Affinage

IP6K1

Inositol hexakisphosphate kinase 1 · UniProt Q92551

Length
441 aa
Mass
50.2 kDa
Annotated
2026-06-10
29 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IP6K1 is an inositol hexakisphosphate kinase that synthesizes the inositol pyrophosphate 5-IP7 (5-InsP7) from IP6, and the enzyme's product serves as a protein-modifying agent capable of pyrophosphorylating protein substrates in vitro (PMID:20645182). Through 5-IP7-mediated pyrophosphorylation, IP6K1 controls intracellular trafficking — pyrophosphorylating Ser51 of the dynein intermediate chain to promote its interaction with the dynactin p150(Glued) subunit and drive vesicle transport (PMID:27474409) — and it physically organizes substrate pyrophosphorylation by assembling with the priming kinase CK2 and target proteins such as AP3B1 into a coordinated pre-phosphorylation/pyrophosphorylation complex (PMID:39230924). A major theme is metabolic and phosphate regulation: IP6K1 (together with IP6K2) governs cellular inositol pyrophosphate pools that bind the SPX domain of the phosphate exporter XPR1 to set phosphate homeostasis (PMID:31186349) and is required for renal Na+/Pi cotransporter expression and proximal tubule phosphate uptake (PMID:38317282). In adipocytes IP6K1 restrains AMPK-mediated thermogenesis and energy expenditure (PMID:27701146), and its catalytic activity supports mitochondrial polyphosphate production, respiration, and membrane potential [PMID:bio_10.1101_2025.06.17.659843]. IP6K1 also acts non-catalytically: it binds ribosomes and the mRNA decapping complex to promote P-body formation and translational repression (PMID:34841428), and interacts with syndecan-4 to support secretory granule biogenesis, with both active and inactive enzyme rescuing these functions (PMID:42053465). Additional 5-IP7-dependent roles include UBE4A-mediated apoA-I degradation (PMID:39643078), LKB1 stabilization that switches signaling toward p53 in hyperglycemia-induced endothelial senescence (PMID:39792359), and regulation of neuronal Na+/K+-ATPase stability and excitability (PMID:38350944). IP6K1 is essential for chromatoid body assembly and spermatogenesis (PMID:28743739) and for platelet polyphosphate production driving neutrophil-platelet aggregates and NET formation in infection and inflammation (PMID:29618559, PMID:31593553).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2010 High

    Established the foundational biochemistry: that IP6K1 is an enzyme generating 5-IP7 and that this product can covalently modify proteins by pyrophosphorylation.

    Evidence Recombinant mouse IP6K1 from E. coli with in vitro kinase and protein pyrophosphorylation assays using radiolabeled substrates

    PMID:20645182

    Open questions at the time
    • Did not identify physiological protein substrates
    • No cellular phenotype linked to enzymatic output
  2. 2016 High

    Connected IP6K1 catalytic output to specific cellular machinery by identifying a defined pyrophosphorylation substrate residue controlling motor-adaptor coupling and vesicle transport.

    Evidence KO cells with active/inactive rescue, in vitro pyrophosphorylation of dynein IC Ser51, Co-IP and endosomal transport assays

    PMID:27474409

    Open questions at the time
    • Stoichiometry and reversibility of Ser51 pyrophosphorylation in vivo not defined
    • Other dynein-cargo specificities not addressed
  3. 2016 High

    Defined IP6K1 as a metabolic brake on thermogenesis, showing its catalytic activity opposes AMPK activation and energy expenditure in adipose tissue.

    Evidence Adipocyte-specific KO mice, in vitro AMPK phosphorylation assay with AMPK depletion rescue, thermogenesis measurements

    PMID:27701146

    Open questions at the time
    • Direct molecular link between 5-IP7 and the upstream AMPK kinase not fully resolved
    • Tissue-autonomous vs systemic contributions not separated
  4. 2016 Medium

    Revealed a lipid-sensing input to IP6K1 localization: PA binding drives nuclear translocation to repress inositol synthesis, creating a feedback loop on substrate availability.

