Protein Variants | Comment | Organism |
---|---|---|
D144N | site-directed mutagenesis | Homo sapiens |
D144N/K146A | site-directed mutagenesis | Homo sapiens |
K146A | site-directed mutagenesis | Homo sapiens |
K327Q/K328Q | site-directed mutagenesis, generation of an IPMK mutant with inactivated nuclear localization signal, NLS, whose intracellular distribution is unaffected by inhibition of conventional protein import | Homo sapiens |
additional information | overexpression of catalytically inactive IPMK mutants is sufficient to reduce RAD51 foci formation | Homo sapiens |
Metals/Ions | Comment | Organism | Structure |
---|---|---|---|
Mg2+ | required | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate | Homo sapiens | - |
ADP + 1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate | - |
? | |
ATP + 1D-myo-inositol 1,4,5,6-tetrakisphosphate | Homo sapiens | - |
ADP + 1D-myo-inositol 1,3,4,5,6-pentakisphosphate | - |
? | |
ATP + 1D-myo-inositol 1,4,5-trisphosphate | Homo sapiens | - |
ADP + 1D-myo-inositol 1,4,5,6-tetrakisphosphate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8NFU5 | gene impk | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
breast carcinoma cell | - |
Homo sapiens | - |
CAL-51 cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate | - |
Homo sapiens | ADP + 1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate | - |
? | |
ATP + 1D-myo-inositol 1,4,5,6-tetrakisphosphate | - |
Homo sapiens | ADP + 1D-myo-inositol 1,3,4,5,6-pentakisphosphate | - |
? | |
ATP + 1D-myo-inositol 1,4,5-trisphosphate | - |
Homo sapiens | ADP + 1D-myo-inositol 1,4,5,6-tetrakisphosphate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
inositol phosphate multikinase | - |
Homo sapiens |
IPMK | - |
Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
ATP | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | IPMK depletion or catalytic inactivation selectively decreases RAD51 protein abundance and the nuclear export of RAD51 mRNA, thereby impairing homologous recombination. Depletion or catalytic inactivation of IPMK selectively inhibits the nuclear export of the poly(A)+ mRNAs that encode essential homologous recombination factors such as RAD51, CHK1, or FANCD2, decreasing protein abundance, whereas, in contrast, several genes involved in NHEJ are unaffected. IPMK inactivation inhibits RAD51 recombinase assembly, provokes sensitivity to genotoxic lesions repaired by homologous recombination, and causes structural chromosome aberrations typical of defective homologous recombination. Overexpression of catalytically inactive IPMK mutants is sufficient to reduce RAD51 foci formation | Homo sapiens |
metabolism | the enzyme IPMK is involved in a transcript-selective mRNA export pathway controlled by phosphoinositide turnover that preserves genome integrity in humans | Homo sapiens |
physiological function | inositol phosphate multikinase regulates transcript-selective nuclear mRNA export to preserve genome integrity. The transcript-selective nuclear export mechanism affecting certain human transcripts, enriched for functions in genome duplication and repair, is controlled by inositol polyphosphate multikinase, an enzyme catalyzing inositol polyphosphate and phosphoinositide turnover. Function for human IPMK in RAD51 assembly and DNA repair by homologous recombination, overview | Homo sapiens |