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Higher expression of GLUT-4 is associated with Oral Epithelial Dysplasia compared to Oral Squamous Cell Carcinoma.
Adipose tissue sirtuin 1 was related to insulin sensitivity. The relationship was still present after controlling for BMI, however, it disappeared after controlling for adipose tissue SLC2A4. Muscle sirtuin 1 was not related to insulin sensitivity.
Results showed that GLUT4 translocation is regulated by TBC1D15 affecting glucose uptake.
This review will summarize the effects of phytochemicals and their action on insulin signaling pathways accelerating GLUT4 translocation based on the current literature.
Our results demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are effective in lowering serum RBP4 levels.
Cell-autonomous adiposity results from increased cell surface GLUT4 due to ankyrin-B deficiency in humans and mice.
The authors show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphorylation of the kinase domain but not mTORC2 phosphorylation of the hydrophobic domain. Nonetheless, an intact hydrophobic domain is required for Glut4-mediated glucose uptake.
rs5435 was not associated with T1D in the Euro-Brazilian population.
Three polymorphisms (rs2654185, rs5415, and rs5417) in SLC2A4 were positively correlated with hip circumference and the rs2654185 locus was also positively associated with thigh circumference. Consumption of n-3 polyunsaturated fatty acids modifies associations between SCD, SLC2A4, and SREBF1 polymorphisms and anthropometric variables and metabolic phenotypes.
increased GLUT4 expression in oral squamous cell carcinoma patients was significantly associated with a poor overall survival (OS, P = 0.035) and recurrence-free survival (RFS, P = 0.001). Furthermore, the ectopic overexpression of GLUT4 in cell lines with low endogenous GLUT4 expression resulted in a significant increase in migratory ability both in vitro and in vivo
The results of the study confirmed the presence of GLUT-1, GLUT-4 and GLUT-9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin therapy may increase placental expression of GLUT-4 and GLUT-9, and partially GLUT-1, in women with pregestational and gestational diabetes mellitus.
our study has found that BMI, hypertension, myometrial invasion, pathological type, and Glut4 positive expression might be prognostic factors of EC [Endometrial cancer ]
Our work highlights the convenience and efficiency of this novel pH-sensitive fluorescent probe and reveals the new biological activity of staurosporine as an agonist for GLUT4 translocation and as an effective insulin additive analogue.
studies demonstrate that Elmo2 is a new regulator of insulin-dependent Glut4 membrane translocation through modulating Rac1 activity and Akt membrane compartmentalization.
This review focuses on recent advances on the role of these signaling pathways and transcription factors involved in the regulation of CD36 and GLUT4.
effects of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4 and GLUT3. The anionic phospholipids, phosphatidic acid, phosphatidylserine, phosphatidylglycerol, and phosphatidylinositol, were found to be essential for transporter function by activating it and stabilizing its structure.
These results suggest that the initial event caused by overnutrition may be oxidative stress, which produces insulin resistance, at least in part, via carbonylation and oxidation-induced inactivation of GLUT4.
A single bout of exercise elicited similar GLUT4 translocation in skeletal muscle of PCOS and Controls. The absence of impairment in GLUT4 translocation suggests that PCOS patients with obesity and insulin resistance may benefit from exercise training.
SLC2A4 gene expression level was slightly lower within type 2 diabetic patients in both type of tissues. Furthermore, the negative correlation between SLC2A4 gene expression level in visceral adipose tissue and BMI has been noticed
Leptin at concentrations used in the study does not change glucose transport into lymphocytes and seems to have no influence on the expression of GLUT1, GLUT3, GLUT4 and and leptin receptors
Feed intake remains low whereas respiratory frequency and body temperature remain higher and expression of HSP90, CAT1, SGLT1 and GLUT4 increases in some tissues in pigs under chronic heat stress conditions.
TBC1D4, insulin receptor and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.
analysis of time- and breed-specific expression patterns of GLUT2 and GLUT4, which highlight their potential as candidate genes for assessing adipose deposition and muscle development in pigs
Chronic elevated calcium blocks AMPK-induced GLUT-4 expression in skeletal muscle.
Insulin resistance was associated with a significantly reduced total GLUT4 content in omental adipose tissue, without a change in content in other visceral or subcutaneous adipose sites.
There was a significant difference when pooled means for Glut-4 expression in muscle compared with adipose tissue from different anatomical sites.
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.
Results of the present study suggest that myostatin inhibits the expression of GLUT4 mRNA and that the greater ability of double muscled cattle to produce muscle may be due to their greater sensitivity to insulin and greater use of glucose.
GLUT4 gene expression increased during late lactation.
These results suggest that goat GLUT4 functions in the transport of glucose and it may play a positive role in amino acid uptake in mammary glands.
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. In the absence of insulin, this integral membrane protein is sequestered within the cells of muscle and adipose tissue. Within minutes of insulin stimulation, the protein moves to the cell surface and begins to transport glucose across the cell membrane. Mutations in this gene have been associated with noninsulin-dependent diabetes mellitus (NIDDM).
, glucose transporter type 4, insulin-responsive
, insulin-responsive glucose transporter type 4
, solute carrier family 2, facilitated glucose transporter member 4
, glucose transporter 4
, glucose transporter type 4
, solute carrier family 2 (facilitated glucose transporter), member 4
, solute carrier family 2, facilitated glucose transporter member 4-like
, Insulin-responsive glucose transporter
, insulin-responsive glucose transporter 4
, insulin-responsive glucose transporter
, Glucose transporter 4 insuline-responsive
, Glucose transporter 4, insuline-responsive
, solute carrier family 2 member 4
, solute carrier family 2 , member 4