Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Human SLC2A4 Antikörper:
anti-Mouse (Murine) SLC2A4 Antikörper:
anti-Rat (Rattus) SLC2A4 Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
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
Show all 7 Pubmed References
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
Show all 4 Pubmed References
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
Show all 2 Pubmed References
Human Monoclonal SLC2A4 Primary Antibody für 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 für 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 für 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 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 Polyclonal SLC2A4 Primary Antibody für 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
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
This review will summarize the effects of phytochemicals and their action on insulin (zeige INS Antikörper) signaling pathways accelerating GLUT4 translocation based on the current literature.
Our results demonstrate that IR is associated with high circulating RBP4 (zeige POLR2D Antikörper) and that suppressed RBP4 (zeige POLR2D Antikörper) adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF (zeige Vcan Antikörper) are effective in lowering serum RBP4 (zeige POLR2D Antikörper) levels.
Cell-autonomous adiposity results from increased cell surface GLUT4 due to ankyrin-B (zeige ANK2 Antikörper) deficiency in humans and mice.
The authors show that insulin (zeige INS Antikörper)-stimulated Glut4-mediated glucose uptake requires PDPK1 (zeige PDPK1 Antikörper) phosphorylation of the kinase domain but not mTORC2 (zeige CRTC2 Antikörper) 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 (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 (zeige RAC1 Antikörper) activity and Akt (zeige AKT1 Antikörper) membrane compartmentalization.
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.
1,2-dioleoyl-sn-glycero-3-phosphoethanolamine retains cell surface GLUT4 by suppressing PKC alpha (zeige PKCa Antikörper)-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 (zeige SIRT1 Antikörper) activation, which in turn increases IRS1 (zeige IRS1 Antikörper) phosphorylation and GLUT4 translocation in myotubes.
G4+/- offspring on a High Fat Diet displayed early hypertension associated with increased renal gene expression of renin (zeige REN Antikörper) and the AT1 (zeige SLC33A1 Antikörper)- 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 (zeige DNM1 Antikörper) is a molecular motor (zeige MYO1B Antikörper) which would be involved in GLUT4 translocation by facilitating exocytosis
Insulin (zeige INS Antikörper)-stimulated translocation of GLUT4 and GLUT8 (zeige SLC2A8 Antikörper) was down-regulated in the atria of insulin (zeige INS Antikörper) 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 (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.
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