EC Number   |
General Information |
Reference |
|---|
   5.4.2.3 | evolution |
the enzyme belongs to the alpha-D-phosphohexomutase superfamily of enzymes |
-, 728329 |
| 5.4.2.3 | malfunction |
loss-of-function mutations in the nst gene, which encodes PGM3, block fibroblast growth factor signaling during embryonic mesoderm and tracheal development. In nst mutants with an 80% reduction in the amount of UDP-GlcNAc, O-GlcNAcylation is compromised. Embryos maternally and zygotically mutant for nst exhibit defects in mesoderm layer formation during gastrulation that are similar to those observed in embryos with mutations in the gene encoding the fibroblast growth factor receptor Heartless (Htl). Zygotic nst mutants (nstZ) exhibit normal dorsal mesoderm differentiation, embryos homozygous for the hypomorphic htlYY262 allele show a reduction in dorsal mesoderm. Phenotypes, overview. Dof is the critical component in MAPK activation affected in nst mutants |
728799 |
| 5.4.2.3 | metabolism |
Nst acts downstream of fibroblast growth factor receptor signaling |
728799 |
| 5.4.2.3 | physiological function |
the enzyme is essential for parasite growth. It takes over the function of phosphoglucomutase, EC 5.4.2.2, whose gene is lost in Trypanosoma brucei, together with phosphomannomutase, EC 5.4.2.8, producing D-glucose 1-phosphate from D-glucose 6-phosphate, kinetics, overview |
-, 728329 |
| 5.4.2.3 | physiological function |
the enzyme is required for normal cellular levels of UDP-GlcNAc and essential in UDP-GlcNAc biosynthesis, and for fibroblast growth factor signaling in early embryos. Role for Nst in fibroblast growth factor receptor Heartless (Htl) signaling |
728799 |
