Affinage

INPP5A

Inositol polyphosphate-5-phosphatase A · UniProt Q14642

Length
412 aa
Mass
47.8 kDa
Annotated
2026-06-10
72 papers in source corpus 14 papers cited in narrative 14 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

INPP5A is a membrane-tethered inositol 1,4,5-trisphosphate (IP3) 5-phosphatase that terminates IP3/Ca2+ signaling and, through its action on phosphoinositides, restrains PI3K/Akt activation (PMID:11706019, PMID:32107387). In vitro it hydrolyzes PI(3,4,5)P3 with ~10-fold higher affinity than other 5-phosphatases, and its overexpression depletes PI(4,5)P2 and PI(3,4,5)P3, suppressing growth-factor-driven Akt phosphorylation and sensitizing cells to apoptosis (PMID:11706019). Membrane targeting is conferred by C-terminal farnesylation and palmitoylation, which distribute the enzyme across the plasma membrane, ER, nuclear envelope, and lysosomes; loss of palmitoylation reduces plasma-membrane localization, while loss of farnesylation confines INPP5A to the nucleoplasm (PMID:40812428). In the cerebellum, INPP5A enzymatic activity is required for Purkinje cell survival: its genetic deletion causes IP3 accumulation and progressive Purkinje cell degeneration with ataxia, while its overexpression lowers IP3 and rescues degeneration in spinocerebellar ataxia models, where it acts as a neuroprotective effector downstream of SP1- and TBP-dependent transcription (PMID:26051944, PMID:32107387, PMID:22973002). By controlling IP3 levels and downstream ER Ca2+ release, INPP5A also governs OSBP dynamics and lipid exchange at ER–Golgi membrane contact sites (PMID:33976123), and constitutes a synthetic-lethal dependency in GNAQ/11-mutant uveal melanoma, where it prevents IP3-receptor-driven cytosolic Ca2+ overload and p53-dependent apoptosis (PMID:38233483, PMID:40812428). INPP5A expression is transcriptionally repressed by a PKA/MBD2 axis in pituitary tumor cells, where it suppresses proliferation via IP3 degradation and PI3K/Akt inhibition (PMID:41857481).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2001 High

    Established INPP5A as a 5-phosphatase with high affinity for PI(3,4,5)P3, linking its catalytic activity to negative control of Akt signaling and apoptotic susceptibility.

    Evidence In vitro kinetic assays, phosphoinositide quantification, and Akt phosphorylation/apoptosis readouts in overexpressing 293 cells

    PMID:11706019

    Open questions at the time
    • Substrate preference between IP3 and 3-phosphoinositides under physiological conditions not resolved
    • No endogenous loss-of-function context in this study
  2. 2006 Medium

    Placed INPP5A within hypothalamic insulin/PI3K signaling, showing it is tyrosine-phosphorylated upon insulin and modulates feeding and body weight.

    Evidence Intracerebroventricular insulin in rats, antisense knockdown, inositol phosphate measurement, behavioral readouts

    PMID:16916951

    Open questions at the time
    • Kinase responsible for INPP5A tyrosine phosphorylation not identified
    • Direct phosphoinositide substrate changes in vivo not fully resolved
  3. 2012 High

    Demonstrated that boosting INPP5A activity suppresses IP3/Ca2+ signaling and rescues Purkinje cell dysfunction in SCA2, establishing INPP5A as a functional regulator of cerebellar Ca2+ homeostasis.

    Evidence AAV-mediated overexpression in SCA2 transgenic mice with electrophysiology, rotarod, and histology

    PMID:22973002

    Open questions at the time
    • Whether endogenous INPP5A is limiting in disease not addressed
    • Direct measurement of IP3 hydrolysis kinetics in vivo absent
  4. 2015 High

    Showed that INPP5A enzymatic activity is required for Purkinje cell survival, defining a cell-autonomous neuroprotective role.

    Evidence Gene-trap Inpp5a knockout mice with histology, motor testing, and cerebellar phosphatase activity assays

    PMID:26051944

    Open questions at the time
    • Cause of perinatal lethality not defined
    • Downstream IP3/Ca2+ targets in Purkinje cells not directly measured here
  5. 2020 High

    Connected INPP5A to transcriptional control by SP1/TBP and confirmed bidirectionally that its IP3-hydrolyzing activity is neuroprotective in cerebellar degeneration.

    Evidence SCA17 knock-in mice, CRISPR cerebellar deletion, AAV overexpression, IP3 measurement, ChIP/reporter assays

    PMID:32107387

    Open questions at the time
    • Tissue specificity of neuroprotection mechanistically unexplained
    • Relationship between SP1 and other INPP5A transcriptional regulators unclear
  6. 2021 High

    Revealed a non-canonical role for INPP5A in regulating lipid exchange at ER–Golgi contact sites through IP3-dependent ER Ca2+ control of OSBP localization.

