EC Number   |
Natural Substrates |
|---|
   2.7.4.21 | ATP + 1D-myo-inositol 1-diphosphate 2,3,4,5,6-pentakisphosphate |
- |
| 2.7.4.21 | ATP + 1D-myo-inositol 1-diphosphate pentakisphosphate |
- |
| 2.7.4.21 | ATP + 1D-myo-inositol 5-diphosphate 1,2,3,4,6-pentakisphosphate |
- |
| 2.7.4.21 | ATP + 1D-myo-inositol 5-diphosphate 2,3,4,5,6-pentakisphosphate |
- |
| 2.7.4.21 | ATP + 1D-myo-inositol hexakisphosphate |
enzyme is responsible for the biosynthesis of diphospho-myo-inositol pentakisphosphate. The enzyme also has a ATP synthase activity, implying that 5-diphospho-1D-myo-inositol pentakisphosphate functions as high-energy phosphate donor |
| 2.7.4.21 | ATP + 1D-myo-inositol hexakisphosphate |
apoptosis regulation |
| 2.7.4.21 | ATP + 1D-myo-inositol hexakisphosphate |
- |
| 2.7.4.21 | more |
role of the enzyme as a mediator of growth inhibition and apoptosis in response to interferon-beta treatment. The cellular level of the enzyme is posttranscriptionally enhanced by interferon-beta, in ovarian carcinoma cells |
| 2.7.4.21 | more |
IHPK2 binds to tumor necrosis factor receptor-associated factor 2 and interferes with phosphorylation of transforming growth factor beta-activated kinase 1, TAK1, thereby inhibiting NF-kappaB signaling. IHPK2 contains two sites required for TRAF2 binding, Ser347 and Ser359. IHPK2-TRAF2 binding leads to attenuation of TAK1- and NF-kappa B-mediated signaling and is partially responsible for the apoptotic activity of IHPK2. A portion of the death-promoting function of IHPK2 is independent of its kinase activity |
| 2.7.4.21 | more |
IP6K2 belongs to a family of enzymes generating the inositol pyrophosphate IP7 [diphosphoinositol pentakisphosphate (5-PP-IP5)], it mediates apoptosis, increased IP6K2 activity sensitizes cancer cells to stressors, whereas its depletion blocks cell death |
