IPMK: A Versatile Regulator of Nuclear Signaling Events
Abstract
Inositol-derived metabolites (e.g., phosphoinositides and inositol polyphosphates) are key second messengers that are essential for controlling a wide range of cellular events. Inositol polyphosphate multikinase (IPMK) exhibits complex catalytic activities that eventually yield water-soluble inositol polyphosphates (e.g., IP4 and IP5) and lipid-bound phosphatidylinositol 3,4,5-trisphosphate. A series of recent studies have suggested that IPMK may be a multifunctional regulator in the nucleus of mammalian cells. In this review, we highlight the novel modes of action of IPMK in transcriptional and epigenetic regulation, and discuss its roles in physiology and disease.
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IPMK is a dual-specificity 6-/3-kinase that generates InsP4 and InsP5 species.
“A key enzyme in this pathway is inositol polyphosphate multikinase (IPMK), a dual-specificity 6-/3-kinase that generates InsP4 and InsP5 species [11,12].”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [11]
IPMK has dual inositol and lipid kinase activities.
“With dual inositol and lipid kinase activities, IPMK generates pivotal signaling molecules such as InsP4 (inositol tetraphosphate), InsP5 (inositol pentaphosphate), and PIP3 (phosphoinositide 3,4,5-trisphosphate), positioning it as a critical regulator of cellular mechanisms.”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [11]
IPMK generates InsP4, InsP5, and PIP3.
“With dual inositol and lipid kinase activities, IPMK generates pivotal signaling molecules such as InsP4 (inositol tetraphosphate), InsP5 (inositol pentaphosphate), and PIP3 (phosphoinositide 3,4,5-trisphosphate), positioning it as a critical regulator of cellular mechanisms.”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [11]
The HOIP pathway uses InsP3 as a precursor and involves a series of phosphorylation events catalyzed by various kinases.
“The HOIP pathway, which uses InsP3 as a precursor, involves a series of phosphorylation events catalyzed by various kinases [10,11] (Figure 1).”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [11]
IPMK can modulate cellular signaling independently of its kinase activity through protein-protein interaction.
“This enzyme can modulate cellular signaling through multiple mechanisms: by generating highly phosphorylated inositol phosphates (HOIPs) [10,12,14], producing phosphatidylinositol 3,4,5-trisphosphate (PIP3) [10,12,14], or even functioning independently of its kinase activity through protein–protein interaction [10,11,12,14].”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [11]
Cites
Histone acetylation and transcriptional regulatory mechanisms
Struhl, K. (1998) · Genes & Development · doi:10.1101/gad.12.5.599 · Cited by 1,815 · see citing works
Steroidogenic factor 1: a key determinant of endocrine development and function
Parker, K. L., & Schimmer, B. P. (1997) · Endocrine Reviews · doi:10.1210/edrv.18.3.0301 · Cited by 764 · see citing works
Structure of Hdac3 Bound to Co-Repressor and Inositol Tetraphosphate
Watson, P. J., Fairall, L., Santos, G. M., & Schwabe, J. W. R. (2012) · Nature · doi:10.1038/nature10728 · Cited by 505 · see citing works
Yoon, H., Chan, D. W., Huang, Z., Li, J., Fondell, J. D., Qin, J., & Wong, J. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg120 · Cited by 444 · see citing works
A Role for Nuclear Inositol 1,4,5-Trisphosphate Kinase in Transcriptional Control
Odom, A. R., Stahlberg, A., Wente, S. R., & York, J. D. (2000) · Science · doi:10.1126/science.287.5460.2026 · Cited by 394 · see citing works
Bartsch, D., Casadio, A., Karl, K. A., Serodio, P., & Kandel, E. R. (1998) · Cell · doi:10.1016/s0092-8674(00)81752-3 · Cited by 373 · see citing works
Inositol pyrophosphates: between signalling and metabolism
Wilson, M. S. C., Livermore, T. M., & Saiardi, A. (2013) · Biochemical Journal · doi:10.1042/bj20130118 · Cited by 256 · see citing works
NALASKOWSKI, M. M., DESCHERMEIER, C., FANICK, W., & MAYR, G. W. (2002) · Biochemical Journal · doi:10.1042/bj20020327 · Cited by 89 · see citing works
El Alami, M., Messenguy, F., Scherens, B., & Dubois, E. (2003) · Molecular Microbiology · doi:10.1046/j.1365-2958.2003.03562.x · Cited by 83 · see citing works
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From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease
Mishra, S. H., Chatterjee, S., Viera-Preval, L., & Guha, P. (2025) · Biomolecules · doi:10.3390/biom15091266 · Cited by 1 · see citing works
“A key enzyme in this pathway is inositol polyphosphate multikinase (IPMK), a dual-specificity 6-/3-kinase that generates InsP4 and InsP5 species [11,12].”
- Authors
- Kim, E., Beon, J., Lee, S., Park, J., & Kim, S.
- Affiliations
- Korea Advanced Institute of Science and Technology (KR)
- Corresponding author
- Kim, Seyun
- Venue
- Advances in Biological Regulation
- Publisher
- Elsevier BV
- Published
- 2016-05
- Volume
- 61
- Pages
- 25-32
- ISSN
- 2212-4926 (ISSN-L)
- OpenAlex
- W2184794753
- Cited by
- 39
- References
- 9
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 6 · 2018: 2 · 2017: 9 · 2016: 4
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Advances in Biological Regulation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea
- Ministry of Education (NRF-2012H1A2A1048895, NRF-2014H1A2A1020802, NRF-2013M3C7A1056102)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- inositol polyphosphate multikinase, inositol polyphosphates, phosphoinositides, nuclear signaling, transcriptional regulation, epigenetic regulation, phosphatidylinositol 3,4,5-trisphosphate, second messengers, inositol tetrakisphosphate
- MeSH terms
- Animals, Carcinoma, Cell Nucleus, Epithelial Cells, Humans, Intestinal Neoplasms, Mutation, Transcription, Genetic, Signal Transduction, Phosphotransferases (Alcohol Group Acceptor), Phosphatidylinositol Phosphates, Phosphatidylinositol 3-Kinases, Epigenesis, Genetic
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