Affinage

IP6K1

Inositol hexakisphosphate kinase 1 · UniProt Q92551

Length
441 aa
Mass
50.2 kDa
Annotated
2026-04-28
28 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IP6K1 is a conserved inositol hexakisphosphate kinase that synthesizes 5-IP7 (5-PP-InsP5) from IP6 and exerts both catalytic and scaffolding functions across diverse cellular processes including vesicle transport, energy metabolism, phosphate homeostasis, mRNA translational control, and secretory granule biogenesis. The 5-IP7 product pyrophosphorylates serine residues on substrates such as dynein intermediate chain to promote dynactin binding and dynein-driven vesicle transport, activates FAK/Paxillin signaling for cell migration, and recruits UBE4A to apoA-I for ubiquitin-mediated degradation (PMID:27474409, PMID:27140681, PMID:39643078). IP6K1 suppresses AMPK-mediated thermogenesis in adipocytes, regulates phosphate export via XPR1 SPX-domain engagement by inositol pyrophosphates, and controls renal Na+/Pi cotransporter expression (PMID:27701146, PMID:31186349, PMID:38317282). Independent of catalytic activity, IP6K1 scaffolds the mRNA decapping complex (EDC4, DCP1A/B, DCP2, DDX6) to promote P-body assembly and translational repression, coordinates CK2-mediated pre-phosphorylation of pyrophosphorylation substrates via an AP3B1–CK2α complex, and supports secretory granule biogenesis in gastric chief cells (PMID:34841428, PMID:39230924).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2010 High

    Establishing that IP6K1 directly converts IP6 to 5-IP7 and can pyrophosphorylate protein serines resolved the fundamental enzymatic activity and opened investigation into protein-level signaling by inositol pyrophosphates.

    Evidence Recombinant mouse IP6K1 purified from E. coli, in vitro kinase assay with radiolabeled substrates

    PMID:20645182

    Open questions at the time
    • Endogenous substrate selectivity for protein pyrophosphorylation not defined
    • Structural basis for 5-position specificity not resolved
  2. 2016 High

    Demonstration that IP6K1-generated 5-IP7 pyrophosphorylates dynein IC-Ser51 to promote dynactin binding and membrane recruitment revealed the first specific in vivo protein substrate and linked IP6K1 to cytoplasmic dynein-driven vesicle transport and Golgi maintenance.

    Evidence IP6K1 KO cells, catalytically active vs. inactive mutant rescue, in vitro pyrophosphorylation, Co-IP, live vesicle imaging

    PMID:27474409

    Open questions at the time
    • Whether other dynein-associated cargoes are similarly regulated is unknown
    • Quantitative contribution of pyrophosphorylation vs. canonical phosphorylation at Ser51 not resolved
  3. 2016 High

    Parallel work showed IP6K1 catalytic activity drives FAK/Paxillin phosphorylation, cell spreading, and migration, broadening the kinase's role to adhesion-dependent signaling and actin remodeling.

    Evidence IP6K1 KO MEFs, active vs. inactive rescue, migration/invasion assays, FAK/Paxillin immunoblot

    PMID:27140681

    Open questions at the time
    • Whether 5-IP7 acts directly on FAK or through an intermediate is not resolved
    • Relevance to in vivo tumor invasion not tested
  4. 2016 High

    Adipocyte-specific IP6K1 deletion showed the kinase suppresses AMPK-mediated thermogenesis and UCP1 expression, establishing IP6K1 as a metabolic regulator of energy expenditure and a potential anti-obesity target.

    Evidence Adipocyte-specific KO mice, AMPK epistasis, in vitro kinase assays, energy expenditure calorimetry

    PMID:27701146

    Open questions at the time
    • Direct molecular mechanism connecting 5-IP7 to AMPK inhibition not fully delineated
    • Whether IP6K1 acts on AMPK directly or upstream kinases in vivo remains unclear
  5. 2016 High

    Discovery that IP6K1 binds phosphatidic acid and translocates to the nucleus to repress MIPS/Isyna1 transcription revealed a lipid-sensing mechanism coupling IP6K1 to inositol biosynthesis regulation.

