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B4GALNT2 catalyzes the last step in the biosynthesis of the human Sd(a) antigen through the addition of an N-acetylgalactosamine residue via a beta-1,4 linkage to a subterminal galactose residue substituted with an alpha-2,3-linked sialic acid.
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Human Polyclonal B4GALNT2 Primary Antibody für IHC, IHC (fro) - ABIN4282651
Chicoine, Rodino-Klapac, Shao, Xu, Bremer, Camboni, Golden, Montgomery, Shontz, Heller, Griffin, Lewis, Coley, Walker, Clark, Sahenk, Mendell, Martin: Vascular delivery of rAAVrh74.MCK.GALGT2 to the gastrocnemius muscle of the rhesus macaque stimulates the expression of dystrophin and laminin α2 surrogates. in Molecular therapy : the journal of the American Society of Gene Therapy 2014
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B4GALNT2 overexpression prevented the infection of every avian influenza virus strain tested, including the H5, H9, and H7 subtypes, which have previously caused disease in humans.
In normal colon samples a significant relationship between sLe(x) expression and the ratio between FUT6 (zeige FUT6 Antikörper)/B4GALNT2 activities exists, demonstrating for the first time a role for B4GALNT2 in sLe(x) inhibition in vivo.
molecular cloning; cDNA predicts a 566 aa protein showing 66.6% and 39% identity with mouse CT beta4GalNAc-T and human GM2/GD2 synthase (zeige B4GALNT1 Antikörper)
A putative CpG island encompassing the promoter and exon 1 regions in the human Sd(a) beta4GalNAcT (zeige CSGALNACT1 Antikörper)-II gene was identified.
Epigenetic changes in a group of glycosyltransferases including B4GALNT2 and ST3GAL6 (zeige ST3GAL6 Antikörper) represent a malignant phenotype of gastric cancer caused by silencing of the activity of these enzymes
B4galnt2 displays an interesting spatial allelic distribution in Western Europe, likely due to the recent action of natural selection.
Overexpression of Galgt2 failed to inhibit skeletal muscle pathology in dystroglycan-deficient muscles
These data support a critical role for B4galnt2 in gastrointestinal infections
Galgt2 is required for postsynaptic expression of the CT carbohydrate at the neuromuscular junction.
We describe changes that result from overexpression of Galgt2, a normally synaptic muscle glycosyltransferase (zeige GTDC2 Antikörper) that can modify alpha dystroglycan and inhibit the development of muscular dystrophy when it is overexpressed.
Study describes detailed characterization of mouse gastrointestinal bacterial communities in 7 distinct locations from the duodenum to the colon and provide evidence for a significant effect of B4galnt2 expression on intestinal bacterial populations.
Data suggest that B4GALNT2 and Sd(a) antigen are essential for embryo implantation.
Expression of B4galnt2 in pregnant mice is regulated by progesterone. The naturally occurring up-regulation of B4galnt2 during pregnancy contributes to normal embryo implantation.
we show that overexpression of the cytotoxic T cell (CT) GalNAc transferase (Galgt2) is effective in inhibiting the development of muscle pathology in the dy(W) mouse model of MDC1A
These experiments demonstrate that Galgt2 can control growth by modulating the expression of myostatin (zeige MSTN Antikörper) and myostatin (zeige MSTN Antikörper) inhibitors during particular periods of muscle development.
B4GALNT2 catalyzes the last step in the biosynthesis of the human Sd(a) antigen through the addition of an N-acetylgalactosamine residue via a beta-1,4 linkage to a subterminal galactose residue substituted with an alpha-2,3-linked sialic acid. B4GALNT2 also catalyzes the last step in the biosynthesis of the Cad antigen (Montiel et al., 2003
, UDP-GalNAc:Neu5Acalpha2-3Galbeta-R beta1,4-N-acetylgalactosaminyltransferase
, beta 1,4 N-acetylgalactosaminyltransferase/betal,4 GalNAcT/Sda-GalNAcT
, beta-1,4 N-acetylgalactosaminyltransferase 2
, sd(a) beta-1,4-GalNAc transferase
, sda beta-1,4-GalNAc transferase
, CT-Gal NAc transferase
, UDP-N-acetyl-alpha-D-galactosamine:(N-acetylneuraminyl)-galactosyl-N-acetylglucosaminylpolypeptide-beta-1, 4-N-acetylgalactosaminyltransferase
, dolichos lectin binding 1