|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for SLC2A1(NM_006516.3) Search again
Product ID:
HQP109761
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
CSE, DYT17, DYT18, DYT9, EIG12, GLUT, GLUT-1, GLUT1, GLUT1DS, HTLVR, PED, SDCHCN
Gene Description:
solute carrier family 2 member 1
Target Gene Accession:
NM_006516.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a major glucose transporter in the mammalian blood-brain barrier. Mutations in this gene have been found in a family with paroxysmal exertion-induced dyskinesia.
Gene References into function
- GLUT1 mediates the transport of glucose across the plasma membrane down a concentration gradient without a specifc requirement for energy or hydrolysis of ATP, however, the ATP-binding domains are critical for transporter activity and kinetic properties.
- Review: structure of the human erythrocyte facilitative glucose transporter (GLUT1)
- GLUT1 is a cooperative tetramer of proteins, each presenting a translocation pathway that alternates between uptake and export states in which, at any instant, two subunits must present sugar uptake and two subunits must present sugar exit states.
- marker for discriminating hepatocellular carcinoma from other carcinomas
- consistent marker of ovarian epithelial malignancy
- Carcinoma samples displaying reduced levels of MCT1 were found to express the high affinity glucose transporter, GLUT1, suggesting that there is a switch from butyrate to glucose as an energy source in colonic epithelia during transition to malignancy
- GLUT1 is expressed by normal articular chondrocytes.
- observed differential response of individual isoforms GLUT1, GLUT3, & GLUT4 in neutrophils and granulocytes to hypoglycemia may represent a mechanism to protect the cells from the stress of glucose deprivation
- polymorphism has an effect on susceptibility to diabetic nephropathy in IDDM
- glucose transporter 1 and 3 in the placenta
- Coexpression of glucose transporter 1 and matrix metalloproteinase-2 in human cancers
- Results describe a possible non-genomic site of estrogen action near the hydrophilic pore of GLUT1.
- The expression of the glucose transporter 1 was downregulated by up to 80% in the failing heart.
- Cooperative nucleotide binding to GLUT1 and nucleotide modulation of GLUT1-mediated sugar transport are regulated by a proton-sensitive saltbridge (Glu329-Arg333/334).
- TNP-ATP binding to glucose transporter GLUT1 has been modeled as a cooperative process in which each GLUT1 protein in a complex of four proteins (subunits) presents a single nucleotide binding domain.
- Basal membrane GLUT1 is upregulated over gestation, increased in diabetic pregnancy, and decreased in chronic hypoxia, while microvillous membrane GLUT1 is unaffected. (review)
- To characterize seizure types and electroencephalographic features of glucose transporter type 1 deficiency syndrome (Glut-1 DS).
- Data show that by using RNA interference, glucose transporter 1 (GLUT1) mRNA and protein expression is reduced, leading to inhibition of a serum-mediated increase in glucose transport.
- increased GLUT-1 expression in rectal tumours was an adverse prognostic factor
- Overexpression of GLUT1 leads to cytosolic alkalinization of mesangial cells depending on functional Na+/H+ exchanger but not on Na+ independent H+ transport.
- GLUT-1 is a receptor for HTLV
- differences in GLUT1 receptor mRNA expression in two breast cancer cell lines with higher expression in MDA-MB-231; results show that invasiveness of cancer cells may be associated with the expression of glucose transporters, including GLUT1
- description of two-dimensional models for the orientation of the 12 transmembrane helices and the conformation of the exofacial glucose binding site of GLUT1
- Differentiation of THP-1 monocytes into macrophages was associated with marked induction of GLUT 3 and GLUT 5 protein expression, and high levels of GLUT 1, GLUT 3, and GLUT 5 were maintained after transformation to foam cells.
- There are two fundamentally different hepatic vascular lesions in infants and young children: GLUT1-positive hepatic infantile hemangioma (HIH) and GLUT1-negative hepatic vascular malformation with capillary proliferation (HVMCP).
- Relative proximity and orientation of helices 4 and 8 of the GLUT1 glucose transporter
- Glut1 is a useful marker of intraneural perineurioma
- hnRNP A2 acts on GLUT1 mRNA to inhibit expression of GLUT1 in a brain cancer cell line.
- High GLUT1 mRNA levels were observed only in ovarian cancer. The intensity of GLUT1 expression in malignant ovarian neoplasms was associated neither with tumor characteristics nor with patient survival.
- Basal or stimulated ROS production and Glut1 activity were significantly reduced by pretreating both cell lines with EUK-134
- Levels of GLUT1 mRNA expression in skin fibroblasts from "slow-track" patients were greater than those from "fast-track" patients with diabetic nephropathy.
- Data support a GluT1-mediated red blood cell sugar transport mechanism in which newly bound sugars are transiently sequestered within the translocation pathway where they become inaccessible to extra- and intracellular water.
