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Validated All-in-One™ qPCR Primer for SLC2A4(NM_001042.2) Search again
Product ID:
HQP053960
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GLUT4
Gene Description:
solute carrier family 2 member 4
Target Gene Accession:
NM_001042.2(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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene is a member of the solute carrier family 2 (facilitated glucose transporter) family and encodes a protein that functions as an insulin-regulated facilitative glucose transporter.
Gene References into function
- The insulin-sensitive glucose transporter, GLUT4, interacts physically with Daxx
- Regulated transport of the glucose transporter GLUT4. A review.
- 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
- The expression of the glucose transporter 4 was downregulated by up to 80% in the failing heart.
- an effect of acid maltase deficiency extending to various vesicle systems linked to lysosomes. The enzyme defect may also affect the homoeostasis of receptors cycling through these organelles such as glucose transporter 4.
- Data describe the expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) co-activator 1, PPAR gamma, insulin receptor substrate-1, glucose transporter isoform-4, and mitochondrial uncoupling protein-1 in adipose tissue.
- Embedded in microvillous (maternal-facing) and basal (fetal-facing) membranes of syncytiotrophoblast, main placental barrier layer. (review)
- upregulation of the p38 mitogen-activated protein kinase pathway might contribute to the loss of GLUT4 protein expression observed in adipose tissue from type 2 diabetic patients
- Data suggest that GLUT4 is transported from the cell surface to a subdomain of the trans-Golgi network that is enriched in syntaxins 6 and 16 and that an acidic targeting motif in the C-terminal tail of GLUT4 plays an important role in this process.
- The regulation of the GLUT4 gene is of special clinical interest because insulin-mediated glucose homeostasis is highly sensitive to the levels of GLUT4 protein in muscle and adipose tissue, as evidenced in this review.
- Expression in human slow-twitch muscle fibres is not correlated with intracellular triglyceride content.
- AICAR increases glucose transport and cell-surface GLUT4 content in skeletal muscle from subjects with type 2 diabetes.
- TUG traps endocytosed GLUT4 and tethers it intracellularly, and insulin mobilizes this pool of retained GLUT4 by releasing this tether
- GLUT4 transcription activation depends on the protein-protein interaction of GEF and MEF2A
- Strength training increases the muscle content of GLUT4.
- ATPase inhibitors block translocation of GLUT4 in adipose cells by inhibiting formation of small insulin-responsive vesicles on donor intracellular membranes.
- Muscle samples were obtained before the start of cycle exercise training and 24 h after the first and seventh exercise sessions. GLUT-4 protein expression was increased after 7 days of exercise training compared to baseline.
- EHD1 and EHBP1, but not EHD2, are required for perinuclear localization of GLUT4 and reveal that loss of EHBP1 disrupts insulin-regulated GLUT4 recycling in cultured adipocytes.
- GLUT4 is present in endometrium of normal and polycystic ovary syndrome (PCOS)subjects. hyperinsulinism and obesity seem to have negative effect on endometrial GLUT4 expression in PCOS.
- 8 weeks of exercise training increases insulin-stimulated glucose disposal primarily by increasing GLUT4 protein expression without enhancing insulin-stimulated phosphatidylinositol 3-Kinase signaling.
- Expression in response to exercise training in glucose intolerant elderly men.
- The insulin-regulatable GLUT4 is expressed in the cytosol of first trimester syncytiotrophoblasts compatible with a role for GLUT4 in placental glucose transport in early pregnancy.
- endometrial GLUT4 expression is not affected by polycystic ovary syndrome itself, whereas it is reduced by obesity in those patients.
- Enhanced insulin-stimulated glycogen synthesis in human skeletal muscle cell culture coincides with increased GLUT4 mRNA expression following treatment with various antidiabetic agents.
- Hyperlipidemia, exhibited as a high free fatty acid level, modulates GLUT4 gene expression in cardiac muscle via a complex mechanism including GLUT4 and the PPARgamma genes
- Our findings that AS160 knockdown only partially releases basal GLUT4 retention provides evidence that insulin signals to GLUT4 exocytosis by both AS160-dependent and -independent mechanisms.
- GLUT4 expression is not required for adipogenic differentiation but is necessary for full lipogenic capacity of differentiated adipocytes
- Glut4 plasma membrane translocation and glucose uptake are induced by insulin and leptin in a human neuronal cell line by a phosphatidylinositol 3-kinase- dependent mechanism
- In conclusion, exercise at approximately 40 and approximately 80% V(O2 peak), with total work equal, increased GLUT4 mRNA and GLUT4 protein in human skeletal muscle to a similar extent, despite differences in exercise intensity and duration.
- results suggest that upregulation of GLUT4 gene transcription might be directly mediated by SREBP-1c in adipose tissue
- GLUT4 and GLUT12 were predominantly expressed in type I oxidative fibers; however, GLUT5 was expressed predominantly in type II (white) fibers
- Results suggest involvement of AMP-activated protein kinase in the control of expression of both metabolic genes, UCP3 and GLUT4, in the skeletal muscle of mice and of human newborns.
- Adipose LPIN1 gene expression associates with basal and insulin-mediated subcutaneous adipocyte glucose transport as well as mRNA levels of glucose transporter 4.
- Differences in GLUT4 transcription when whole adipose tissue and cell culture model systems are compared can be correlated to a posttranslational phosphorylation of the transcription factor MEF2A.
- the luminal Vps10p domain of sortilin plays the predominant role in targeting to insulin-responsive Glut4-containing vesicles
- enhanced GLUT4 activity was paralleled by increased transporter abundance in the plasma membrane. Disruption of the SGK1 phosphorylation site on GLUT4 ((S274A)GLUT4) abrogated the stimulating effect of SGK1.
- Our findings implicate the muscular GLUT4 system in the glucose intolerance of liver cirrhosis by a mechanism different from that in diabetes.
- signaling connections spanning the insulin receptor and GLUT4 [REVIEW]
- 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.
- Study indicated that further progress in teasing apart the GLUT4 code will require the development and application of novel and advanced technologies that can discriminate one molecule from another in the living cell.
- an exercise protocol designed to strain muscle carbohydrate reserves and to result in large increases in lactic acid results in a rapid upregulation of both GLUT-4 and MCT-4
- McArdle's disease muscle had higher phosphofructokinase protein content and activity as well as glucose transporter 4 (GLUT4) protein content and lower GLUT4 mRNA content than controls
- AMP-activated protein kinase (AMPK) regulates GLUT4 transcription through the histone deacetylase (HDAC)5 transcriptional repressor.
- In hyperthyroidism: 1) basal abundance of GLUT3 and GLUT4 on the plasma membrane is increased and 2) the sensitivity of the recruitment of GLUT3 and GLUT4 transporters on the plasma membrane in response to IGF-I is increased
- GLUT4 was reduced by 28% in vastus lateralis in chronic obstructive pulmonary disease.
- FXR is a new transcription factor of GLUT4, further elucidating the potential role for FXR in glucose metabolism.
- A novel GLUT4 translocation assay that is optimal for identifying negative regulators of GLUT4 translocation.