AS160 _ TBC1D4
- Known as:
- AS160 _ TBC1D4
- Catalog number:
- Y212667
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AS160 _ TBC1D4
Related genes to: AS160 _ TBC1D4
- Gene:
- TBC1D4 NIH gene
- Name:
- TBC1 domain family member 4
- Previous symbol:
- -
- Synonyms:
- KIAA0603, AS160, DKFZp779C0666
- Chromosome:
- 13q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-29
- Date modifiied:
- 2015-11-18
Related products to: AS160 _ TBC1D4
Akt substrate of 160 kDa,AS160,AS160,Homo sapiens,Human,KIAA0603,TBC1 domain family member 4,TBC1D4Akt substrate of 160 kDa,AS160,As160,Kiaa0603,Mouse,Mus musculus,TBC1 domain family member 4,Tbc1d4Anti- AS160 TBC1D4 AntibodyAnti-Mouse TBC1D4 (KIAA0603), Rabbit PolyclonalAnti-Mouse TBC1D4 (KIAA0603), Rabbit Polyclonalanti-TBC1D4 (C-Terminus)anti-TBC1D4 (Internal)anti-TBC1D4 (Internal)Anti-TBC1D4 Antibodyanti-TBC1D4, Goat polyclonal to TBC1D4, Isotype IgG, Host GoatAnti-TBC1D4, Rabbit Polyclonal to TBC1D4, Isotype , Host RabbitAntibodies: AS160 _ TBC1D4 HOST: Goat Clonality: pAbAS160 Primary Antibody, TBC1D4, Species: Human Synthetic peptide Source: Rabbit PolyclonalAS160 TBC1D4 Immunizing PeptideAS160 Polyclonal Antibody, Reactivity: H, Gene ID: 9882, Synonyms: TBC1D4 Related articles to: AS160 _ TBC1D4
- Glucose transporter type 4 (GLUT4), encoded by the gene, is the final effector of insulin-stimulated glucose uptake in insulin-sensitive tissues: skeletal muscle, adipose tissue, and cardiac muscle. Its dynamic localization, retained intracellularly under basal conditions and extensively translocated to the plasma membrane upon stimulation, makes it a master regulator of glycemic homeostasis. While the canonical insulin pathway (PI3K/Akt/TBC1D4) is the most potent and specific mechanism in the postprandial state, its dysfunction is centrally associated with insulin resistance and type 2 diabetes mellitus (T2DM). Crucially, robust alternative signaling networks function completely independently of insulin to regulate GLUT4 synthesis and translocation. Prominent among these are contraction-mediated pathways in skeletal muscle, which employ calcium signaling (via CaMKII), mechanical/metabolic stress sensors (via p38 MAPK γ/δ), and AMP-activated protein kinase (AMPK). This review critically integrates current knowledge, linking the molecular architecture and post-translational modifications of GLUT4 to the complex, tissue-specific signaling networks that govern its vesicular trafficking. We emphasize the hierarchy, redundancy, and interdependence of these pathways, highlighting differences between acute translocation and chronic transcriptional adaptations. Finally, we discuss how deciphering insulin-independent mechanisms offers promising therapeutic opportunities, particularly in identifying pharmacological targets that mimic the metabolic benefits of physical exercise. - Source: PubMed
Publication date: 2026/04/13
Ramos-Jiménez ArnulfoRubio-Valles MariazelGuereca-Arvizuo JaimeJuárez-Oropeza Marco ARamos-Hernández Javier AChávez-Guevara Isaac AGonzález-Rodríguez EverardoMoreno-Brito VerónicaHernández Torres Rosa P - Homozygous carriers of a loss-of-function variant in the sucrase-isomaltase (SI) gene (c.273_274delAG) are unable to digest sucrose and parts of starch. The variant is common only in Indigenous Arctic populations such as the Greenlandic Inuit and has been associated with a healthier metabolic profile. In a unique gene-diet intervention, we aimed to study whether the SI genotype modulates the effect of two different diets on glucose homeostasis and lipids. - Source: PubMed
Publication date: 2026/04/17
Senftleber NinnaChristensen Marie Mathilde BCarstensen BendixStæger Frederik FilipFrøst Michael BGillum Matthew PHansen TorbenJørgensen Marit E - Skeletal muscle glucose transporter 4 (GLUT4) translocation to the plasma membrane determines glucose uptake in response to insulin and exercise and is disrupted in insulin resistance, making its experimental measurement critical. Confocal light microscopy is widely used for this purpose because of its ability to provide quantitative, high-resolution spatial information from small tissue amounts. However, conventional immunofluorescence colocalization microscopy lacks sensitivity and specificity in the detection of GLUT4 translocation. We validated the use of exofacial epitope-specific GLUT4 antibodies to quantify sarcolemmal GLUT4 translocation in fixed, nonpermeabilized adult human and rodent muscle fibers. Across human, mouse, and rat muscles, these antibodies sensitively detected stimulus-induced GLUT4 translocation, and labeling was abolished in muscle-specific GLUT4-knockout muscle, confirming specificity. Importantly, this study includes the first unambiguous visualization of endogenous GLUT4 translocation in intact human skeletal muscle fibers after insulin stimulation and exercise. In TBC1D4-knockout rats, insulin-stimulated GLUT4 translocation was absent despite wild-type-level GLUT4 expression, confirming an essential role for TBC1D4 in this process. Thus, exofacial GLUT4 antibodies provide a straightforward, sensitive, and specific approach to quantify endogenous GLUT4 translocation in fixed adult skeletal muscle. - Source: PubMed
Persson Kaspar WFjeldsøe CasperFrandsen Lukas WKnudsen Jonas RKwak SeongEunWang HaiyanVoldstedlund Christian TLeandersson Magnus RWitczak Carol AWojtaszewski Jørgen F PRichter Erik ACartee Gregory DJensen Thomas E - Our previous work demonstrated that wild Ehrh. possesses notable in vitro hypoglycemic activity. This study further evaluated the effects of wild Ehrh. polyphenol extract (WPPE) on T2DM mice. WPPE treatment significantly lowered blood glucose, improved insulin resistance, and reduced hepatic oxidative stress and inflammation in T2DM mice. It could promote the production of short-chain fatty acids and regulate the relative abundance of T2DM-associated bacteria like and , and enhance hepatic glycogen synthesis through activation of the key gene involved in the PI3K/AKT/TBC1D4 pathway, resulting in hypoglycemic effect based on the gut-liver axis. These findings support WPPE as a promising dietary candidate for T2DM management. - Source: PubMed
Publication date: 2026/02/08
Cheng XinpengXie XingLuo ShiboXie QuanyuanXiang HaiyanPeng ChunyanDing QiaoFan HongbingLiu WeiZhang Lu - RNF186, which encodes a ring-finger domain-containing E3 ubiquitin-protein ligase, has previously been implicated in the regulation of lipid metabolic disorders associated with metabolic dysfunction-related fatty liver disease (MAFLD). However, the precise mechanism by which RNF186 influences glucose metabolism in the context of MAFLD remains unclear. In this study, we aimed to elucidate the role of RNF186 in the regulation of glucose metabolism, with a particular focus on skeletal muscle. - Source: PubMed
Publication date: 2025/11/28
Du JiangDu QizhangZhang YuxuanGao JingwenWang ChihengKou BeilinJiang YanZhao DunyongLin Juntang