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The gene changes of SLC2A1 pathogenic variants leading to GLUT1 deficiency and generalized epilepsies.
genetic variation in GLUT1 is associated with Early-Stage Non-small Cell Lung Cancer.
This meta-analysis indicates that GLUT1 expression is associated with poor prognostic and a series of clinicopathological features in breast cancer
The distribution of glucose transporter 1 expression compared with heme oxygenase 1 expression in HCT116 cell spheroids seemed consistent with differential dependence of hypoxic expression of these molecules on fatty acid beta-oxidation
SLC2A1 variants and haplotypes may be involved in the pathogenesis of diabetic nephropathy [meta-analysis]
These findings promote development of metabolic-based cancer detection technologies, and suggest that 2GF-GNPs may enable specific cancer detection in a wide range of tumors characterized by high GLUT-1 expression
Kazakh and Han patients with esophageal squamous cell carcinoma with Glut1 c-myc co-expression had poorer prognosis.
miR-328 expression is reduced in colon cancer patients and thus inversely correlates with the classically reported upregulated SLC2A1/GLUT1 expression in tumors.
Glucose transporter-1 could play a role not only in the onset of psoriasis but also in the progression and severity of the disease. It may participate in the pathogenesis of psoriasis through the facilitation of epidermal hyperproliferation, inflammation, and angiogenesis.
Data suggest that GLUT1 functions as tetramer of adjacent dimers of allosteric, alternating access transporters in which (a) cis-allostery is mediated by intra-subunit interaction and (b) trans-allostery requires inter-subunit interaction. Endofacial (vs exofacial) cis-allostery obtains when affinity of un-liganded e1 (endofacial) GLUT1 subunit in one dimer is increased by occupancy of e1 GLUT1 subunit of adjacent dimer.
Results show that GLUT1 is sensitive and specific marker for colorectal cancer (CRC). It is overexpressed in young age patients, poor performance status, and stage IV patients. Although this was not statistically significant, GLUT 1 showed higher expression level in patients with lesser survival.
GLUT1 ectopic overexpression makes PCa cells more resistant to glucose deprivation and oxidative stress-induced cell death. Under glucose deprivation, GLUT1 overexpressing PCa cells sustains mitochondrial SOD2 activity, compromised after glucose removal, and significantly increases reduced glutathione (GSH)
Results confirm the positive expression of Glut1 in colorectal neoplasm (CRC) and its involvement in proliferation and cell survival of cancer cells. Its silencing inhibits the proliferation and promoted apoptosis of CRC cells by inactivating TGF-beta/PI3K-AKT-mTOR signaling pathway.
p-ERK-mediated phosphorylation and stabilization of JMJD2B during glucose deprivation contributes to its role in glucose uptake and cell viability, which may be modulated through epigenetically upregulation of GLUT1 in colon cancer cells.
work characterized the clustering distribution of GLUT1 and linked its spatial structural organization to the functions, which would provide insights into the activation mechanism of the transporter.
This study present the results from the molecular genetics study of the SLC2A1 gene in Bulgarian patients with different forms of genetic generalized epilepsy having emerged in childhood.
Expression of SLC5A5 mRNA was negatively correlated with SLC2A1 mRNA. This finding provides a molecular basis for the management of PTC with negative WBS using F-FDG PET scans. In addition, higher expression of SLC5A5 mRNA was associated with less PTC [papillary thyroid cancer] recurrence, but not with deaths.
GLUT-1 in nasopharyngeal carcinoma and its clinical significance
PPAR-gamma and Akt regulate GLUT1 and GLUT3 surface localization during Mycobacterium tuberculosis infection.
YAP1 interacted with TEAD1, exerted their transcriptional control of the functional target, glucose transporter 1 (Glut1).
Biochemical studies identify a Bmp-mTORC1-Hif1a signaling cascade resulting in upregulation of Glut1 in chondrocytes that is essential for murine skeletal development.
Adequate Glut1 protein is indispensable for the proper development and maintenance of the capillary network of the brain.
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
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.
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.
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.
TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retromer-dependent GLUT1 trafficking.
inhibition of GLUT1 activity and/or expression is shown to impair TGF-beta-driven fibrogenic processes, including cell proliferation and production of profibrotic mediators
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
This study demonstrates a strict requirement for GLUT1 in the early stages of mammary tumorigenesis in vitro and in vivo.
GLUT1-dependent glycolysis regulates fibrogenesis in aged lung.
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.
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.
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.
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
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.
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.
Enhanced GLUT1 expression in melanoma cells favors their metastatic behavior.
bright-field microscopy designed to automatically identify and segment microvessels containing the protein glucose transporter 1.
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
pGlcT, together with MEX1, contributes significantly to the export of starch degradation products from chloroplasts in A. thaliana leaves and and that this starch-mediated pathway for photoassimilate export via pGlcT and MEX1 is essential for the growth and development of A. thaliana. [pGlcT]
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.
the different conformations of the GLUT-1 transporter in luminal (blood facing) and abluminal (brain facing) membranes of bovine cerebral endothelial cells arise from differential phosphorylation of GLUT-1
Significant increases in GLUT1 gene expression were observed during early lactation.
Hyperthermia-induced Hsp90.eNOS preserves mitochondrial respiration in hyperglycemic endothelial cells by down-regulating Glut-1 and up-regulating G6PD activity.
distinct regulation by glucose deprivation in chromaffin cells
distinct domains of the glucose transporter GLUT1 mediate HTLV envelope binding and virus entry
Expression of GLUT1 was evaluated in LLC-PK1 cells grown on porous membranes for the development of an artificial kidney.
results suggest that glucose is transported to the axonal cleft intracytoplasmically and delivered to the cleft by GLUT1 transporters
This gene encodes a major glucose transporter in the mammalian blood-brain barrier. The encoded protein is found primarily in the cell membrane and on the cell surface, where it can also function as a receptor for human T-cell leukemia virus (HTLV) I and II. Mutations in this gene have been found in a family with paroxysmal exertion-induced dyskinesia.
, glucose transporter type 1, erythrocyte/brain
, hepG2 glucose transporter
, human T-cell leukemia virus (I and II) receptor
, solute carrier family 2, facilitated glucose transporter member 1
, solute carrier family 2, member 1
, Solute carrier family 2 a 1 (facilitated glucose transporter) brain
, Solute carrier family 2, facilitated glucose transporter member 1
, solute carrier family 2 (facilitated glucose transporter), member 1
, solute carrier family 2 member 1
, glucose transporter protein
, glucose transporter type 1
, solute carrier family 2 (facilitated glucose transporter), member 1 L homeolog
, glucose transport protein