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The gene changes of SLC2A1 pathogenic variants leading to GLUT1 deficiency and generalized epilepsies.
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genetic variation in GLUT1 is associated with Early-Stage Non-small Cell Lung Cancer.
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This meta-analysis indicates that GLUT1 expression is associated with poor prognostic and a series of clinicopathological features in breast cancer
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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
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SLC2A1 variants and haplotypes may be involved in the pathogenesis of diabetic nephropathy [meta-analysis]
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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
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Kazakh and Han patients with esophageal squamous cell carcinoma with Glut1 c-myc co-expression had poorer prognosis.
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miR-328 expression is reduced in colon cancer patients and thus inversely correlates with the classically reported upregulated SLC2A1/GLUT1 expression in tumors.
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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.
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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.
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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.
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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)
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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.
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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.
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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.
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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.
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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.
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GLUT-1 in nasopharyngeal carcinoma and its clinical significance
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PPAR-gamma and Akt regulate GLUT1 and GLUT3 surface localization during Mycobacterium tuberculosis infection.
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YAP1 interacted with TEAD1, exerted their transcriptional control of the functional target, glucose transporter 1 (Glut1).
