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anti-Human SLC2A4 Antikörper:
anti-Mouse (Murine) SLC2A4 Antikörper:
anti-Rat (Rattus) SLC2A4 Antikörper:
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Human Polyclonal SLC2A4 Primary Antibody für FACS, ICC - ABIN4314628
Gauger, Bassa, Henchey, Wyman, Bentley, Brown, Shimono, Schneider: Mice deficient in Sfrp1 exhibit increased adiposity, dysregulated glucose metabolism, and enhanced macrophage infiltration. in PLoS ONE 2013
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Human Polyclonal SLC2A4 Primary Antibody für IHC, WB - ABIN1742482
Boyle, Logan, Jones, Small, Sattar, Connell, Cleland, Salt: AMP-activated protein kinase is activated in adipose tissue of individuals with type 2 diabetes treated with metformin: a randomised glycaemia-controlled crossover study. in Diabetologia 2011
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Human Polyclonal SLC2A4 Primary Antibody für IHC (fro), IHC (p) - ABIN2473824
Tokunaga, Uyama, Tooya, Kumamoto, Araki: [Oculopharyngeal muscular dystrophy in a Japanese family]. in Rinsh? shinkeigaku = Clinical neurology 1990
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Human Monoclonal SLC2A4 Primary Antibody für CyTOF, ELISA - ABIN4314635
Albert, Svensson, Shimobayashi, Colombi, Muñoz, Jimenez, Handschin, Bosch, Hall: mTORC2 sustains thermogenesis via Akt-induced glucose uptake and glycolysis in brown adipose tissue. in EMBO molecular medicine 2016
Human Polyclonal SLC2A4 Primary Antibody für IHC, IHC (p) - ABIN4314630
Huang, Beiting, Gebreselassie, Gagliardo, Ruyechan, Lee, Lee, Appleton: Eosinophils and IL-4 Support Nematode Growth Coincident with an Innate Response to Tissue Injury. in PLoS pathogens 2016
Mouse (Murine) Polyclonal SLC2A4 Primary Antibody für ELISA, WB - ABIN4314629
Hosgood, Menashe, He, Chanock, Lan: PTEN identified as important risk factor of chronic obstructive pulmonary disease. in Respiratory medicine 2009
Human Monoclonal SLC2A4 Primary Antibody für ICC, FACS - ABIN1724743
Sano, Peck, Kettenbach, Gerber, Lienhard: Insulin-stimulated GLUT4 protein translocation in adipocytes requires the Rab10 guanine nucleotide exchange factor Dennd4C. in The Journal of biological chemistry 2011
Human Monoclonal SLC2A4 Primary Antibody für IF - ABIN2473821
James, Strube, Mueckler: Molecular cloning and characterization of an insulin-regulatable glucose transporter. in Nature 1989
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Human Monoclonal SLC2A4 Primary Antibody für IHC (fro), WB - ABIN2473822
Berger, Biswas, Vicario, Strout, Saperstein, Pilch: Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting. in Nature 1989
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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 (zeige SCD Antikörper), SLC2A4, and SREBF1 (zeige SREBF1 Antikörper) 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 (zeige SLC2A1 Antikörper), GLUT-4 and GLUT-9 (zeige SLC2A6 Antikörper) proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin (zeige INS Antikörper) therapy may increase placental expression of GLUT-4 and GLUT-9 (zeige SLC2A6 Antikörper), and partially GLUT-1 (zeige SLC2A1 Antikörper), 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 (zeige INS Antikörper) additive analogue.
studies demonstrate that Elmo2 (zeige ELMO2 Antikörper) is a new regulator of insulin (zeige INS Antikörper)-dependent Glut4 membrane translocation through modulating Rac1 activity and Akt (zeige AKT1 Antikörper) membrane compartmentalization.
This review focuses on recent advances on the role of these signaling pathways and transcription factors involved in the regulation of CD36 (zeige CD36 Antikörper) and GLUT4.
effects of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4 and GLUT3 (zeige SLC2A3 Antikörper). 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 (zeige INS Antikörper) 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 (zeige INS Antikörper) resistance may benefit from exercise training.
