Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human SLC2A4 Antibodies:
anti-Mouse (Murine) SLC2A4 Antibodies:
anti-Rat (Rattus) SLC2A4 Antibodies:
Go to our pre-filtered search.
Human Polyclonal SLC2A4 Primary Antibody for 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
Show all 7 Pubmed References
Human Polyclonal SLC2A4 Primary Antibody for IHC (fro), IHC (p) - ABIN2473824
Tokunaga, Uyama, Tooya, Kumamoto, Araki: [Oculopharyngeal muscular dystrophy in a Japanese family]. in Rinsh? shinkeigaku = Clinical neurology 1990
Show all 4 Pubmed References
Human Polyclonal SLC2A4 Primary Antibody for 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
Show all 2 Pubmed References
Human Monoclonal SLC2A4 Primary Antibody for IHC (fro), WB - ABIN2473822
James, Strube, Mueckler: Molecular cloning and characterization of an insulin-regulatable glucose transporter. in Nature 1989
Show all 4 Pubmed References
Human Monoclonal SLC2A4 Primary Antibody for IF - ABIN2473821
Berger, Biswas, Vicario, Strout, Saperstein, Pilch: Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting. in Nature 1989
Show all 4 Pubmed References
Human Monoclonal SLC2A4 Primary Antibody for IHC (fro), IF - ABIN2473819
James, Brown, Navarro, Pilch: Insulin-regulatable tissues express a unique insulin-sensitive glucose transport protein. in Nature 1988
Show all 4 Pubmed References
Human Monoclonal SLC2A4 Primary Antibody for 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 Polyclonal SLC2A4 Primary Antibody for IF (p), IHC (p) - ABIN739445
Zhang, Yang, Ren, Qiao, He, Li, Zeng et al.: Effects of isoleucine on glucose uptake through the enhancement of muscular membrane concentrations of GLUT1 and GLUT4 and intestinal membrane concentrations of Na+/glucose co-transporter 1 (SGLT-1) ... in The British journal of nutrition 2016
Human Polyclonal SLC2A4 Primary Antibody for 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
This review will summarize the effects of phytochemicals and their action on insulin (show INS Antibodies) signaling pathways accelerating GLUT4 translocation based on the current literature.
Our results demonstrate that IR is associated with high circulating RBP4 (show POLR2D Antibodies) and that suppressed RBP4 (show POLR2D Antibodies) adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF (show Vcan Antibodies) are effective in lowering serum RBP4 (show POLR2D Antibodies) levels.
Cell-autonomous adiposity results from increased cell surface GLUT4 due to ankyrin-B (show ANK2 Antibodies) deficiency in humans and mice.
The authors show that insulin (show INS Antibodies)-stimulated Glut4-mediated glucose uptake requires PDPK1 (show PDPK1 Antibodies) phosphorylation of the kinase domain but not mTORC2 (show CRTC2 Antibodies) phosphorylation of the hydrophobic domain. Nonetheless, an intact hydrophobic domain is required for Glut4-mediated glucose uptake.
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 (show SCD Antibodies), SLC2A4, and SREBF1 (show SREBF1 Antibodies) 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 (show SLC2A1 Antibodies), GLUT-4 and GLUT-9 (show SLC2A6 Antibodies) proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin (show INS Antibodies) therapy may increase placental expression of GLUT-4 and GLUT-9 (show SLC2A6 Antibodies), and partially GLUT-1 (show SLC2A1 Antibodies), 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 (show INS Antibodies) additive analogue.
studies demonstrate that Elmo2 (show ELMO2 Antibodies) is a new regulator of insulin (show INS Antibodies)-dependent Glut4 membrane translocation through modulating Rac1 activity and Akt (show AKT1 Antibodies) membrane compartmentalization.
Feed intake remains low whereas respiratory frequency and body temperature remain higher and expression of HSP90 (show HSP90 Antibodies), CAT1 (show SLC7A1 Antibodies), SGLT1 (show SLC5A1 Antibodies) and GLUT4 increases in some tissues in pigs under chronic heat stress conditions.
TBC1D4 (show TBC1D4 Antibodies), insulin receptor (show INSR Antibodies) and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.
analysis of time- and breed-specific expression patterns of GLUT2 (show SLC2A2 Antibodies) and GLUT4, which highlight their potential as candidate genes for assessing adipose deposition and muscle development in pigs
Chronic elevated calcium blocks AMPK (show PRKAA1 Antibodies)-induced GLUT-4 expression in skeletal muscle.
Insulin (show INS Antibodies) 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.
1,2-dioleoyl-sn-glycero-3-phosphoethanolamine retains cell surface GLUT4 by suppressing PKC alpha (show PKCa Antibodies)-driven endocytic internalization of GLUT4, to enhance glucose uptake into cells and restrict an increase in the blood glucose levels after glucose loading in type 2 Diabetes Mellitus.
The data, therefore, suggest that 1,25(OH)2D3 increases glucose consumption by inducing SIRT1 (show SIRT1 Antibodies) activation, which in turn increases IRS1 (show IRS1 Antibodies) phosphorylation and GLUT4 translocation in myotubes.
G4+/- offspring on a High Fat Diet displayed early hypertension associated with increased renal gene expression of renin (show REN Antibodies) and the AT1 (show SLC33A1 Antibodies)- receptors compared to G4+/- on a C diet. This group showed decreased cardiac expression of key genes involved in fatty acid oxidation compared to WT on a C diet.
dynamin (show DNM1 Antibodies) is a molecular motor (show MYO1B Antibodies) which would be involved in GLUT4 translocation by facilitating exocytosis
Insulin (show INS Antibodies)-stimulated translocation of GLUT4 and GLUT8 (show SLC2A8 Antibodies) was down-regulated in the atria of insulin (show INS Antibodies) resistance animals, as well as their total protein expression.
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 (show FDXR Antibodies) levels; high glucose availability up-regulates total NADH/NADPH (show FDXR Antibodies) 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 (show TBK1 Antibodies) directly interacts with Exo84 (show EXO84 Antibodies) through the coiled-coil domain of TBK1 (show TBK1 Antibodies) and helical domain of Exo84 (show EXO84 Antibodies), and knockdown of TBK1 (show TBK1 Antibodies) blocked insulin (show INS Antibodies)-stimulated glucose uptake and GLUT4 translocation.
Low GLUT1 (show SLC2A1 Antibodies) and GLUT3 (show SLC2A3 Antibodies) expression in nonclassical monocytes was unaltered during differentiation into macrophages. GLUT4 mRNA was only detectable in unstimulated macrophages. Neither monocytes nor macrophages were insulin (show INS Antibodies) responsive.
Results of the present study suggest that myostatin (show MSTN Antibodies) 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 (show INS Antibodies) 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