    Evidence IP6K1 KO MEFs, PA-binding assay, nuclear fractionation, qRT-PCR for Isyna1

    PMID:26953345

    Open questions at the time
    • How IP6K1 mediates transcriptional repression of MIPS at the chromatin level is unresolved
    • PA-binding domain on IP6K1 not mapped
  6. 2017 High

    Localization of IP6K1 to the chromatoid body and demonstration that its loss abolishes chromatoid body formation and derepresses TNP2/PRM2 translation established IP6K1 as essential for post-transcriptional control during spermiogenesis.

    Evidence Ip6k1 KO mice, immunofluorescence of chromatoid body markers, immunoblot for TNP2/PRM2

    PMID:28743739

    Open questions at the time
    • Whether this function requires catalytic activity or scaffolding is not determined
    • Direct RNA or RNP targets of IP6K1 in chromatoid body not identified
  7. 2018 High

    IP6K1 was shown to be required for platelet inorganic polyphosphate production that drives neutrophil-platelet aggregate formation via the bradykinin pathway, extending IP6K1 function to innate immunity and thromboinflammation.

    Evidence Ip6k1 KO mice, pharmacological IP6K1 inhibition, polyP rescue, NPA flow cytometry, bacterial pneumonia model

    PMID:29618559

    Open questions at the time
    • Mechanism by which IP6K1 controls mitochondrial/platelet polyP synthesis is undefined
    • Contribution of IP6K1 vs. IP6K2 to platelet polyP not separated
  8. 2019 High

    Double KO of IP6K1/2 eliminated IP7/IP8, elevated intracellular ATP and phosphate, and impaired phosphate export via XPR1 SPX-domain binding, unifying inositol pyrophosphate signaling with cellular phosphate homeostasis.

    Evidence CRISPR IP6K1/2 DKO in HCT116, PAGE/HPLC inositol phosphate profiling, 32Pi flux, XPR1 SPX-domain binding assay

    PMID:31186349

    Open questions at the time
    • Individual contributions of IP6K1 vs. IP6K2 to phosphate export not fully dissected
    • In vivo tissue-specific phosphate phenotype of single IP6K1 KO not addressed here
  9. 2021 High

    IP6K1 was found to scaffold the mRNA decapping complex and promote P-body assembly independently of catalytic activity, establishing a kinase-independent role in translational repression and mRNA turnover.

    Evidence IP6K1 KD/KO, reciprocal Co-IPs of decapping complex, ribosome fractionation, P-body quantification, catalytically inactive mutant rescue

    PMID:34841428

    Open questions at the time
    • Structural basis for IP6K1-decapping complex interaction unknown
    • Whether P-body scaffolding and chromatoid body functions share a common mechanism is untested
  10. 2022 High

    The upstream signal for IP6K1 nuclear translocation was traced to PLD-generated PA at the plasma membrane, regulated by AMPK, linking metabolic stress and mood-stabilizing drugs to MIPS repression and inositol depletion.

    Evidence Pharmacological PLD stimulation, AMPK activation by glucose deprivation/valproate/lithium, organelle-specific PA manipulation, nuclear translocation imaging

    PMID:35963434

    Open questions at the time
    • Whether PA-dependent nuclear import uses a classical NLS or alternative mechanism is unresolved
    • Contribution of IP6K1 nuclear translocation to mood-stabilizer therapeutic efficacy not established
  11. 2024 Medium

    IP6K1 forms a ternary complex with AP3B1 and CK2α, acting as a scaffold to coordinate CK2-mediated pre-phosphorylation and subsequent 5-IP7-dependent pyrophosphorylation of substrates, revealing a general mechanism for substrate targeting.