    Evidence INPP5A loss-of-function in cell lines, IP3/Ca2+ measurement, OSBP localization, cholesterol/Gb3 and Shiga toxin endocytosis assays

    PMID:33976123

    Open questions at the time
    • Direct INPP5A localization at contact sites not shown
    • Whether INPP5A physically associates with OSBP/VAP not established
  7. 2024 High

    Identified INPP5A as a genome-scale synthetic-lethal dependency in GNAQ/11-mutant uveal melanoma, mechanistically tied to IP3 accumulation, Ca2+ elevation, and p53-dependent apoptosis.

    Evidence Genome-scale CRISPR screens, in vitro and in vivo INPP5A depletion, IP3/IP4 and cytosolic Ca2+ measurement, p53 pathway analysis

    PMID:38233483

    Open questions at the time
    • Whether IP4 is a reliable clinical biomarker untested in patients prospectively
    • Mechanism coupling Ca2+ overload to p53 activation not detailed
  8. 2025 High

    Defined the lipid-modification-driven subcellular targeting of INPP5A and showed it tunes the rate of GNAQ/11-driven Ca2+ oscillations to prevent Ca2+ overload.

    Evidence GFP-INPP5A imaging, palmitoylation/farnesylation site mutagenesis, INPP5A inhibitor YU144369, single-cell Ca2+ imaging, GNAQ/11 inhibitor FR900359

    PMID:40812428

    Open questions at the time
    • Functional significance of nuclear-envelope and lysosomal pools not defined
    • Dynamics/regulation of reversible palmitoylation cycle unknown
  9. 2013 Medium

    Extended INPP5A's role to peripheral insulin signaling, showing its upregulation in obesity impairs glucose homeostasis.

    Evidence Antisense knockdown in obese rodent models with enzymatic activity assays, insulin-signaling immunoblotting, and clamp studies

    PMID:23349329

    Open questions at the time
    • Direct phosphoinositide substrate in muscle/adipose not quantified
    • Mechanism of obesity-induced INPP5A upregulation unknown
  10. 2017 Medium

    Identified INPP5A as a direct miR-181a-5p target whose restoration suppresses cervical cancer cell proliferation and invasion.

    Evidence Dual-luciferase reporter assay and overexpression/mimic rescue experiments in HeLa/SiHa cells

    PMID:28653606

    Open questions at the time
    • Downstream signaling effector in cervical cancer not defined
    • In vivo tumor relevance not tested
  11. 2026 Medium

    Established a PKA/MBD2 transcriptional axis repressing INPP5A in pituitary tumors and linked INPP5A loss to PI3K/Akt-driven proliferation.

    Evidence ChIP, PKA activation, S99 phosphorylation analysis, MBD2–14-3-3σ co-IP, bidirectional INPP5A manipulation with pathway immunoblotting

    PMID:41857481

    Open questions at the time
    • Whether MBD2 repression operates in non-pituitary tissues unknown
    • Direct demonstration that INPP5A acts through phosphoinositide hydrolysis here is inferred from PI3K/Akt readouts

Open questions

Synthesis pass · forward-looking unresolved questions
  • How INPP5A's distinct subcellular pools and dual phosphoinositide/IP3 substrate activities are coordinated to achieve tissue-specific outcomes — from Purkinje cell survival to tumor dependency — remains unresolved.
  • No structural model of substrate recognition in the timeline
  • Regulation of localization-specific activity not established
  • Direct protein partners largely uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 5 GO:0140098 catalytic activity, acting on RNA 1
Localization
GO:0005635 nuclear envelope 2 GO:0005654 nucleoplasm 2 GO:0005764 lysosome 2 GO:0005783 endoplasmic reticulum 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 2 R-HSA-5653656 Vesicle-mediated transport 1
Partners
OSBPVAP