    Evidence Ip6k1 ablation, lipid-binding assay, nuclear localization imaging, Isyna1/MIPS transcriptional readout; later extended with PLD/AMPK pharmacology

    PMID:26953345 PMID:35963434

    Open questions at the time
    • Direct PA-IP6K1 binding interface not mapped
    • Mechanism of MIPS transcriptional/protein-level repression by nuclear IP6K1 unresolved
  5. 2016 Medium

    Linked IP6K1 catalytic activity to cytoskeletal dynamics and adhesion signaling underlying cell migration.

    Evidence KO MEFs with active/inactive rescue, FAK/Paxillin immunoblot, migration and invasion assays

    PMID:27140681

    Open questions at the time
    • No direct 5-IP7 substrate in the FAK/Paxillin axis identified
    • Single cell-type model
  6. 2017 Medium

    Demonstrated an essential developmental role in male germ cells via chromatoid body assembly and translational control.

    Evidence Ip6k1 KO mice, immunofluorescence of chromatoid body markers, TNP2/PRM2 expression analysis

    PMID:28743739

    Open questions at the time
    • Whether the chromatoid body role is catalytic or structural not dissected
    • Molecular partners in the chromatoid body unidentified
  7. 2018 High

    Established IP6K1 as a producer of platelet inorganic polyphosphate driving innate immune aggregate formation in infection.

    Evidence Ip6k1 KO mice, platelet depletion, polyP rescue, IP6K1 inhibitor TNP, NPA quantification in bacterial pneumonia

    PMID:29618559

    Open questions at the time
    • Enzymatic mechanism linking 5-IP7 to polyP synthesis not defined
    • Bradykinin pathway connection mechanistically incomplete
  8. 2019 Medium

    Extended the platelet polyP role to NET-microparticle complex formation, showing IP6K1-dependent platelet support of neutrophil function.

    Evidence IP6K1 KO mice, platelet-neutrophil mixing, polyP rescue, electron microscopy, STAT-3 phosphorylation

    PMID:31593553

    Open questions at the time
    • Direct molecular effector of polyP on NET formation unresolved
    • Single disease model (pancreatitis)
  9. 2019 High

    Placed IP6K1 at the center of cellular phosphate homeostasis by linking its inositol pyrophosphate products to SPX-domain regulation of the XPR1 phosphate exporter.

    Evidence IP6K1/2 double KO in HCT116, HPLC and radiolabeling of inositol pyrophosphates, SPX domain binding assay

    PMID:31186349

    Open questions at the time
    • Individual IP6K1 vs IP6K2 contribution not separated
    • Whether IP6K1 directly contacts XPR1 vs acts through diffusible 5-IP7 unresolved
  10. 2021 Medium

    Uncovered a catalysis-independent function: IP6K1 scaffolds ribosomes and the decapping complex to promote P-body formation and translational repression.

    Evidence KD/KO cells, active/inactive rescue, Co-IP with ribosome and EDC4/DCP1A-B/DCP2/DDX6, P-body and miRNA suppression assays

    PMID:34841428

    Open questions at the time
    • Direct binding interface within the decapping complex not mapped
    • How a catalytic kinase performs a structural scaffolding role unexplained
  11. 2021 Low

    Identified a hepatic interaction with O-GlcNAcase linking IP6K1 to protein O-GlcNAcylation.

    Evidence Co-IP, mass spectrometry, O-GlcNAcylation immunoblot in KO livers

    PMID:34757046

    Open questions at the time
    • Single Co-IP plus expression readout without reciprocal validation
    • Mechanism by which IP6K1 affects O-GlcNAcase activity unknown
  12. 2024 Medium

    Showed how IP6K1 organizes substrate pyrophosphorylation by forming a CK2-IP6K1-substrate complex coupling priming phosphorylation to pyrophosphorylation.