    Evidence Mass spectrometry interactome, Co-IP of IP6K1-AP3B1-CK2α, in vivo pyrophosphorylation assay with IP6K1-binding mutant of AP3B1

    PMID:39230924

    Open questions at the time
    • Whether this scaffolding mechanism applies broadly to all pyrophosphorylation substrates is untested
    • Structural details of the ternary complex are unknown
    • Single-lab finding
  12. 2024 High

    Renal tubular double KO of IP6K1/2 demonstrated that inositol pyrophosphates are required for NaPi-IIa/IIc cotransporter expression and renal phosphate reabsorption, establishing an in vivo tissue-specific phosphate homeostasis role.

    Evidence Renal tubular-specific Ip6k1/2 DKO mice, brush border membrane vesicle phosphate uptake, FGF23 measurement, cotransporter immunoblot

    PMID:38317282

    Open questions at the time
    • Individual contribution of IP6K1 vs. IP6K2 in renal phosphate handling not resolved
    • Mechanism by which 5-IP7 regulates cotransporter expression is undefined
  13. 2024 High

    IP6K1-generated 5-IP7 binds apoA-I and recruits UBE4A for ubiquitination, establishing a direct mechanism linking IP6K1 to apoA-I degradation and atherosclerosis susceptibility.

    Evidence Co-IP, 5-IP7 chemical binding assays, hepatocyte-specific IP6K1 KO mice, apoA-I KO epistasis, atherosclerotic plaque analysis

    PMID:39643078

    Open questions at the time
    • Structural basis of 5-IP7-apoA-I interaction not determined
    • Whether IP6K1 similarly regulates other apolipoproteins is unknown
  14. 2025 Medium

    IP6K1 was shown to stabilize LKB1 by disrupting Hsp/Hsc70-CHIP-mediated degradation, redirecting LKB1 signaling from AMPK to p53 to drive hyperglycemia-induced endothelial senescence.

    Evidence Multiple Co-IPs, endothelial-specific IP6K1 KO and overexpression mice, immunoblot for AMPK/p53/senescence markers