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 INPP5A (5ptase IV) has approximately 10-fold greater affinity for PI(3,4,5)P3 (Km = 0.65 µM) compared to other 5-phosphatases including SHIP, OCRL, and 5ptase II. Overexpression in 293 cells depletes both PI(4,5)P2 and PI(3,4,5)P3, generating PI(4)P and PI(3,4)P2. By selective depletion of PI(3,4,5)P3, INPP5A overexpression inhibits Akt phosphorylation in response to growth factors or heat shock, demonstrating that Akt activation correlates with PI(3,4,5)P3 levels rather than PI(3,4)P2 levels. Inhibition of Akt phosphorylation makes cells highly susceptible to FAS-induced apoptosis. In vitro enzymatic assay (Km determination), stable cell line overexpression, phosphoinositide measurement, immunoblotting for Akt phosphorylation, apoptosis assay The Journal of biological chemistry High 11706019
2006 INPP5A (5ptase IV) undergoes time-dependent tyrosine phosphorylation in hypothalamic neurons following intracerebroventricular insulin treatment, following the same pattern as canonical insulin signaling (insulin receptor → IRS-2 → PI3K). Antisense-mediated knockdown of 5ptase IV in the hypothalamus (~80% reduction) increases basal phosphorylated inositol accumulation, reduces food intake, and causes body weight loss, placing 5ptase IV as a regulator of PI3K signaling in the hypothalamus. Intracerebroventricular insulin treatment in rats, antisense oligonucleotide knockdown, immunoprecipitation/tyrosine phosphorylation assay, inositol phosphate measurement, food intake and body weight measurement Endocrinology Medium 16916951
2012 Adeno-associated virus-mediated overexpression of INPP5A (Inpp5a/5PP) in cerebellar Purkinje cells of SCA2 transgenic mice suppresses IP3-mediated Ca2+ signaling and alleviates age-dependent Purkinje cell firing dysfunction, rescues motor incoordination, and reduces Purkinje cell death, establishing INPP5A as a functional regulator of IP3/Ca2+ homeostasis in Purkinje cells relevant to SCA2 pathogenesis. AAV-mediated gene delivery in transgenic mice, rotarod motor testing, electrophysiology (Purkinje cell firing), histology (Purkinje cell counting) The Journal of neuroscience High 22973002
2015 Deletion of Inpp5a in mice (gene-trap insertion) causes early-onset, slowly progressive Purkinje cell degeneration and ataxia. Homozygous mutants show ~90% perinatal lethality; survivors exhibit locomotor instability at P16 and widespread Purkinje cell loss by P60. Phosphatase activity toward phosphoinositol substrates is reduced in mutant cerebellum, establishing that Inpp5a enzymatic activity is required for Purkinje cell survival. Gene-trap mouse model, qRT-PCR, immunohistochemistry, Western blot, rotarod, β-galactosidase staining, phosphatase activity assay Neurogenetics High 26051944
2020 In SCA17 knock-in mice, mutant TBP inhibits SP1-mediated transcription to downregulate INPP5A. CRISPR/Cas9-mediated deletion of Inpp5a in the cerebellum of wild-type mice leads to Purkinje cell degeneration. Conversely, Inpp5a overexpression decreases IP3 levels and ameliorates Purkinje cell degeneration in SCA17 knock-in mice, demonstrating that INPP5A is a tissue-specific neuroprotective protein acting via IP3 hydrolysis downstream of SP1 transcription. SCA17 knock-in mouse model, stereotaxic AAV injection, CRISPR/Cas9 cerebellar deletion, IP3 measurement, histology (PC counting), SP1 transcription factor ChIP/reporter assays Nature communications High 32107387
2021 Loss of INPP5A causes IP3 accumulation that triggers ER Ca2+ efflux. This Ca2+ release induces dissociation of oxysterol binding protein (OSBP) from the Golgi complex and from VAP-containing ER–Golgi membrane contact sites, thereby depleting cholesterol and Gb3 from the cell surface and blocking clathrin-independent endocytosis (CIE) of Shiga toxin. INPP5A-mediated IP3 hydrolysis is thus required for lipid exchange at ER–Golgi membrane contact sites. INPP5A loss-of-function (cell lines), IP3/Ca2+ measurement, cholesterol/Gb3 cell surface assay, OSBP localization (immunofluorescence/co-fractionation), Shiga toxin CIE assay, receptor-triggered IP3 accumulation Nature communications High 33976123
2024 Genome-scale CRISPR screens identify INPP5A as a selective synthetic lethal dependency in GNAQ/11-mutant uveal melanoma (UM) cells in vitro and in vivo. Suppression of INPP5A in mutant cells causes accumulation of IP3, hyperactivation of IP3-receptor signaling, increased cytosolic calcium, and p53-dependent apoptosis. UM cells and patient tumors exhibit elevated IP4 (a biomarker of enhanced IP3 production) that correlates with sensitivity to INPP5A depletion; GNAQ/11 inhibition abolishes elevated IP4. Genome-scale CRISPR screens, INPP5A KD/KO in cell lines and in vivo xenografts, IP3/IP4 measurement, cytosolic Ca2+ measurement, p53 pathway analysis, GNAQ/11 inhibitor treatment Nature cancer High 38233483
