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Mouse Anti-IMPA1 Recombinant Antibody (CBYY-I0244) (CBMAB-I0638-YY)


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Summary

Host Animal
Mouse
Specificity
Human, Mouse
Clone
CBYY-I0244
Antibody Isotype
IgG1, κ
Application
WB, FC, ELISA, IF

Basic Information

Specificity
Human, Mouse
Antibody Isotype
IgG1, κ
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Concentration
1 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Inositol Monophosphatase 1
Introduction
This gene encodes an enzyme 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.
Entrez Gene ID
Human3612
Mouse55980
UniProt ID
HumanP29218
MouseO55023
Alternative Names
Inositol Monophosphatase 1
Function
Responsible for the provision of inositol required for synthesis of phosphatidylinositol and polyphosphoinositides and has been implicated as the pharmacological target for lithium action in brain. Has broad substrate specificity and can use myo-inositol monophosphates, myo-inositol 1,3-diphosphate, myo-inositol 1,4-diphosphate, scyllo-inositol-phosphate, D-galactose 1-phosphate, glucose-1-phosphate, glucose-6-phosphate, fructose-1-phosphate, beta-glycerophosphate, and 2'-AMP as substrates.
Biological Process
Inositol biosynthetic processIEA:UniProtKB-UniPathway
Inositol metabolic processManual Assertion Based On ExperimentIBA:GO_Central
Inositol phosphate dephosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
Phosphate-containing compound metabolic processManual Assertion Based On ExperimentIMP:UniProtKB
Phosphatidylinositol biosynthetic processManual Assertion Based On ExperimentIMP:UniProtKB
Phosphatidylinositol phosphate biosynthetic processIEA:InterPro
Signal transductionManual Assertion Based On ExperimentIMP:UniProtKB
Cellular Location
Cytoplasm
Involvement in disease
Mental retardation, autosomal recessive 59 (MRT59):
A form of mental retardation, a disorder characterized by significantly below average general intellectual functioning associated with impairments in adaptive behavior and manifested during the developmental period. MRT59 transmission pattern is consistent with autosomal recessive inheritance.
More Infomation

Yang, S. Y., Xie, Y. F., Zhang, T. M., Deng, L., Liao, L., Hu, S. Y., ... & Li, D. Q. (2023). Inositol monophosphatase 1 (IMPA1) promotes triple‐negative breast cancer progression through regulating mTOR pathway and EMT process. Cancer Medicine, 12(2), 1602-1615.

Pessoa, A. L. S., Quesada, A. A., Nóbrega, P. R., Viana, A. P. O., de Oliveira, K. T., Figueiredo, T., ... & Kok, F. (2023). Neuropsychological Characterization of Autosomal Recessive Intellectual Developmental Disorder 59 Associated with IMPA1 (MRT59). Brain Sciences, 13(7), 1048.

Padinjat, R., Saha, S., & Krishnan, H. (2022). IMPA1 dependent regulation of plasma membrane phosphatidylinositol 4, 5-bisphosphate turnover and calcium signalling by lithium. bioRxiv, 2022-10.

Andreassi, C., Luisier, R., Crerar, H., Darsinou, M., Blokzijl-Franke, S., Lenn, T., ... & Riccio, A. (2021). Cytoplasmic cleavage of IMPA1 3′ UTR is necessary for maintaining axon integrity. Cell Reports, 34(8).

Figueiredo, T., Mendes, A. P., Moreira, D. P., Goulart, E., Oliveira, D., Kobayashi, G. S., ... & Zatz, M. (2021). Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. Molecular Psychiatry, 26(7), 3558-3571.

Pillai, R. A., Islam, M. O., Selvam, P., Sharma, N., Chu, A. H., Watkins, O. C., ... & Chan, S. Y. (2021). Placental inositol reduced in gestational diabetes as glucose alters inositol transporters and IMPA1 enzyme expression. The Journal of Clinical Endocrinology & Metabolism, 106(2), e875-e890.

Bogatikov, E., Lindblad, I., Punga, T., & Punga, A. R. (2020). miR-1933-3p is upregulated in skeletal muscles of MuSK+ EAMG mice and affects Impa1 and Mrpl27. Neuroscience research, 151, 46-52.

Walker, C. P., Pessoa, A. L., Figueiredo, T., Rafferty, M., Melo, U. S., Nóbrega, P. R., ... & Cho, R. Y. (2019). Loss-of-function mutation in inositol monophosphatase 1 (IMPA1) results in abnormal synchrony in resting-state EEG. Orphanet Journal of Rare Diseases, 14(1), 1-10.

Rosette, C., & Murray PhD, M. (2018). P-29 Preparing to Test the Effects of Omega-3 Fatty Acids on Inositol Levels and ISYNA & IMPA1 Gene Expression in Mammalian Cells.

de Farias, A. A., Nunes, K., Lemes, R. B., Moura, R., Fernandes, G. R., Melo, U. S., ... & Santos, S. (2018). Origin and age of the causative mutations in KLC2, IMPA1, MED25 and WNT7A unravelled through Brazilian admixed populations. Scientific reports, 8(1), 16552.

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For research use only. Not intended for any clinical use.

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