    PMID:39792359

    Open questions at the time
    • Whether this mechanism requires 5-IP7 or is catalysis-independent is not addressed
    • Relevance to diabetic vascular disease in humans not validated
    • Single-lab finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for IP6K1's dual catalytic and scaffolding functions; how substrate selectivity for protein pyrophosphorylation is achieved in vivo; the mechanism linking IP6K1 to mitochondrial polyphosphate synthesis; and whether kinase-dependent vs. kinase-independent functions segregate by subcellular compartment or tissue.
  • No crystal structure of full-length IP6K1 with substrates
  • No systematic delineation of catalytic vs. non-catalytic functions across tissues
  • Mechanism of mitochondrial polyP regulation by IP6K1 is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0060090 molecular adaptor activity 3 GO:0008289 lipid binding 2 GO:0098772 molecular function regulator activity 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005739 mitochondrion 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-162582 Signal Transduction 3 R-HSA-382551 Transport of small molecules 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-8953854 Metabolism of RNA 2 R-HSA-168256 Immune System 1 R-HSA-5653656 Vesicle-mediated transport 1
Partners
AP3B1CSNK2A1DCP2DDX6DIC (DYNEIN INTERMEDIATE CHAIN)EDC4SDC4UBE4A
Complex memberships
IP6K1-AP3B1-CK2α complexchromatoid bodymRNA decapping complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2016 IP6K1 catalytic activity is required for cytoplasmic dynein-driven vesicle transport; IP7 pyrophosphorylates Ser51 of dynein intermediate chain (IC), promoting IC interaction with p150(Glued) subunit of dynactin, and IC recruitment to membranes. Cells lacking IP6K1 show defects in endosomal sorting, vesicle movement, and Golgi maintenance that are reversed by catalytically active but not inactive IP6K1. KO cell lines, catalytically inactive mutant rescue, in vitro pyrophosphorylation assay, Co-IP, membrane fractionation, live imaging of vesicle movement The Biochemical journal High 27474409
2016 IP6K1 promotes cell migration and actin cytoskeleton remodeling via FAK and Paxillin activation; IP6K1-null MEFs show defects in adhesion-dependent signaling, cell spreading, and migration that are reversed by catalytically active but not inactive IP6K1, indicating 5-IP7 synthesis drives cell locomotion. KO MEFs, catalytically inactive mutant rescue, immunoblot for FAK/Paxillin phosphorylation, migration and invasion assays, gene expression analysis Cellular signalling High 27140681
2016 IP6K1 regulates adipocyte energy metabolism by suppressing AMPK-mediated thermogenesis; adipocyte-specific deletion of Ip6k1 enhances AMPK activation, UCP1/PGC1α expression, and thermogenic energy expenditure. IP6 and IP6K1 differentially regulate upstream kinase-mediated AMPK stimulatory phosphorylation in vitro. Adipocyte-specific KO mice, in vitro kinase assays, immunoblot, UCP1/PGC1α expression, AMPK depletion epistasis, energy expenditure measurement The Journal of clinical investigation High 27701146
2016 IP6K1 preferentially binds phosphatidic acid (PA), and this binding is required for IP6K1 nuclear localization and transcriptional repression of myo-inositol-3-phosphate synthase (MIPS/Isyna1), thereby negatively regulating inositol synthesis in mammalian cells. Ip6k1 ablation in MEFs, PA-binding assay, subcellular fractionation/nuclear localization, DNA methylation analysis, qRT-PCR for Isyna1 expression The Journal of biological chemistry High 26953345
2022 Phosphatidic acid (PA) synthesized at the plasma membrane by phospholipase D (PLD) induces nuclear translocation of IP6K1 and represses MIPS expression. AMPK activates PLD-mediated PA synthesis, linking glucose deprivation or mood-stabilizing drugs (valproate, lithium) to IP6K1 nuclear translocation and MIPS repression. Pharmacological PLD stimulation, direct PA supplementation, AMPK activation by glucose deprivation/drugs, nuclear translocation imaging, MIPS immunoblot, organelle-specific PA manipulation The Journal of biological chemistry High 35963434
