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inositol monophosphatase, IMPase, ImpA, IMPA2
This gene encodes an enyzme that dephosphorylates myo-inositol monophosphate to generate free myo-inositol, a precursor of phosphatidylinositol, and is therefore an important modulator of intracellular signal transduction via the production of the second messengers myoinositol 1,4,5-trisphosphate and diacylglycerol. This enzyme can also use myo-inositol-1,3-diphosphate, myo-inositol-1,4-diphosphate, scyllo-inositol-phosphate, glucose-1-phosphate, glucose-6-phosphate, fructose-1-phosphate, beta-glycerophosphate, and 2'-AMP as substrates. This enzyme shows magnesium-dependent phosphatase activity and is inhibited by therapeutic concentrations of lithium. Inhibition of inositol monophosphate hydroylosis and subsequent depletion of inositol for phosphatidylinositol synthesis may explain the anti-manic and anti-depressive effects of lithium administered to treat bipolar disorder. Alternative splicing results in multiple transcript variants encoding distinct isoforms. A pseudogene of this gene is also present on chromosome 8q21.13. [provided by RefSeq, Nov 2009] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, V1a, fibrillin-1
Papers on inositol monophosphatase
Combined therapy with m-TOR-dependent and -independent autophagy inducers causes neurotoxicity in a mouse model of Machado-Joseph disease.
Maciel et al., Braga, Portugal. In Neuroscience, Feb 2016
Temsirolimus (CCI-779) inhibits the mammalian target of rapamycin (m-TOR), while lithium chloride (LiCl) acts by inhibiting inositol monophosphatase, both being able to induce autophagy.
Effects of the potential lithium-mimetic, ebselen, on brain neurochemistry: a magnetic resonance spectroscopy study at 7 tesla.
Cowen et al., Oxford, United Kingdom. In Psychopharmacology (berl), Feb 2016
The antioxidant drug, ebselen, may be a possible lithium-mimetic based on its ability to inhibit inositol monophosphatase (IMPase), an action which it shares with lithium.
Evaluation of a DLA-79 allele associated with multiple immune-mediated diseases in dogs.
Meurs et al., Raleigh, United States. In Immunogenetics, Jan 2016
As many immune-mediated diseases in humans share polymorphisms among a common set of genes, we conducted a candidate gene study of 15 of these genes across four immune-mediated diseases (immune-mediated hemolytic anemia, immune-mediated thrombocytopenia, immune-mediated polyarthritis (IMPA), and atopic dermatitis) in 195 affected and 206 unaffected dogs to assess whether causative or predictive polymorphisms might exist in similar genes in dogs.
Effect of the Putative Lithium Mimetic Ebselen on Brain Myo-Inositol, Sleep, and Emotional Processing in Humans.
Churchill et al., Newark, United States. In Neuropsychopharmacology, Dec 2015
We previously reported that ebselen inhibits inositol monophosphatase (IMPase) and exhibits lithium-like effects in animal models through lowering of inositol.
Integrated Microfluidics for Protein Modification Discovery.
Tzur et al., Ramat Gan, Israel. In Mol Cell Proteomics, Oct 2015
Based on this approach, we introduce a modular integrated microfluidic platform for multiple post-translational modifications analysis of freshly synthesized protein arrays (IMPA).
A homozygous loss-of-function mutation in inositol monophosphatase 1 (IMPA1) causes severe intellectual disability.
Santos et al., João Pessoa, Brazil. In Mol Psychiatry, Oct 2015
WES identified a homozygous deleterious variant in inositol monophosphatase 1 (IMPA1) (NM_005536), consisting of a 5-bp duplication (c.489_493dupGGGCT; chr8: 82,583,247; GRCh37/hg19) leading to a frameshift and a premature stop codon (p.Ser165Trpfs*10) that cosegregated with the disease in 26 genotyped family members.
Drugs under early investigation for the treatment of bipolar disorder.
Michalopoulou et al., Athens, Greece. In Expert Opin Investig Drugs, Apr 2015
Glycogen synthase kinase 3, casein kinase 1, inositol monophosphatase inhibition, histone deacetylase inhibition pathways are known targets that should proceed from preclinical to the clinical trial level.
Molecular actions and clinical pharmacogenetics of lithium therapy.
Gould et al., Baltimore, United States. In Pharmacol Biochem Behav, 2014
Here we discuss preclinical research suggesting mechanisms likely to underlie lithium's therapeutic actions including direct targets inositol monophosphatase and glycogen synthase kinase-3 (GSK-3) among others, as well as indirect actions including modulation of neurotrophic and neurotransmitter systems and circadian function.