- Oolymorphisms in the GLUT1 gene are associated with susceptibility to diabetic nephropathy.
- results provide additional evidence that glut-1 is a receptor for HTLV
- it is reported in this study that TGF-beta induces binding of HTLV virions and expression of glucose transporter type 1 in primary CD4(+) T lymphocytes that remain quiescent
- operational properties of GLUT1 are determined by host cell environment
- CA IX and GLUT 1 as well as VEGF and IL 6 have roles in response of in head and neck squamous cell carcinoma to radiotherapy +/- chemotherapy
- distinct domains of the glucose transporter GLUT1 mediate HTLV envelope binding and virus entry
- Glut-1, HK-II, and PCNA expression are related to uptake of 18F-FDG uptake in lung cancer
- We present an alternative hypothesis centring on presumed deficits in membrane bound glucose transporter proteins GLUT 1 and GLUT 3, either in absolute numbers or functional capacity.
- during human thymopoiesis, GLUT1 is up-regulated after beta-selection
- This review presents a model incorporating hypoxia responsive facilitative GLUT1 and GLUT3 as putative components of the glucose sensing apparatus in chondrocytes
- HIF-1alpha may have a role in recurrence and survival in superficial bladder cancer, while Glut-1 may have a role in survival in invasive bladder cancer
- GLUT1 may play a role in cementogenesis
- the exoplasmic end of helix 4 lies outside the inner helical bundle in the exofacial configuration of Glut1
- Glut1 has a role in vitamin C entry into mitochondria and confers mitochondrial protection against oxidative injury
- The GLUT-1 expression in borderline and malignant ovarian epithelial tumors was analyzed against prognosis, no statistically significant difference was identified.
- GLUT-1 may play an important role in the advancement of papillary carcinoma and lymph node metastasis.
- basal membrane fractions GLUT1 was positively correlated with birth weight at high, but not low altitude
- Data suggest that endocyclic hexose hydrogens, as with maltosaccharides in maltoporins, form pi-bonds with aromatic rings and slide between sites instead of being translocated via a single alternating site in GLUT1.
- SGK1 regulates GLUT1 and may contribute to or account for the PI3 kinase-dependent but PKB-independent stimulation of GLUT1 by insulin.
- results demonstrate the utilization of cell surface GLUT-1 in HTLV-1 infection of CD4(+) T lymphocytes and implicate a critical role for the ECL1 region in viral tropism
- Altered expression of GLUT1 was found in head and neck squamous intraepithelial neoplasia.
- In keratinizing carcinomas, GLUT1 was immunodetected peripherally, with loss of expression in central keratinized zones.
- Some detergents stabilize while others destabilize GLUT1 quaternary structure but GLUT1 does not appear to exchange rapidly between protein/lipid/detergent micelles.
- GLUT1 is expressed in the vast majority of endometrial intraepithelial and uterine serous papillary carcinoma, suggesting a biological role during the early steps of carcinogenesis in endometrial serous neoplasms.
- helix 12 of Glut1 plays a passive stabilizing role in the structure of Glut1 and is not directly involved in the transport mechanism
- GLUT1 may be a major pathway uptake of both inorganic and methylated arsenicals in erythrocytes or the epithelial cells of the blood-brain barrier, contributing to arsenic-related cardiovascular problems and neurotoxicity.
- GLUT1 expression may provide useful prognostic information in patients with salivary gland carcinoma
- The central part of the colorectal tumor, thought to be relatively hypoxic, had stronger GLUT-1 expression and a higher SUV than the periphery, in both the primary tumor and hepatic metastatic foci.
- Icreased GLUT1 levels lead to excess glucose metabolism under normoglycemic conditions and altered gene expression of pathogenetic factors involved in diabetic kidney disease.
- GLUT-1 is a sensitive and specific immunohistochemical marker enabling differential diagnosis of reactive mesothelium from malignant mesothelioma.
- GLUT-1 expression have a role in gastric carcinoma, as shown by FDG uptake representing tumor metabolism
- comparison of the expression of HIF-1alpha and GLUT-1 with various clinicopathological features of colorectal cancer
- Significant coexpression of GLUT-1, Bcl-xL, and Bax points to cooperation of all three regulatory proteins in elimination due to irreversible injury, adaptation to hypoxia, reduction of further damage, and survival of colorectal cancer cells.
- During trophoblast hypoxia glucose transporters (GLUT1/3) are upregulated via HIF-1 alpha pathway.
- glycosylation change & decrease of transport activity of GLUT1 may be 1 possible mechanism of ER stress induced by down-regulating GnT-V, & GnT-V may contribute to the regulation of glucose uptake by modifying glycosylation of GLUT1 in some tumor cells.
- The role of protein expression of hypoxia-inducible factor (HIF)-1alpha, HIF-2alpha, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1) in patients with colorectal adenocarcinomas.
