EC Number   |
General Information |
Reference |
|---|
   2.7.4.21 | evolution |
in Dictyostelium discoideum, the IP7 target Ser is conserved, but the neighboring Asp and Glu residues are replaced with Thr. These Thr residues may undergo phosphorylation to mimic Asp/Glu and create a consensus site for diphosphorylation |
737654 |
| 2.7.4.21 | evolution |
IP6Ks are members of a wider inositol phosphate kinase family (Pfam PF03770) that includes IPMKs and IP3Ks. These enzymes all share a PxxxDxKxG, PDKG, catalytic motif. Phylogenetic analysis indivates that this kinase family arose from a primordial IP6K precursor |
739144 |
| 2.7.4.21 | evolution |
the absence of diphosphorylation in the IC(1-70)fragment suggests that the Ser-Pro cluster (residues 71-111) is required to facilitate pyrophosphorylation on Ser51. The site of diphosphorylation in mouse IC-2C is well conserved in human and rat, suggesting that the effect of IP7 on dynein is likely to be conserved in these species |
-, 737654 |
| 2.7.4.21 | malfunction |
analysis of the impact of siRNA-mediated knockdown of the two more abundant IP6Ks on Runx2 transcriptional activity. Knockdown of IP6K1 inhibits the FGF2-induced Runx2 activity, both basally and in response to Cx43 overexpression, more potently than knockdown of IP6K2. Knockdown of expression and/or inhibition of function of phospholipase Cgamma1, inositol polyphosphate multikinase, which generates inositol 1,3,4,5-tetrakisphosphate (InsP4) and InsP5, and inositol hexakisphosphate kinase 1/2, which generates inositol pyrophosphates, prevented the ability of Cx43 to potentiate FGF2 induced signaling through Runx2. Overexpression of phospholipase Cgamma1 and inositol hexakisphosphate kinase 1/2 enhances FGF2 activation of Runx2 and the effect of Cx43 overexpression on this response. Enzyme inhibition by TNP abolishes the basal and Cx43-potentiated Runx2 activity in response to FGF2 treatment relative to DMSO treated controls |
738740 |
| 2.7.4.21 | malfunction |
analysis of the impact of siRNA-mediated knockdown of the two more abundant IP6Ks on Runx2 transcriptional activity. Knockdown of IP6K1 inhibits the FGF2-induced Runx2 activity, both basally and in response to Cx43 overexpression, more potently than knockdown of IP6K2Knockdown of expression and/or inhibition of function of phospholipase Cgamma1, inositol polyphosphate multikinase, which generates inositol 1,3,4,5-tetrakisphosphate (InsP4) and InsP5, and inositol hexakisphosphate kinase 1/2, which generates inositol pyrophosphates, prevented the ability of Cx43 to potentiate FGF2 induced signaling through Runx2. Overexpression of phospholipase Cgamma1 and inositol hexakisphosphate kinase 1/2 enhances FGF2 activation of Runx2 and the effect of Cx43 overexpression on this response. Enzyme inhibition by TNP abolishes the basal and Cx43-potentiated Runx2 activity in response to FGF2 treatment relative to DMSO treated controls |
738740 |
| 2.7.4.21 | malfunction |
cells lacking isoform IP6K1 arrest after genotoxic stress, and markers associated with DNA repair are recruited to DNAdamage sites indicating that homologous recombination repair is initiated in these cells. However, repair does not proceed to completion. Enzyme loss increases chromosomal damage susceptibility |
722814 |
| 2.7.4.21 | malfunction |
deletion of inositol hexakisphosphate kinase 1 ( IP6K1) alters probability of presynaptic vesicle release and short-term facilitation of glutamatergic synapses in mouse hippocampus. IP6K1-knockout mice exhibit decreased prepulse inhibition with no defects in Y-maze and elevated plus maze tests. IP6K1 knockout leads to impaired shortterm memory formation in a contextual fear memory retrieval test with no effect on long-term memory. Both hippocampal long-term potentiation and long-term depression in IP6K1-knockout mice are similar to those in the wild-type control |
761879 |
| 2.7.4.21 | malfunction |
deletion of inositol hexakisphosphate kinase 3 (IP6K3) causes defects in cell motility and neuronal dendritic growth, eventually leading to brain malformations |
762284 |
| 2.7.4.21 | malfunction |
deletion of inositol hexakisphosphate kinase-1 (IP6K1) protects mice from high fat diet induced obesity and insulin resistance in mice. IP6K1-KO mice are lean due to enhanced energy expenditure. IP6K1-KO mice display enhanced basal lipolysis. IP6K1 modulates lipolysis via its interaction with the lipolytic regulator protein perilipin1 (PLIN1) |
738392 |
| 2.7.4.21 | malfunction |
deletion of IP6K2 in male/female mice elicits substantial defects in synaptic influences of granule cells upon Purkinje cells as well as notable impairment of locomotor function. The disruption of IP6K2- 4.1N interactions impairs cell viability |
761721 |