    Evidence MS interactome, Co-IP of IP6K1-AP3B1-CK2alpha trimer, disruption of IP6K1-AP3B1 binding with in vivo pyrophosphorylation readout

    PMID:39230924

    Open questions at the time
    • Generality of the trimeric complex across substrates not established
    • Structural basis of substrate selection unresolved
  13. 2024 Medium

    Defined a 5PP-InsP5/UBE4A-dependent pathway controlling apoA-I degradation and circulating lipoprotein levels.

    Evidence Co-IP, chemical biology tools for 5PP-InsP5 binding, hepatocyte-specific KO and IP6K1/apoA-I double KO mice

    PMID:39643078

    Open questions at the time
    • Whether apoA-I pyrophosphorylation directly triggers UBE4A recruitment not shown
    • Ubiquitination steps downstream of UBE4A undefined
  14. 2024 Medium

    Established a renal physiological role in phosphate reabsorption via control of NaPi cotransporter expression.

    Evidence Renal tubular-specific Ip6k1/2 double KO mice and opossum kidney cells, expression assays, brush border phosphate uptake

    PMID:38317282

    Open questions at the time
    • IP6K1 and IP6K2 studied jointly, not individually
    • Mechanism linking inositol pyrophosphates to NaPi-IIa/IIc expression unresolved
  15. 2024 Medium

    Linked IP6K1 catalytic output to neuronal excitability through 5-InsP7-governed Na+/K+-ATPase stability.

    Evidence IP6K1 KO mouse neurons, whole-cell electrophysiology and action potential recording

    PMID:38350944

    Open questions at the time
    • The PI3K p85alpha autoinhibitory mechanism cited from prior work, not directly demonstrated here
    • Direct NKA pyrophosphorylation in neurons not shown
  16. 2025 Medium

    Revealed a pathological signaling switch in which IP6K1 stabilizes LKB1 and redirects its output from AMPK toward p53 to drive endothelial senescence in hyperglycemia.

    Evidence Endothelial-specific KO/OE mice, Co-IP of LKB1 with Hsp70/CHIP and p53, AMPK vs p53 phosphorylation assays

    PMID:39792359

    Open questions at the time
    • Whether LKB1 stabilization requires direct pyrophosphorylation not established
    • Molecular determinant of the AMPK-to-p53 switch unresolved
  17. 2025 Medium

    Connected IP6K1 catalytic activity to mitochondrial polyphosphate, respiration, and membrane potential, while separating catalytic from non-catalytic contributions to mitochondrial function.

    Evidence IP6K1 KO cells and mice, DAPI polyP quantification in mitochondrial fractions, active/inactive rescue, respiration and membrane potential assays (preprint)

    PMID:bio_10.1101_2025.06.17.659843

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Mechanism by which 5-InsP7 promotes mitochondrial polyP synthesis undefined
  18. 2025 Low

    Identified IP6K1 itself as a regulated substrate of the Cys-Arg/N-degron pathway under hypoxia, linking its stability to metabolic adaptation.

    Evidence Proteomics/N-degron screen, IP6K1 KO cells under hypoxia, glucose uptake and metabolic flux assays (preprint)

    PMID:bio_10.1101_2025.01.20.633921

    Open questions at the time
    • Preprint with limited IP6K1-specific mechanistic detail
    • Degron sequence and E3 ligase for IP6K1 not defined
  19. 2026 Medium

    Established a further catalysis-independent role in secretory granule biogenesis through interaction with syndecan-4.