Feed intake remains low whereas respiratory frequency and body temperature remain higher and expression of HSP90 (zeige HSP90 Antikörper), CAT1 (zeige SLC7A1 Antikörper), SGLT1 (zeige SLC5A1 Antikörper) and GLUT4 increases in some tissues in pigs under chronic heat stress conditions.
TBC1D4 (zeige TBC1D4 Antikörper), insulin receptor (zeige INSR Antikörper) and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.
analysis of time- and breed-specific expression patterns of GLUT2 (zeige SLC2A2 Antikörper) and GLUT4, which highlight their potential as candidate genes for assessing adipose deposition and muscle development in pigs
Chronic elevated calcium blocks AMPK (zeige PRKAA1 Antikörper)-induced GLUT-4 expression in skeletal muscle.
Insulin (zeige INS Antikörper) 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.
The disruption of SM22alpha enhances PDGF-BB-induced GLUT4 translocation and glucose uptake by promoting actin dynamics and cortical actin polymeriza- tion.
Data suggest that Glut4 expression is glucose-dependent in white adipocytes; low glucose availability reduces total NADH/NADPH (zeige FDXR Antikörper) levels; high glucose availability up-regulates total NADH/NADPH (zeige FDXR Antikörper) levels, promotes adipogenesis and lipogenesis, and induces Glut4 expression.
Glucose transporter 4 (GLUT4) is required for myocardial adaptations to exercise, and its absence accelerates heart dysfunction after pressure overload.
Data show that TBK1 (zeige TBK1 Antikörper) directly interacts with Exo84 (zeige EXO84 Antikörper) through the coiled-coil domain of TBK1 (zeige TBK1 Antikörper) and helical domain of Exo84 (zeige EXO84 Antikörper), and knockdown of TBK1 (zeige TBK1 Antikörper) blocked insulin (zeige INS Antikörper)-stimulated glucose uptake and GLUT4 translocation.
E4-ORF1 (zeige MED14 Antikörper) activation of PI3K in adipocytes recapitulates insulin (zeige INS Antikörper) regulation of FoxO1 (zeige FOXO1 Antikörper) but not regulation of Glut4. This uncoupling of PI3K effects occurs despite E4-ORF1 (zeige MED14 Antikörper) activating PI3K and downstream signaling to levels achieved by insulin (zeige INS Antikörper).
Authors suggest that sortilin (zeige SORT1 Antikörper)- and retromer-mediated Glut4 retrieval from endosomes may represent a step in the Glut4 pathway vulnerable to the development of insulin (zeige INS Antikörper) resistance and diabetes.
It was concluded that ILK (zeige ILK Antikörper) depletion modifies the transcription of GLUT4, which results in reduced peripheral insulin (zeige INS Antikörper) sensitivity and glucose uptake, suggesting ILK (zeige ILK Antikörper) as a molecular target and a prognostic biomarker of insulin (zeige INS Antikörper) resistance.
Data, including data from studies using knockout/transgenic mice, suggest that PrPC (zeige PRNP Antikörper) is involved in development of insulin (zeige INS Antikörper) resistance and obesity; primary embryonic fibroblasts cultured from PrPC (zeige PRNP Antikörper) knockout mice exhibit reduced glucose uptake upon insulin (zeige INS Antikörper) stimulation due to reduced translocation of glucose transporter Glut4 to cell membrane. (PrPC (zeige PRNP Antikörper) = cellular prion protein (zeige PRNP Antikörper); Glut4 = facilitated glucose transporter (zeige SLC2A12 Antikörper) 4)
Our findings implicate Rac1 as a regulatory element critical for controlling glucose uptake during exercise via regulation of GLUT4 translocation.
insulin (zeige INS Antikörper) and insulin (zeige INS Antikörper) resistance regulate the spatial organization of GLUT4 in adipocytes.
Low GLUT1 (zeige SLC2A1 Antikörper) and GLUT3 (zeige SLC2A3 Antikörper) expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin (zeige INS Antikörper) responsive.
Results of the present study suggest that myostatin (zeige MSTN Antikörper) 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 (zeige INS Antikörper) 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