- Glut-1 is induced by TCR engagement, resulting in massive increases in glucose uptake and binding of HTLV-1 and -2 envelopes to both CD4 and CD8 T lymphocytes
- Findings suggest that characteristic differences in the patterns of glucose uptake can exist according to the histological type and that GLUT1, GLUT3 and GLUT4 could be related to tumor angiogenesis in epithelial ovarian carcinoma.
- Transport regulation involves ATP-dependent conformational changes in (or interactions between) the GLUT1 C terminus and the C-terminal half of GLUT1 cytoplasmic loop 6-7.
- Gatifloxacin affects GLUT1 gene transcription, reduces GLUT1 mRNA expression and glucose transport in HepG2 cells. This may contribute to gatifloxacin induced dysglycemia especially in patients predisposed to disturbances of glycemic control.
- GLUT-1 overexpression is to some extent regulated by HIF-1alpha and is also strongly associated with histological features.
- GLUT1 expression was studied in normal and degenerate intervertebral discs.
- GLUT1 and 9 are preferentially localized to the plasma membrane and thus can account for the transport activity.
- Glut-1 plays a crucial role in determining FDG uptake in neuroendocrine (NE) lung tumors
- single nucleotide polymorphisms on gene involved with glucose metabolism and obesity may be associated with increased susceptibility to spina bifida
- in 5 cases of follicular dendritic cell sarcoma, study found diffuse intense positivity of the tumor cells for Glut-1 in all 5 cases and focal and weak immunoreaction for Claudin-1 in 3 cases
- helix 6 of Glut1 contains amino acid side chains that are critical for transport activity and structurally analogous outer helices may play distinct roles in the function of membrane transporters
- the expression of Glut 1 with (18)F-FDG [(18)F]-2-fluro-2-deoxy-D-glucose uptake, indicating that Glut 1 is a major glucose transporter expressed inCholangiocellular carcinoma
- A role for GLUT1 as an endogenous marker of tumor hypoxia is currently not supported by the available clinical data.
- GLUT-1 XbaI gene polymorphism is associated with vascular calcifications in nondiabetic uremic patients.
- In the ampulla of Vater, GLUT1 expression was associated with malignant change, and might be a useful marker of malignancy.
- Glut 1 expression levels in tumor cell lines corresponds to 2-gluSNAP cytotoxicity.
- Upregulation of HIF-1 alpha and its downstream targets GLUT1 and SDF-1 in colorectal adenomas and carcinomas may be due to hypoxia.
- intracellular charges at the MFS TM2-3 and TM8-9 signature loops and flanking TMs 3, 5, and 6 are critical for the structure of GLUT1 as are TM glycines
- GLUT-1 gene expression level and protein expression were correlated with lymph node metastasis, poor survival and clinical stage of head and neck carcinoma.
- GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak
- Expression of GLUT-1 in psoriasis and the relationship between GLUT-1 upregulation induced by hypoxia and proliferation of keratinocyte growth.
- co-occurring PED and epilepsy can be due to autosomal dominant heterozygous SLC2A1 mutations, expanding the phenotypic spectrum associated with GLUT1 deficiency and providing a potential new treatment option for this clinical syndrome.
- The TAT haplotype of the GLUT1 gene confers susceptibility to T2DM in the Tunisian population.
- Functional studies of the T295M mutation causing Glut1 deficiency: glucose efflux preferentially affected by T295M.
- No relationship between the immunohistochemical expression of Glut-1, -3, Hex I or II and glucose metabolism measured using [18F]FDG-PET in patients with high-grade glioma is observed.
- Expression of GLUT-1 is significantly reduced in low-grade oligodendroglial tumors harboring LOH 1p.
- results suggest that glucose transporter Glut-1 expression can significantly discriminate between human malignant melanoma and benign melanocytic nevi
- The GLUT1 gene confers susceptibility to diabetic nephropathy in type 2 diabetes patients in the Tunisian population.
- GLUT1 expression is increased in human ESCs when decidualized in vitro with P(4) and dibutyryl cAMP, suggesting a similar role for P(4) in human endometrium.
- Apigenin inhibits the GLUT-1 glucose transporter and the phosphoinositide 3-kinase/Akt pathway in human pancreatic cancer cells.
- analysis of glucose transporter GLUT1 topology and structural dynamics
- Erythrocyte GLUT1 transports alpha and beta sugars with equal avidity in an ATP independent manner.
- Deficiency may result in cerebral hypoxia and hyperglycemia.
- The C-terminal PDZ-binding motif of Glut1 plays a key role in growth factor regulation of glucose uptake by both allowing GIPC to promote Glut1 trafficking to the cell surface and protecting intracellular Glut1 from lysosomal degradation.
- Glut-1 may have a role in progression of oral squamous cell carcinoma
- lysyl oxidase and glucose transporter-1 expression have roles in prostate cancer progression
- Glucose transporter-1 is expressed and has a role in pancreatic carcinogenesis
