Application | Comment | Organism |
---|---|---|
medicine | delivery of IPMK in a transgenic Huntington's disease model improves pathological changes and motor performance. The Ctip2-IPMK-Akt signaling pathway provides a previously unidentified therapeutic target for Huntington's disease | Homo sapiens |
Cloned (Comment) | Organism |
---|---|
gene impk, adeno-associated virus serotype 2-mediated delivery of IPMK into mouse brain, in the striatum of R6/2 Huntington's disease mice | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
soluble | - |
Homo sapiens | - |
- |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | Homo sapiens | inositol polyphosphate multikinase is an enzyme that displays soluble inositol phosphate kinase activity, lipid kinase activity, and various noncatalytic interactions | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8NFU5 | gene impk | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
brain | from Huntington's disease patients and healthy persons | Homo sapiens | - |
brain cortex | - |
Homo sapiens | - |
cerebellum | - |
Homo sapiens | - |
hippocampus | - |
Homo sapiens | - |
striatum | from Huntington's disease patients and healthy persons, severe loss of IPMK in the striatum of Huntington's disease patients | Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | inositol polyphosphate multikinase is an enzyme that displays soluble inositol phosphate kinase activity, lipid kinase activity, and various noncatalytic interactions | Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
Impk | - |
Homo sapiens |
inositol polyphosphate multikinase | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | severe loss of IPMK in the striatum of Huntington's disease patients, the depletion reflects mHtt-induced impairment of COUP-TF-interacting protein 2 (Ctip2), a striatal-enriched transcription factor for IPMK, as well as alterations in IPMK protein stability. IPMK overexpression reverses the metabolic activity deficit in a cell model of Huntington's disease. IPMK depletion appears to mediate neural dysfunction, because intrastriatal delivery of IPMK abates the progression of motor abnormalities and rescues striatal pathology in transgenic murine models of Huntington's disease | Homo sapiens |
metabolism | IPMK expression rescues mHtt-induced deficits in mitochondrial metabolic activity. Delivery of IPMK in a transgenic Huntington's disease model improves pathological changes and motor performance. The Ctip2-IPMK-Akt signaling pathway provides a previously unidentified therapeutic target for Huntington's disease | Homo sapiens |