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Data suggest that lncRNA lnc-p23154 (lnc-p23154) may play an important role in solute carrier family 2 member 1 (Glut1)-mediated glycolysis by inhibiting miR-378a-3p transcription and accelerate OSCC metastasis.
MT1 high expression was associated with good prognosis subtype (Luminal A), while GLUT1 high expression was related to poor prognosis subtype (triple-negative)
To increase CD71 and Glut1 expression.
It suggests that the reduced expression of GLUT-1 and overexpression of SGLT-2 are associated with false-negative lymph node metastases in NSCLC.
Evidence suggests that poor CD4+ T cell recovery in treated HIV-positive individuals is linked to the homozygous genotype (GG) associated with SLC2A1 SNP rs1385129 when compared to those with a recessive allele (GA/AA). Furthermore, poor response to therapy is less likely among Australian participants when compared against American participants.
Inhibiting the expression of GLUT1 in neuroblastoma cells inhibits cell proliferation, and the ability of cell invasion and migration were reduced.
Metabolic analysis showed that YC-1 shifted glucose metabolism in hypoxic cells from anaerobic glycolysis to oxidative phosphorylation (OXPHOS). Additional GI accelerated membranous GLUT1 translocation, elevating glucose uptake, and increased acetyl-CoA levels, leading to more ROS generation in hypoxic YC-1-treated cells.
Study demonstrated that downregulation of GLUT1 expression had a strong anti-proliferative effect in esophageal squamous cell carcinoma (ESCC) cells and improved their sensitivity to cisplatin. These findings provide evidence that GLUT1 plays a role in cisplatin-resistance of ESCC cells.
The authors describe two sporadic children with pure and complex hereditary spastic paraplegia (HSP) without paroxysmal non-epileptic movement disorders harboring heterozygous de novo SLC2A1 pathogenic variants
Exogenous GLUT1 expression after AAV-GLUT1 injection approximated that of physiological human GLUT1 expression. Local central nervous system administration of AAV-GLUT1 improved CSF glucose levels and motor function of GLUT1-deficient mice and minimized off-target effects.
SIRT1/GLUT1 axis promotes bladder cancer progression via regulation of glucose uptake.
Corticotropin releasing hormone and 8-Br-cAMP led to robust GLUT1 upregulation and increased membrane translocation.
Placental expression of at least three GLUT isoforms, i.e. GLUT-1, GLUT-4, and GLUT-9, may be involved in the intensification of intrauterine fetal growth in pregnancies complicated by gestational diabetes mellitus and pregnancy complicated by diabetes mellitus, type 1.
Besides GLUT1, GLUT5 seems to be regulated under hypoxia.
High glut1 expression is associated with Malignant Melanoma.
This study provides evidence that SLC2A1 gene variants might be implicated in the development of Type 2 diabetes microvascular complications.
A positive expression of GLUT1 significantly predicts a poor prognosis in lung cancer patients. GLUT1 may server as a helpful biomarker and a potential target for the treatment strategies of lung cancer.[review;meta-analysis]
SLC2A1 gene variants do not play a causative role in genetic generalized epilepsy patients with eyelid myoclonia.
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.
Although lack of Slc2a1 blunted glycolysis and the pentose phosphate pathway, MPhi were metabolically flexible enough that inflammatory cytokine release was not dramatically regulated, yet phagocytic defects hindered MPhi function in chronic diseases.
Data showed downregulation of GLUT1 expression in the retinae of mice treated with levetiracetam.
In this work, it was observed that chronic HFD administration aggravated the metabolic alterations by causing reduced ATP production, imbalanced oxidative stress and altered class 1 GLUTs expression.
Glucose uptake in microglia is facilitated predominately by GLUT1, particularly under inflammatory conditions
AQP7 and GLUT1 mRNA and protein have a higher expression in T1DM mice, but the levels of AQP9 mRNA and protein are not changed in the lung difference between normal and T1DM mice. T1DM may increase the expression of transporters of trivalent inorganic arsenic.
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.
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