2019 IP6K1 and IP6K2 together control inositol pyrophosphate (IP7/IP8) metabolism; IP6K1/2-knockout HCT116 cells lack IP7/IP8, have elevated intracellular ATP and free phosphate, and show reduced phosphate import and export. Inositol pyrophosphates regulate phosphate export via binding to the SPX domain of the phosphate exporter XPR1. CRISPR KO of IP6K1/2, PAGE and HPLC inositol phosphate analysis, nucleotide analysis, Malachite green phosphate assay, [32Pi] pulse labeling, XPR1 SPX-domain binding assay The Journal of biological chemistry High 31186349
2018 Platelet IP6K1-mediated inorganic polyphosphate (polyP) production is essential for infection-induced neutrophil-platelet aggregate (NPA) formation; IP6K1 inhibition reduces serum polyP levels, which regulates NPAs via the bradykinin pathway and bradykinin-mediated neutrophil activation, thereby reducing pulmonary neutrophil accumulation. Ip6k1 KO mice, pharmacological IP6K1 inhibition (TNP), platelet polyP measurement, NPA flow cytometry, bradykinin pathway analysis, polyphosphate rescue experiment, bacterial pneumonia model Science translational medicine High 29618559
2017 IP6K1 is a component of the chromatoid body in round spermatids and is required for its formation; Ip6k1-null spermatids lack chromatoid bodies and show premature translational derepression of TNP2 and PRM2, resulting in abnormal chromatin remodeling, failure of spermatid differentiation, and azoospermia. Ip6k1 KO mice, immunofluorescence/localization of IP6K1 to chromatoid body, immunoblot for TNP2/PRM2/histones, spermatogenesis phenotype analysis Journal of cell science High 28743739
2021 IP6K1 upregulates processing body (P-body) formation independently of its catalytic activity by binding to ribosomes and interacting with the mRNA decapping complex (EDC4, DCP1A/B, DCP2, DDX6); IP6K1 augments DDX6-4E-T interaction and binding to eIF4E on the 5' mRNA cap, tipping the balance toward translational repression. IP6K1-depleted cells show reduced microRNA-mediated translational suppression and increased stability of DCP2-regulated transcripts. IP6K1 KD/KO, Co-IP of decapping complex components, ribosome fractionation, P-body quantification, mRNA stability assays, catalytically inactive mutant analysis Journal of cell science High 34841428
2021 IP6K1 interacts with O-GlcNAcase in human NASH liver tissue and its deletion reduces protein O-GlcNAcylation in mouse liver, linking IP6K1 to regulation of protein O-GlcNAc modification in hepatic metabolism. Co-immunoprecipitation, mass spectrometry, immunoblot for O-GlcNAcylation in KO vs WT mouse livers and human NASH samples Molecular metabolism Medium 34757046
2017 IP6K1 deletion in MSCs results in higher MDM2 and lower p53 protein levels, leading to reduced intrinsic mitochondrial ROS, enhanced osteogenesis and hematopoiesis-supporting activity, and reduced adipogenic differentiation. Ip6k1 KO mice, MSC isolation, immunoblot for MDM2/p53, mitochondrial ROS measurement, osteogenic/adipogenic differentiation assays Stem cells (Dayton, Ohio) Medium 28577302
2024 IP6K1 forms a complex with AP3B1 and CK2α; IP6K1 interacts with multiple proteins that undergo 5-InsP7-mediated pyrophosphorylation (NOLC1, TCOF, UBF1, AP3B1), and disrupting IP6K1 binding to AP3B1 lowers its in vivo pyrophosphorylation, suggesting IP6K1 acts as a scaffold to coordinate CK2-mediated pre-phosphorylation and subsequent pyrophosphorylation of substrates. Mass spectrometry interactome, Co-IP of IP6K1-AP3B1-CK2α complex, in vivo pyrophosphorylation assay with IP6K1-binding mutant Bioscience reports Medium 39230924
