Cloned (Comment) | Organism |
---|---|
gene Csgalnact1 | Mus musculus |
Protein Variants | Comment | Organism |
---|---|---|
additional information | construction of RNAi-mediated gene Csgalnact1 knockout mice, mutant T1KO. T1KO mice are viable, but they have abnormal bone development and 10% shorter bodies compared to wild-type mice. Heparan sulfate synthesis increases in injured spinal cords of T1KO mice | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
additional information | heparan sulfate-synthesis enzymes inhibits chondroitin sulfate as extracellular inhibitor of axon growth | Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
UDP-N-acetyl-D-galactosamine + beta-D-glucuronyl-(1->3)-D-galactosyl-proteoglycan | Mus musculus | - |
UDP + N-acetyl-D-galactosaminyl-(1->4)-beta-D-glucuronyl-(1->3)-beta-D-galactosylproteoglycan | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | Q8BJQ9 | gene csgalnact1 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
cartilage | - |
Mus musculus | - |
spinal cord | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
UDP-N-acetyl-D-galactosamine + beta-D-glucuronyl-(1->3)-D-galactosyl-proteoglycan | - |
Mus musculus | UDP + N-acetyl-D-galactosaminyl-(1->4)-beta-D-glucuronyl-(1->3)-beta-D-galactosylproteoglycan | - |
? |
Synonyms | Comment | Organism |
---|---|---|
chondroitin sulphate N-acetylgalactosaminyl-transferase-1 | - |
Mus musculus |
CS N-acetylgalactosaminyltransferase-1 | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | mice carrying a gene knockout for chondroitin sufate N-acetylgalactosaminyltransferase-1, mutant T1KO, recover more completely from spinal cord injury than wild-type mice and even chondroitinase ABC-treated mice. Synthesis of heparan sulfate, a glycosaminoglycan promoting axonal growth, is also upregulated in TI knockout mice because heparan sulfate-synthesis enzymes are induced in the mutant neurons. Chondroitinase ABC treatment never induces heparan sulfate upregulation. T1KO mice are viable, but they have abnormal bone development and 10% shorter bodies compared to wild-type mice. Reduced chondroitin sulfate levels are associated with reduced scar formation in T1KO mice. Phenotype of enzyme knockout mutant mice, overview | Mus musculus |
metabolism | chondroitin sulfate N-acetylgalactosaminyl-transferase-1 is a key enzyme in chondroitin sulfate biosynthesis | Mus musculus |