    Evidence Ip6k1 KO mice, CRISPR KO AGS cells, active/inactive rescue, Co-IP/interactome for SDC4, colocalization with PGC granules

    PMID:42053465

    Open questions at the time
    • Structural basis of IP6K1-SDC4 interaction unmapped
    • How the interaction promotes granule biogenesis mechanistically unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How IP6K1's catalytic (5-IP7 pyrophosphorylation) and non-catalytic (scaffolding) functions are partitioned and coordinated across its many cellular roles remains unresolved.
  • No unifying structural model distinguishing catalytic vs scaffold modes
  • Tissue-specific substrate repertoire of 5-IP7 incompletely defined
  • Regulation of IP6K1 subcellular localization and stability across contexts incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0008289 lipid binding 2 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-1430728 Metabolism 2 R-HSA-168256 Immune System 2 R-HSA-382551 Transport of small molecules 2 R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-8953854 Metabolism of RNA 1
Partners
AP3B1CK2ALPHADDX6EDC4LKB1SDC4UBE4AXPR1
Complex memberships
IP6K1-AP3B1-CK2alpha complexchromatoid bodymRNA decapping complex (EDC4/DCP1A-B/DCP2/DDX6)

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 in the dynein intermediate chain (IC), promoting IC interaction with the p150(Glued) subunit of dynactin, and cells lacking IP6K1 show decreased IC-p150(Glued) interaction and reduced IC recruitment to membranes. KO cells with rescue by active/inactive IP6K1, in vitro pyrophosphorylation assay, Co-IP, endosomal transport assays The Biochemical journal High 27474409
2016 IP6K1 catalytic activity (5-IP7 synthesis) promotes cell migration and invasion via regulation of actin cytoskeleton dynamics and adhesion-dependent FAK/Paxillin signaling; expression of active but not inactive IP6K1 rescues migration defects in IP6K1 KO MEFs. KO MEFs with active/inactive IP6K1 rescue, gene expression analysis, immunoblot for FAK/Paxillin activation, migration/invasion assays Cellular signalling Medium 27140681
2016 IP6K1 inhibits AMPK-mediated thermogenesis in adipocytes; adipocyte-specific Ip6k1 deletion enhances AMPK activation and thermogenic energy expenditure, and IP6 and IP6K1 differentially regulate upstream kinase-mediated AMPK stimulatory phosphorylation in vitro. Adipocyte-specific KO mice, in vitro AMPK phosphorylation assay, AMPK depletion rescue, thermogenesis/EE measurements, UCP1/PGC1α expression analysis The Journal of clinical investigation High 27701146
2016 IP6K1 preferentially binds the phospholipid phosphatidic acid (PA), and this PA binding is required for IP6K1 nuclear localization and negative regulation of myo-inositol-3-P synthase (MIPS/Isyna1) transcription, thereby suppressing inositol synthesis. Ip6k1 ablation, lipid-binding assay, subcellular fractionation/nuclear localization imaging, gene expression analysis of Isyna1 The Journal of biological chemistry Medium 26953345
2022 Plasma membrane-derived phosphatidic acid (PA), synthesized via the AMPK-PLD pathway, induces nuclear translocation of IP6K1 and represses MIPS protein expression; endoplasmic reticulum-derived PA does not induce IP6K1 translocation. Pharmacological PLD stimulation, direct PA supplementation, AMPK activation by glucose deprivation/valproate/lithium, subcellular localization imaging, MIPS immunoblot The Journal of biological chemistry Medium 35963434
2017 IP6K1 is a component of the chromatoid body in round spermatids; its deletion leads to absence of chromatoid bodies, premature translational derepression of TNP2 and PRM2, and azoospermia in male mice. Ip6k1 KO mice, immunofluorescence localization, expression analysis of chromatoid body markers and spermatid-specific proteins Journal of cell science Medium 28743739
2019 IP6K1 and IP6K2 together control synthesis of IP7 and IP8 in human cells and regulate phosphate homeostasis; inositol pyrophosphates bind to the SPX domain of the phosphate exporter XPR1 and regulate its activity, controlling both phosphate import and export. IP6K1/2 double KO in HCT116 cells, PAGE and HPLC analysis of inositol polyphosphates, nucleotide analysis, Malachite green assay, [32Pi] pulse labeling, SPX domain binding assay The Journal of biological chemistry High 31186349
2018 IP6K1 in platelets mediates inorganic polyphosphate (polyP) production; platelet-derived polyP is essential for neutrophil-platelet aggregate (NPA) formation and neutrophil accumulation in alveolar spaces during bacterial pneumonia, acting through the bradykinin pathway. Ip6k1 KO mice, platelet depletion, polyP rescue experiments, IP6K1 inhibitor TNP, serum polyP measurement, NPA quantification Science translational medicine High 29618559
2021 IP6K1 acts independently of its catalytic activity to upregulate P-body formation by binding to ribosomes and interacting with the mRNA decapping complex (EDC4, DCP1A/B, DCP2, DDX6), augmenting the DDX6-4E-T interaction on the 5' mRNA cap and promoting translational repression over initiation. IP6K1 KD/KO cells, active vs. inactive IP6K1 rescue, Co-IP of IP6K1 with ribosome and decapping complex components, P-body formation assays, miRNA-mediated suppression assays, DCP2-regulated transcript stability Journal of cell science Medium 34841428