2024 IP6K1 and its product 5PP-InsP5 bind apoA-I and recruit UBE4A to induce apoA-I ubiquitination and degradation; depleting 5PP-InsP5 by IP6K1 deletion or inhibition disrupts UBE4A-apoA-I interaction, preventing apoA-I degradation and elevating circulating apoA-I, thereby reducing atherosclerosis. Co-immunoprecipitation, chemical biology 5PP-InsP5 binding assays, hepatocyte-specific IP6K1 KO mice, apoA-I KO epistasis, Oil Red O/H&E plaque assessment Metabolism: clinical and experimental High 39643078
2025 IP6K1 mediates hyperglycemia-induced endothelial senescence by stabilizing LKB1 (disrupting Hsp/Hsc70 and CHIP-mediated LKB1 degradation), which shifts LKB1 signaling from AMPK activation to p53 pathway activation, resulting in p53-dependent senescence; endothelial-specific IP6K1 KO attenuates and overexpression exacerbates this phenotype. Co-IP (LKB1-IP6K1, LKB1-Hsp70, LKB1-CHIP, LKB1-p53), endothelial cell-specific KO and overexpression mice, immunoblot for AMPK/p53/senescence markers Diabetes Medium 39792359
2010 Recombinant mouse IP6K1 purified from E. coli catalyzes the synthesis of InsP7 (5-IP7) from IP6 in vitro and can pyrophosphorylate protein serine residues in a kinase-independent manner using this product. Recombinant protein purification from E. coli, in vitro kinase assay, radiolabeled [32P]-InsP7 production, in vitro protein pyrophosphorylation Methods in molecular biology (Clifton, N.J.) High 20645182
2024 Renal IP6K1 and IP6K2 together are required for normal expression and function of Na+/Pi cotransporters NaPi-IIa and NaPi-IIc; renal tubular-specific double KO mice show reduced phosphate uptake into proximal brush border membranes, hypophosphatemia, reduced FGF23, and increased bone resorption despite hypophosphatemia. Renal tubular-specific Ip6k1/2 DKO mice, in vitro opossum kidney cell KO, phosphate transport assays, brush border membrane vesicle uptake, FGF23 ELISA, immunoblot for cotransporters Journal of the American Society of Nephrology : JASN High 38317282
2024 IP6K1 KO neurons display lower action potential frequency and deepened afterhyperpolarization, consistent with increased Na+/K+-ATPase (NKA) activity resulting from IP6K1-regulated NKA stability (via PI3K p85α autoinhibitory domain pathway). Electrophysiology of IP6K1 KO neurons, action potential frequency and afterhyperpolarization measurement Molecular brain Medium 38350944
2025 IP6K1 regulates mitochondrial polyphosphate (polyP) levels through 5-InsP7 synthesis; IP6K1 KO mice and cells show significantly reduced mitochondrial polyP, impaired mitochondrial respiration, and reduced membrane potential. Catalytically active but not inactive IP6K1 restores polyP synthesis and membrane potential, while both active and inactive forms rescue mitochondrial respiration, indicating dual catalytic-dependent and independent mechanisms. DAPI fluorescence-based polyP assay, mitochondrial fractionation, mitochondrial respiration (Seahorse), membrane potential measurement, KO cells/mice, active vs. inactive IP6K1 rescue bioRxivpreprint Medium bio_10.1101_2025.06.17.659843
2025 IP6K1 interacts with the proteoglycan SDC4 and supports secretory granule biogenesis in gastric chief cells independently of its catalytic activity; IP6K1 KO AGS cells and Ip6k1-/- mice lack pepsinogen C (PGC) and gastric lipase F (LIPF) granules, and PGC granule formation is restored by reintroduction of either active or inactive IP6K1. Ip6k1 KO mice, CRISPR/Cas9 KO in AGS cells, Co-IP of IP6K1-SDC4, immunofluorescence of granules, active vs. inactive IP6K1 rescue bioRxivpreprint Medium bio_10.1101_2025.09.17.676719
2025 IP6K1 is a substrate of the Cys-Arg/N-degron pathway under hypoxia; loss of IP6K1 impairs glucose uptake, glycolytic ATP production, mitochondrial morphology, and metabolic adaptation under hypoxic conditions. Proteomics/global N-terminal Cys-degron profiling, mutagenesis, IP6K1 KO cells under hypoxia, glucose uptake and ATP production assays, mitochondrial morphology imaging bioRxivpreprint Low bio_10.1101_2025.01.20.633921

