MGAT5 Proteins, cDNA Clones Research Reagents

MGAT5 (Alpha-1,6-Mannosylglycoprotein 6-Beta-N-Acetylglucosaminyltransferase, also known as GNT-V; GNT-VA; MGAT5A; glcNAc-T V), located on 2q21.2-q21.3, is conserved in chimpanzee, dog, cow, mouse, rat, chicken, zebrafish, C.elegans, and frog. The gene produces an 84543 Da protein composed of 741 amino acids. The protein encoded by this gene belongs to the glycosyltransferase family. Diseases such as Hepatocellular Carcinoma and colorectal Cancer are associated with MGAT5. The related pathways of MGAT5 include Transport to the Golgi and subsequent modification and Metabolism of proteins.

MGAT5 Protein (1)

    MGAT5 cDNA Clone (13)

    NM_002410.3

    クローニングベクター cDNA 製品

    In lentiviral vector

    MGAT5 qPCR Primer (1)

    MGAT5 Lysate (1)

      MGAT5 の背景知識

      Alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase A, also known as Alpha-mannoside beta-1,6-N-acetylglucosaminyl-transferase, Mannoside acetylglucosaminyltransferase 5, N-acetylglucosaminyl-transferase V, MGAT5, and GGNT5, is a single-pass type II membrane protein that belongs to the glycosyltransferase 18 family. MGAT5 / GGNT5 catalyzes the addition of N-acetylglucosamine in beta 1-6 linkage to the alpha-linked mannose of biantennary N-linked oligosaccharides. It is one of the most important enzymes involved in the regulation of the biosynthesis of glycoprotein oligosaccharides. The central nervous system (CNS) is rich in glycoconjugates, located on the cell surface and in the extracellular matrix. MGAT5 / GGNT5 modification of complex-type N-glycans on CNS glycoproteins is involved in the regulation of depression-like behavior. Inhibitors of MGAT5 / GGNT5 might be useful in the treatment of malignancies by targeting their dependency on focal adhesion signaling for growth and metastasis.

      MGAT5 の参考文献

      • Morgan,R. et al., 2004,J Immunol  173 (12): 7200-8.
      • Cheung,P. et al., 2007,Glycobiology  17 (7): 767-73.
      • Li,D. et al., 2008, J Immunol 180 (5): 3158-65.
      • Soleimani,L. et al., 2008, Genes Brain Behav. 7 (3):334-43.

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