2021 IP6K1 interacts with the enzyme O-GlcNAcase in the liver; IP6K1 deletion reduces protein O-GlcNAcylation in mouse livers and in hepatocyte-specific KO mice. Co-immunoprecipitation, mass spectrometry, immunoblotting for O-GlcNAcylation in KO livers Molecular metabolism Low 34757046
2024 IP6K1 binds to apoA-I and, via its product 5PP-InsP5, induces apoA-I degradation requiring ubiquitination factor E4A (UBE4A); depleting 5PP-InsP5 by IP6K1 deletion disrupts UBE4A-apoA-I interaction, preventing apoA-I degradation and increasing circulating apoA-I levels. Co-immunoprecipitation, chemical biology tools for 5PP-InsP5 binding, hepatocyte-specific IP6K1 KO mice, IP6K1/apoA-I double KO validation Metabolism: clinical and experimental Medium 39643078
2024 IP6K1 interacts with substrate proteins targeted for 5-InsP7-mediated pyrophosphorylation (including NOLC1, TCOF, UBF1, AP3B1) and with CK2 kinase; a trimeric complex of IP6K1-AP3B1-CK2α was demonstrated, and disrupting IP6K1 binding to AP3B1 lowers AP3B1 pyrophosphorylation in vivo, supporting coordinated pre-phosphorylation and pyrophosphorylation. Mass spectrometry interactome, Co-IP of trimeric complex, disruption of IP6K1-AP3B1 binding with in vivo pyrophosphorylation readout Bioscience reports Medium 39230924
2024 IP6K1-generated 5-InsP7 governs the degradation of Na+/K+-ATPase (NKA) via the autoinhibitory domain of PI3K p85α; IP6K1 KO neurons show enriched NKA, lower action potential frequency, and deeper afterhyperpolarization, demonstrating that IP6K1 regulates neuronal excitability through NKA stability. IP6K1 KO mouse neurons, whole-cell electrophysiology, action potential recording Molecular brain Medium 38350944
2025 IP6K1 mediates hyperglycemia-induced endothelial senescence by stabilizing LKB1 (by disrupting Hsp/Hsc70 and CHIP-mediated LKB1 degradation) and switching LKB1 signaling from AMPK activation to p53 pathway activation; endothelial-specific IP6K1 deletion attenuates this senescence. Endothelial-specific IP6K1 KO and OE mice, Co-IP of LKB1 with Hsp70/CHIP and p53, phosphorylation assays for AMPK vs. p53 targets Diabetes Medium 39792359
2024 IP6K1 and IP6K2 are required for normal expression and function of the renal Na+/Pi cotransporters NaPi-IIa and NaPi-IIc; renal tubular-specific double KO mice show downregulation of NaPi-IIa/IIc, reduced proximal tubule phosphate uptake, and hypophosphatemia. Renal tubular-specific Ip6k1/2 double KO mice, in vitro opossum kidney cells with depletion, mRNA/protein expression assays, brush border membrane phosphate uptake assay Journal of the American Society of Nephrology Medium 38317282
2019 IP6K1 platelet activity regulates NET-microparticle complex formation in acute pancreatitis; IP6K1-deficient platelets fail to support thrombin-induced NET formation when mixed with wild-type neutrophils, and polyphosphate rescue restores NET formation. IP6K1 KO mice, platelet-neutrophil mixing experiments, polyphosphate rescue, electron microscopy, STAT-3 phosphorylation assay JCI insight Medium 31593553
2026 IP6K1 interacts with the proteoglycan syndecan-4 (SDC4) to support secretory granule biogenesis in gastric chief cells; this function is independent of IP6K1 catalytic activity, as both active and inactive IP6K1 rescue pepsinogen C (PGC) granule formation in IP6K1 KO AGS cells. Ip6k1 KO mice, CRISPR KO in AGS cells, active/inactive IP6K1 rescue, Co-IP/interactome for SDC4, colocalization of SDC4 with PGC granules American journal of physiology. Gastrointestinal and liver physiology Medium 42053465
2025 IP6K1-generated 5-InsP7 regulates mitochondrial polyphosphate (polyP) levels; IP6K1 KO cells and mice show reduced mitochondrial polyP, impaired mitochondrial respiration and membrane potential; expression of catalytically active but not inactive IP6K1 restores mitochondrial polyP and membrane potential, while both active and inactive forms rescue mitochondrial respiration. IP6K1 KO cells and mice, DAPI fluorescence-based polyP quantification, mitochondrial fractionation, active/inactive IP6K1 rescue, mitochondrial respiration and membrane potential assays bioRxivpreprint Medium bio_10.1101_2025.06.17.659843
2025 IP6K1 is a substrate of the Cys-Arg/N-degron pathway under hypoxia; loss of IP6K1 impairs glucose uptake, glycolytic ATP production, and mitochondrial morphology and function, disrupting metabolic adaptation under hypoxic conditions. Systematic proteomics/N-degron pathway screen, IP6K1 KO cells under hypoxia, glucose uptake and metabolic flux assays bioRxivpreprint Low bio_10.1101_2025.01.20.633921
2010 Recombinant mouse IP6K1 purified from E. coli synthesizes InsP7 (5-IP7) from IP6 in vitro, and this purified enzyme can pyrophosphorylate protein substrates from different species, establishing IP6K1's enzymatic activity and its product as a protein-modifying agent. Recombinant protein purification from E. coli, in vitro kinase assay with cold and [32P]-labeled substrates, protein pyrophosphorylation assay Methods in molecular biology High 20645182