Neuroprotective effects of lithium: implications for the treatment of Alzheimer's disease and related neurodegenerative disorders.
Diniz et al., São Paulo, Brazil. In Acs Chem Neurosci, 2014
Such a wide range of intracellular responses may be secondary to two key effects, that is, the inhibition of glycogen synthase kinase-3 beta (GSK-3β) and inositol monophosphatase (IMP) by lithium.
The let-7-Imp axis regulates ageing of the Drosophila testis stem-cell niche.
Jones et al., Los Angeles, United States. In Nature, 2012
IGF-II messenger RNA binding protein (Imp) counteracts endogenous small interfering RNAs to stabilize upd RNA; but similar to upd, Imp expression decreases in the hub cells of older males, which is due to the targeting of Imp by the heterochronic microRNA let-7; in the absence of Imp, upd mRNA therefore becomes unprotected and susceptible to degradation
Additive effect of ANRIL and BRAP polymorphisms on ankle-brachial index in a Taiwanese population.
Juo et al., Kao-hsiung, Taiwan. In Circ J, 2011
ANRIL on 9p21 and BRAP were both associated with ankle brachial index in a Taiwanese population.
BRCA1 status in Pakistani breast cancer patients with moderate family history.
Pervez et al., Karāchi, Pakistan. In J Coll Physicians Surg Pak, 2011
Several BRCA1 mutations were observed in Pakistani breast cancer patients with moderate family history.
A phenomics-based strategy identifies loci on APOC1, BRAP, and PLCG1 associated with metabolic syndrome phenotype domains.
Lin et al., Chapel Hill, United States. In Plos Genet, 2011
our approach, which is applicable to any set of interval scale traits that is heritable and exhibits evidence of phenotypic clustering, identified three new loci in or near APOC1, BRAP, and PLCG1, which were associated with multiple phenotype domains.
Synergistic effect between BRAP polymorphism and diabetes on the extent of coronary atherosclerosis in the Chinese population.
Sheu et al., Kao-hsiung, Taiwan. In Cardiology, 2010
BRAP gene is associated with the extent of coronary atherosclerosis and has a synergistic effect with diabetes on the occurrence of significant CAD in the Chinese population
[Toward understanding the molecular mechanism of brain function by molecular and neural circuit elucidation of the C. elegans nervous system].
Mori, Nagoya, Japan. In Nihon Shinkei Seishin Yakurigaku Zasshi, 2010
We found that loss of Inositol Monophosphatase (IMPase) encoded by the ttx-7 gene, an Inositol-producing enzyme regarded as a bipolar disorder-relevant molecule for its Lithium sensitivity, causes defects in thermotaxis behavior and localization of synaptic proteins in RIA neurons in vivo.
Validating GSK3 as an in vivo target of lithium action.
Klein et al., Philadelphia, United States. In Biochem Soc Trans, 2009
However, lithium also inhibits inositol monophosphatase, several structurally related phosphomonoesterases, phosphoglucomutase and the scaffolding function of beta-arrestin-2.
Molecular targets of lithium action.
Klein et al., Philadelphia, United States. In Annu Rev Pharmacol Toxicol, 2000
A number of enzymes have been proposed as potential targets of lithium action, including inositol monophosphatase, a family of structurally related phosphomonoesterases, and the protein kinase glycogen synthase kinase-3.
Interaction of Wnt and a Frizzled homologue triggers G-protein-linked phosphatidylinositol signalling.
Moon et al., Baltimore, United States. In Nature, 1997
This release of intracellular calcium is suppressed by an inhibitor of the enzyme inositol monophosphatase and hence of the phosphatidylinositol signalling pathway; this suppression can be rescued by injection of the compound myo-inositol, which overcomes the decrease in this intermediate caused by the inhibitor.
Lithium-sensitive production of inositol phosphates during amphibian embryonic mesoderm induction.
Busa et al., Baltimore, United States. In Science, 1992
Amounts of the PI cycle-derived second messenger, inositol 1,4,5-trisphosphate, increased during mesoderm induction in normal embryos; addition of Li+ inhibited the embryonic inositol monophosphatase and reversed this increase.
Recent insights in phosphatidylinositol signaling.
Bansal et al., Saint Louis, United States. In Cell, 1990
The recent cDNA cloning of inositol monophosphatase (Diehl et al., 1990), Ins(1,4,5)P3 3-kinase (Choi et al., 1990), and inositol polyphosphate 1-phosphatase (York and Majerus, 1991) should provide tools to define further the cell biology of the phosphatidylinositol signaling pathway.
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