EC Number |
Substrates |
Organism |
Products |
Reversibility |
---|
5.1.3.14 | more |
the enzyme catalyzes the first step of sialic acid biosynthesis |
Rattus norvegicus |
? |
- |
? |
5.1.3.14 | more |
downregulation of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase in hyposialylated HIV-infected T cells with consequential glycosylation modification (the deficiency can be entirely corrected by nutrient complementation with N-acetylmannosamine). The promoter of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase is de novo hypermethylated in HIV-infected CEM cells |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
the bifunctional enzyme UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase is a rate-limiting enzyme of sialic acid biosynthesis |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
the homozygous M712T mutation of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase results in reduced enzyme activities but not in altered overall cellular sialylation in hereditary inclusion body myopathy |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
biosynthesis of sialic acids |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
biosynthesis of sialic acids |
Mus musculus |
? |
- |
? |
5.1.3.14 | more |
role of splice variant GNE1 in basic supply of cells with sialic acids, whereas GNE2 and GNE3 may have a function in finetuning of the sialic acid pathway |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
role of splice variant GNE1 in basic supply of cells with sialic acids, whereas GNE2 and GNE3 may have a function in finetuning of the sialic acid pathway. No significant differences in activities of splice variants mGNE 1 and mGNE2 |
Mus musculus |
? |
- |
? |
5.1.3.14 | more |
GNE interacts with proteins involved in the regulation of development, e.g. the transcription factor promyelotic leukemia zinc finger protein, which might play a crucial role in the hereditary inclusion body myopathy. GNE is regulated by a variety of biochemical means, including tetramerization promoted by the substrate UDP-GlcNAc, phosphorylation by protein kinase C and feedback inhibition by CMP-Neu5Ac, which is defect in the human disease sialuria. Multienzyme complexes of GNE with the other enzymes of the sialic acid biosynthesis pathway, either close to the Golgi CMP sialic acid transporter or in particular with the nuclear localized CMP-sialic acid synthetase, are possible |
Homo sapiens |
? |
- |
? |
5.1.3.14 | more |
GNE interacts with proteins involved in the regulation of development, e.g. the transcription factor promyelotic leukemia zinc finger protein, which might play a crucial role in the hereditary inclusion body myopathy. GNE is regulated by a variety of biochemical means, including tetramerization promoted by the substrate UDP-GlcNAc, phosphorylation by protein kinase C and feedback inhibition by CMP-Neu5Ac. Multienzyme complexes of GNE with the other enzymes of the sialic acid biosynthesis pathway, either close to the Golgi CMP sialic acid transporter or in particular with the nuclear localized CMP-sialic acid synthetase, are possible |
Mus musculus |
? |
- |
? |