17. The SLC2A3 duplication was the most frequent CNV detected and the only significant finding in our combined analysis , indicating that the SLC2A3 duplication might serve as a genetic modifier of congenital heart defect

18. Positive expression of SLC2A1, SLC2A3, and HIF-1alpha genes was noted in 83.9, 82.1, and 71.7% of SCC specimens and in 34.4, 59.4, and 62.5% of laryngeal cancer samples. Higher levels of mRNA/protein for GLUT1 and HIF-1alpha were noted in SCC compared to NCM

19. Glut3 is a downstream target of mTORC1, and it is critical for oncogenic mTORC1-mediated aerobic glycolysis and tumorigenesis.

20. Data from human genetic analysis, molecular biology and a Drosophila Huntington's disease (HD) model strongly support the hypothesis that increased dosage of SLC2A3 ameliorates HD phenotypes.

Mouse (Murine) Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) interaction partners

1. 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.

2. Neonatal hypothyroridism downregulates the expressions of GLUT3 and GLUT8 in the testis of perpubertal mice.

3. GLUT3-mediated glucose utilization and glycogenolysis in platelets promotes alpha-granule release, platelet activation, and postactivation functions.

4. 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

5. 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

6. Glut3 is a downstream target of mTORC1, and it is critical for oncogenic mTORC1-mediated aerobic glycolysis and tumorigenesis.

7. GLUT3 levels in the brains of scrapie-infected animals was significantly downregulated.

8. Placental endoplasmic reticulum stress by administration of Tun causes downregulation of Slc2a1(GLUT1) and upregulation of Slc2a3(GLUT3) mRNA expression.

9. 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

10. 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.

11. 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.

12. 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.

13. In glut3(+/-) mice, a key role of placental Glut3 in mediating transplacental and intraplacental glucose transport was established.

14. Hesperetin and hesperidin downregulate Akt, GLUT3, and GLUT4 of the insulin signaling pathway in Abeta1-42-induced Neuro-2A cells.

15. This study demonistrated that Glut3 haploinsufficiency does not impair brain glucose uptake or utilization.

16. 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

17. phosphorylated CREB and Sp3 induce GLUT 3 expression in response to development/cell differentiation and neurotransmission

18. 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

19. Trophectodermal deficiency of GLUT3 adversely affects in vivo embryonic development in th mouse.

20. Chondrocytes have the capacity to detect and respond to low oxygen availability with changes in expression of oxygen-regulated genes. Hypoxia regulation of facilitated GLUT-1 and -3 was mediated by HIF-1alpha.

Pig (Porcine) Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) interaction partners

1. 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, and SLC16A1, which suggests that HS-induced autophagy may enhance lactate secretion by sertoli cells.

2. Anti-GLUT3 predominantly labels axonal bundles. TEM immunolabeling with colloidal gold displays a very specific distribution of GLUT-1 in the membranes of vascular endothelial cells and in periaxonal astrocyte expansions

Cow (Bovine) Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) interaction partners

1. Low GLUT1 and GLUT3 expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin responsive.

2. GLUT3 gene expression increased during late lactation.

3. distinct regulation by glucose deprivation in chromaffin cells