EC Number   |
General Information |
Reference |
|---|
    3.1.3.25 | evolution |
existence of three distinct evolutionary groups of enzyme: vertebrate IMPA1 proteins, vertebrate IMPA2 proteins and invertebrate IMPA proteins |
714937 |
| 3.1.3.25 | malfunction |
mutations that degrade membrane phosphatidylinositol 4,5-bisphosphate suppress the synaptic defects of the enzyme mutants and confer resistance to lithium treatment |
729804 |
| 3.1.3.25 | malfunction |
the impl2 mutant has an embryo lethal phenotype, while the impl1 and vtc4 mutants do not |
716043 |
| 3.1.3.25 | metabolism |
myo-inositol monophosphatase catalyzes the dephosphorylation of myo-inositol 3-phosphate in the last step of myo-inositol biosynthesis. Expression of IMP genes is correlated with expression of the gene for myo-inositol polyphosphate 1-phosphatase, which is involved in the myo-inositol salvage pathway, suggesting a possible salvage pathway role in seed development. Moreover, the partial rescue of the impl2 phenotype by histidine application implies that IMPL2 is also involved in histidine biosynthesis during embryo development |
716043 |
| 3.1.3.25 | physiological function |
gene expression is essential for viability |
750664 |
| 3.1.3.25 | physiological function |
ImpA1 is a pulmonary arterial hypertension-specific interacting partner of receptor for advanced glycation end products, RAGE. RAGE/IMPA1 form a complex in the pulmonary artery wall. A threefold increase in glucose 6-phosphate levels in lungs of pulmonary arterial hypertension rats correlates with accumulation of phosphatidylinositol (3,4,5)-trisphosphate, membrane translocation of phosphatidylinositol-3-kinase, and a threefold increase in membrane Akt levels and Akt phosphorylation |
749540 |
| 3.1.3.25 | physiological function |
Mycobacteria use inositol in phosphatidylinositol, for anchoring lipoarabinomannan, lipomannan, and phosphatidylinosotol mannosides in the cell envelope, and for the production of mycothiol, which maintains the redox balance of the cell. The protein encoded by gene impA is partly responsible for inositol synthesis, while the impC encoded protein is essential, overview |
-, 714620 |
| 3.1.3.25 | physiological function |
myo-inositol monophosphatase catalyzes the dephosphorylation of myo-inositol 3-phosphate in the last step of myo-inositol biosynthesis. Myo-inositol monophosphatase is also important in phosphate metabolism and is required for the biosynthesis of cell wall polysaccharides, phytic acid, and phosphatidylinositol |
716043 |
| 3.1.3.25 | physiological function |
presence of a crosstalk between Ras signaling and inositol phosphate signaling by inositol monophosphatase. Constitutively active Ras1 leads to the repression of IMPase transcription and lithium inhibition of IMPase activity is compensated by the induction of IMPase at transcriptome level. Presence of lithium induces a considerable shift to inositol phosphate metabolism leading to a massive increase in the level of higher phosphorylated inositol species up to the inositol pyrophosphates |
749526 |
| 3.1.3.25 | physiological function |
Sac2/INPP5F interacts with 5-phosphatase OCRL which is potentiated by Rab5. Rab5 activity is required to recruit Sac2/INPP5F to endosomes |
751172 |