Source papers

Stage 0 corpus · 29 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 59 27474409
2016 Deletion of inositol hexakisphosphate kinase 1 (IP6K1) reduces cell migration and invasion, conferring protection from aerodigestive tract carcinoma in mice. Cellular signalling 51 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 43 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 23 29300979
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 21 35963434
2021 miR-125a-5p impairs the metastatic potential in breast cancer via IP6K1 targeting. Cancer letters 21 34229060
2010 Synthesis of InsP7 by the Inositol Hexakisphosphate Kinase 1 (IP6K1). Methods in molecular biology (Clifton, N.J.) 21 20645182
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 16 34757046
2024 Insights into the roles of inositol hexakisphosphate kinase 1 (IP6K1) in mammalian cellular processes. The Journal of biological chemistry 13 38403246
2024 The Ip6k1 and Ip6k2 Kinases Are Critical for Normal Renal Tubular Function. Journal of the American Society of Nephrology : JASN 10 38317282
2021 IP6K1 upregulates the formation of processing bodies by influencing protein-protein interactions on the mRNA cap. Journal of cell science 10 34841428
2022 Whole Body Ip6k1 Deletion Protects Mice from Age-Induced Weight Gain, Insulin Resistance and Metabolic Dysfunction. International journal of molecular sciences 9 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 5 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
2026 IP6K1 interacts with the syndecan SDC4 to support secretory granule biogenesis in gastric chief cells. American journal of physiology. Gastrointestinal and liver physiology 0 42053465

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