SLC2A4 Membrane Protein Introduction

Introduction of SLC2A4

Solute carrier family 2, facilitated glucose transporter member 4 (SLC2A4), also known as glucose transporter type 4, insulin-responsive (GLUT-4), is a protein in humans that is encoded by the SLC2A4 gene. It is an insulin-regulated glucose transporter which was found primarily in adipose tissues and striated muscle.

Function of SLC2A4 Membrane Protein

GLUT4 (SLC2A4) is one of 13 sugar transporter proteins (GLUT1-GLUT12, and HMIT) encoded in the human genome that catalyzes hexose transport across cell membranes through an ATP-independent, facilitative diffusion mechanism. As a member of the GLUT family, it represents one of the most intensively studied glucose transporters, which is a major mediator of glucose removal from the circulation and a key regulator of whole-body glucose homeostasis. It contains unique sorting motifs at its N-terminus (FQQI) and C-terminal end (dileucine) that are critical for its capability to traffic between specific intracellular compartments and to translocate to the plasma membrane in response to different stimuli. Studies have shown that the expression of GLUT4 in adipocytes was decreased in obesity but increased in adipocytes and muscle cells in response to exercise.

Fig.1 Insulin-stimulated glucose transporter-4 (GLUT4) vesicle translocation to the skeletal muscle transverse tubules and sarcolemmal membranes. (Tunduguru, 2017)

Application SLC2A4 of Membrane Protein in Literature

1. Ebersbach-Silva P., et al. Palmitate-induced Slc2a4/GLUT4 downregulation in L6 muscle cells: evidence of inflammatory and endoplasmic reticulum stress involvement. Lipids in health and disease. 2018, 17(1):64. PubMed ID: 29609616
   
   

   This study aims to investigate the involvement of inflammation and ER stress in the modulation of glucose transporter GLUT4, encoded by Slc2a4 gene, in L6 skeletal muscle cells. It suggests that different pathways are activated in acute and chronic palmitate induced-repression of Slc2a4/GLUT4 expression. Furthermore, this regulation involves the activation of an initial component of ER stress, such as the formation of an IRE1a-TRAF2-IKK complex, and converges to NF-KB-induced repression of Slc2a4/GLUT4.

2. Fang P., et al. Effect of baicalin on GLUT4 expression and glucose uptake in myotubes of rats. Life sciences. 2018, 196:156-61. PubMed ID: 29459024
   
   

   The aim of this study is to survey if baicalin might facilitate glucose uptake and to explore its signal mechanisms in L6 myotubes. It suggests that baicalin could promote glucose uptake in myotubes by differential regulation on P38-MAPK and AKT activity, which providing insight that baicalin is a powerful and promising agent for the treatment of hyperglycemia via AKT/AS160/GLUT4 and P38-MAPK/PGC1α/GLUT4 pathway.

3. Aruleba R.T., et al. Structural Studies of Predicted Ligand Binding Sites and Molecular Docking Analysis of Slc2a4 as a Therapeutic Target for the Treatment of Cancer. International journal of molecular sciences. 2018, 19(2):386. PubMed ID: 29382080
   
   

   This article suggests that all the generated AMPs can serve as a therapeutic drug in treating cancer by inhibiting Slc2a4 which is responsible for the production of energy for cancer cells during angiogenesis.

4. Nishizaki T. Dioleoylphosphoethanolamine Retains Cell Surface GLUT4 by Inhibiting PKCα-Driven Internalization. Cellular Physiology and Biochemistry. 2018, 46(5):1985-98. PubMed ID: 29723855
   
   

   This article is conducted to investigate the role of 1, 2-dioleoyl-sn-glycerol-3-phosphoethanolamine (DOPE) in the trafficking of the glucose transporter GLUT4 and the glucose homeostasis. It shows that DOPE retains cell surface GLUT4 by suppressing PKCα-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 DM.

5. Wende A.R., et al. Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses. American Journal of Physiology-Heart and Circulatory Physiology. 2017, 313(6):H1098-108. PubMed ID: 28822962
   
   

   This article indicates that GLUT4 is required for the maintenance of cardiac structure and function in response to physiological or pathological processes that increase energy demands, in part through secondary changes in mitochondrial metabolism and cellular stress survival pathways such as Akt.

SLC2A4 Preparation Options

To provide high-quality membrane protein services, we have developed an advanced Magic™ membrane protein production platform which enables us to provide numerous membrane protein products. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-SLC2A4 antibody development services.

• Magic™ Membrane Protein Production Platform
• Magic™ Anti-Membrane Protein Antibody Discovery Platform

Based on extensive experience and professional scientists, Creative Biolabs is dedicated to promoting global customers’ programs. In addition to SLC2A4 membrane protein products, we also provide other membrane protein preparation services to meet every client’s specific requirements. To learn more information, please feel free to contact us for more information.

Reference

1. Tunduguru, et al. (2017). Promoting glucose transporter-4 vesicle trafficking along cytoskeletal tracks: PAK-Ing them out. Frontiers in endocrinology. 8: 329.

All listed services and products are For Research Use Only. Do Not use in any diagnostic or therapeutic applications.