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2.4.1.165: N-acetylneuraminylgalactosylglucosylceramide beta-1,4-N-acetylgalactosaminyltransferase

This is an abbreviated version!
For detailed information about N-acetylneuraminylgalactosylglucosylceramide beta-1,4-N-acetylgalactosaminyltransferase, go to the full flat file.

Word Map on EC 2.4.1.165

Reaction

UDP-N-acetyl-alpha-D-galactosamine
+
alpha-N-acetylneuraminyl-(2->3)-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1)-ceramide
=
UDP
+
N-acetyl-beta-D-galactosaminyl-(1->4)-[alpha-N-acetylneuraminyl-(2->3)]-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1)-ceramide

Synonyms

acetylgalactosaminyltransferase, uridine diphosphoacetylgalactosamine-acetylneuraminyl(alpha2-->3)galactosyl(beta1-->4)glucosyl beta1-->4-, beta-1,4-N-acetylgalactosyltransferase II, beta4GalNAc-T, beta4GalNAcT-II, CT GalNAc transferase, cytotoxic T cell GalNAc transferase, Galgt2, More, Sd(alpha) beta4GalNAcT-II, Sda-beta-1,4-N-acetylgalactosaminyltransferase, Sda-beta-GalNAc-transferase, UDP-GalNAc:beta1,4-N-acetylgalactosaminyltransferase

ECTree

     2 Transferases
         2.4 Glycosyltransferases
             2.4.1 Hexosyltransferases
                2.4.1.165 N-acetylneuraminylgalactosylglucosylceramide beta-1,4-N-acetylgalactosaminyltransferase

Disease

Disease on EC 2.4.1.165 - N-acetylneuraminylgalactosylglucosylceramide beta-1,4-N-acetylgalactosaminyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Carcinoma
Molecular cloning of the human beta1,4 N-acetylgalactosaminyltransferase responsible for the biosynthesis of the Sd(a) histo-blood group antigen: the sequence predicts a very long cytoplasmic domain.
Colonic Neoplasms
Biosynthesis and expression of the Sda and sialyl Lewis x antigens in normal and cancer colon.
Colorectal Neoplasms
Biosynthesis and expression of the Sda and sialyl Lewis x antigens in normal and cancer colon.
Gastrointestinal Neoplasms
Expression of the human Sd(a) beta-1,4-N-acetylgalactosaminyltransferase II gene is dependent on the promoter methylation status.
Leukemia
Genome-wide DNA methylation profiling of chronic lymphocytic leukemia allows identification of epigenetically repressed molecular pathways with clinical impact.
Muscular Diseases
Overexpression of Galgt2 reduces dystrophic pathology in the skeletal muscles of alpha sarcoglycan-deficient mice.
Muscular Dystrophies
B4GALNT2 (GALGT2) Gene Therapy Reduces Skeletal Muscle Pathology in the FKRP P448L Mouse Model of Limb Girdle Muscular Dystrophy 2I.
Comparative Proteomic Profiling of Dystroglycan-Associated Proteins in Wild Type, mdx, and Galgt2 Transgenic Mouse Skeletal Muscle.
Congenital muscular dystrophies involving the O-mannose pathway.
Deletion of Galgt2 (B4Galnt2) reduces muscle growth in response to acute injury and increases muscle inflammation and pathology in dystrophin-deficient mice.
Overexpression of Galgt2 in skeletal muscle prevents injury resulting from eccentric contractions in both mdx and wild-type mice.
Overexpression of Galgt2 reduces dystrophic pathology in the skeletal muscles of alpha sarcoglycan-deficient mice.
Overexpression of the CT GalNAc transferase inhibits muscular dystrophy in a cleavage-resistant dystroglycan mutant mouse.
Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx mice.
Postnatal overexpression of the CT GalNAc transferase inhibits muscular dystrophy in mdx mice without altering muscle growth or neuromuscular development: evidence for a utrophin-independent mechanism.
Soluble Heparin Binding Epidermal Growth Factor-Like Growth Factor Is a Regulator of GALGT2 Expression and GALGT2-Dependent Muscle and Neuromuscular Phenotypes.
The synaptic CT carbohydrate modulates binding and expression of extracellular matrix proteins in skeletal muscle: partial dependence on utrophin.
Vascular Delivery of rAAVrh74.MCK.GALGT2 to the Gastrocnemius Muscle of the Rhesus Macaque Stimulates the Expression of Dystrophin and Laminin ?2 Surrogates.
Muscular Dystrophies, Limb-Girdle
B4GALNT2 (GALGT2) Gene Therapy Reduces Skeletal Muscle Pathology in the FKRP P448L Mouse Model of Limb Girdle Muscular Dystrophy 2I.
Overexpression of Galgt2 reduces dystrophic pathology in the skeletal muscles of alpha sarcoglycan-deficient mice.
Muscular Dystrophy, Duchenne
Congenital muscular dystrophies involving the O-mannose pathway.
Deletion of Galgt2 (B4Galnt2) reduces muscle growth in response to acute injury and increases muscle inflammation and pathology in dystrophin-deficient mice.
Overexpression of Galgt2 in skeletal muscle prevents injury resulting from eccentric contractions in both mdx and wild-type mice.
The modulation of skeletal muscle glycosylation as a potential therapeutic intervention in muscular dystrophies.
Stomach Neoplasms
Expression of the human Sd(a) beta-1,4-N-acetylgalactosaminyltransferase II gene is dependent on the promoter methylation status.