Source papers

Stage 0 corpus · 28 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 The inositol hexakisphosphate kinases IP6K1 and -2 regulate human cellular phosphate homeostasis, including XPR1-mediated phosphate export. The Journal of biological chemistry 87 31186349
2016 Adipocyte-specific deletion of Ip6k1 reduces diet-induced obesity by enhancing AMPK-mediated thermogenesis. The Journal of clinical investigation 73 27701146
2016 Inositol hexakisphosphate kinase 1 (IP6K1) activity is required for cytoplasmic dynein-driven transport. The Biochemical journal 58 27474409
2016 Deletion of inositol hexakisphosphate kinase 1 (IP6K1) reduces cell migration and invasion, conferring protection from aerodigestive tract carcinoma in mice. Cellular signalling 50 27140681
2016 TNP [N2-(m-Trifluorobenzyl), N6-(p-nitrobenzyl)purine] ameliorates diet induced obesity and insulin resistance via inhibition of the IP6K1 pathway. Molecular metabolism 47 27689003
2018 Inhibition of IP6K1 suppresses neutrophil-mediated pulmonary damage in bacterial pneumonia. Science translational medicine 41 29618559
2016 Global IP6K1 deletion enhances temperature modulated energy expenditure which reduces carbohydrate and fat induced weight gain. Molecular metabolism 37 28123939
2004 The IHPK1 gene is disrupted at the 3p21.31 breakpoint of t(3;9) in a family with type 2 diabetes mellitus. Journal of human genetics 28 15221640
2017 IP6K1 is essential for chromatoid body formation and temporal regulation of Tnp2 and Prm2 expression in mouse spermatids. Journal of cell science 27 28743739
2016 Inositol Hexakisphosphate Kinase 1 (IP6K1) Regulates Inositol Synthesis in Mammalian Cells. The Journal of biological chemistry 27 26953345
2017 IP6K1 Reduces Mesenchymal Stem/Stromal Cell Fitness and Potentiates High Fat Diet-Induced Skeletal Involution. Stem cells (Dayton, Ohio) 25 28577302
2018 High-Intensity Exercise Decreases IP6K1 Muscle Content and Improves Insulin Sensitivity (SI2*) in Glucose-Intolerant Individuals. The Journal of clinical endocrinology and metabolism 22 29300979
2010 Synthesis of InsP7 by the Inositol Hexakisphosphate Kinase 1 (IP6K1). Methods in molecular biology (Clifton, N.J.) 21 20645182
2022 Phosphatidic acid inhibits inositol synthesis by inducing nuclear translocation of kinase IP6K1 and repression of myo-inositol-3-P synthase. The Journal of biological chemistry 19 35963434
2021 miR-125a-5p impairs the metastatic potential in breast cancer via IP6K1 targeting. Cancer letters 19 34229060
2019 Synthesis and characterization of novel isoform-selective IP6K1 inhibitors. Bioorganic & medicinal chemistry letters 17 31445853
2021 Pleiotropic actions of IP6K1 mediate hepatic metabolic dysfunction to promote nonalcoholic fatty liver disease and steatohepatitis. Molecular metabolism 15 34757046
2024 The Ip6k1 and Ip6k2 Kinases Are Critical for Normal Renal Tubular Function. Journal of the American Society of Nephrology : JASN 10 38317282
2024 Insights into the roles of inositol hexakisphosphate kinase 1 (IP6K1) in mammalian cellular processes. The Journal of biological chemistry 10 38403246
2021 IP6K1 upregulates the formation of processing bodies by influencing protein-protein interactions on the mRNA cap. Journal of cell science 9 34841428
2022 Whole Body Ip6k1 Deletion Protects Mice from Age-Induced Weight Gain, Insulin Resistance and Metabolic Dysfunction. International journal of molecular sciences 8 35216174
2022 Deletion of IP6K1 in mice accelerates tumor growth by dysregulating the tumor-immune microenvironment. Animal cells and systems 8 35308129
2019 Platelet IP6K1 regulates neutrophil extracellular trap-microparticle complex formation in acute pancreatitis. JCI insight 7 31593553
2024 Interaction with IP6K1 supports pyrophosphorylation of substrate proteins by the inositol pyrophosphate 5-InsP7. Bioscience reports 5 39230924
2024 Inhibiting IP6K1 confers atheroprotection by elevating circulating apolipoprotein A-I. Metabolism: clinical and experimental 4 39643078
2024 Deleting IP6K1 stabilizes neuronal sodium-potassium pumps and suppresses excitability. Molecular brain 2 38350944
2025 IP6K1 Rewires LKB1 Signaling to Mediate Hyperglycemic Endothelial Senescence. Diabetes 1 39792359
2024 Shaping the Future of Obesity Treatment: In Silico Multi-Modeling of IP6K1 Inhibitors for Obesity and Metabolic Dysfunction. Pharmaceuticals (Basel, Switzerland) 1 38399478