2025 INPP5A is upregulated in GNAQ/11-mutant uveal melanoma cells and is required for cell survival. INPP5A is reversibly palmitoylated; combined palmitoylation and farnesylation target the enzyme to plasma membrane, nuclear envelope, ER, and lysosomes. Mutation of the palmitoylation site reduces plasma membrane localization; mutation of the farnesylation site confines INPP5A to the nucleoplasm. Acute INPP5A inhibition augments the rate of spontaneous Ca2+ oscillations driven by constitutive GNAQ/11 activity, demonstrating that INPP5A regulates IP3-evoked Ca2+ oscillations to prevent Ca2+ overload in UM cells. GFP-tagged INPP5A localization imaging, palmitoylation/farnesylation site mutagenesis, INPP5A inhibitor (YU144369), single-cell Ca2+ imaging, GNAQ/11 inhibitor FR900359 The Journal of biological chemistry High 40812428
2024 INPP5A is tethered to membranes via C-terminal farnesylation and palmitoylation. GFP-INPP5A localizes to plasma membrane, nuclear envelope, ER, and lysosomes. Palmitoylation site mutation reduces plasma membrane localization; farnesylation site mutation results in purely nucleoplasmic localization. INPP5A inhibitor YU144369 causes significant changes in Ca2+ oscillations in constitutively active GNAQ/11-driven UM cells. GFP-fusion localization imaging, palmitoylation/farnesylation mutagenesis, INPP5A small-molecule inhibitor, single-cell Ca2+ imaging bioRxivpreprint Medium bio_10.1101_2024.09.18.613756
2013 In three models of obesity (high-fat diet rats and mice, ob/ob mice), INPP5A (72k-5ptase) expression is increased in skeletal muscle and adipose tissue. Antisense oligonucleotide knockdown of 72k-5ptase reduces its catalytic activity and improves insulin signal transduction and glucose homeostasis in obese rats, identifying INPP5A as a regulator of peripheral insulin signaling. Antisense oligonucleotide knockdown in obese animal models, enzymatic activity assay, immunoblotting for insulin signaling components, hyperinsulinemic-euglycemic clamp The Journal of endocrinology Medium 23349329
2026 MBD2 directly binds the INPP5A promoter to mediate transcriptional repression. PKA signaling phosphorylates MBD2 at S99, recruits 14-3-3σ to stabilize MBD2 protein, and enhances MBD2-mediated inhibition of INPP5A expression. INPP5A overexpression inhibits pituitary tumor cell proliferation, migration, and hormone secretion while knockdown promotes these phenotypes; the mechanism involves INPP5A-mediated IP3 degradation that negatively regulates the PI3K/Akt pathway. ChIP (MBD2 binding to INPP5A promoter), PKA activation assays, phosphorylation site analysis (S99), co-immunoprecipitation (MBD2–14-3-3σ), INPP5A overexpression/knockdown in pituitary tumor cells, PI3K/Akt pathway immunoblotting, cell proliferation/migration assays CNS neuroscience & therapeutics Medium 41857481
2021 TRIM32 deficiency in mice decreases INPP5A protein levels in the cerebellum, and is associated with decreased dendritic arborization and synaptic contacts of Purkinje cells and motor deficits, suggesting TRIM32 acts upstream of INPP5A in cerebellar function. (Note: the paper does not establish a direct E3-ligase write/erase relationship; it reports an association.) TRIM32 knockout mouse model, immunohistochemistry (INPP5A protein levels), Golgi staining (dendritic morphology), motor behavior testing Frontiers in aging neuroscience Low 34111256
2011 In mature hippocampal neurons, loss of IP3 3-kinase A (itpka) leads to compensatory upregulation of INPP5A and SERCA2b, resulting in decreased duration of IP3 signals and shorter IP3-dependent Ca2+ transients at synapses. This establishes INPP5A as a functional participant in shaping synaptic Ca2+ transients. itpka knockdown in hippocampal neurons, Western blot (INPP5A and SERCA2b levels in synaptosomes), Ca2+ imaging Cellular signalling Low 22120525
2017 miR-181a-5p directly targets INPP5A (validated by dual-luciferase reporter assay). INPP5A overexpression inhibits cervical cancer cell proliferation and invasion and enhances apoptosis; miR-181a-5p mimic attenuates these effects, confirming INPP5A as a functional downstream target of miR-181a-5p in cervical cancer cells. Dual-luciferase reporter assay, INPP5A overexpression in HeLa/SiHa cells, miR-181a-5p mimic/inhibitor transfection, proliferation/invasion/apoptosis assays Oncology research Medium 28653606

Source papers

Stage 0 corpus · 72 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Rapidly inducible changes in phosphatidylinositol 4,5-bisphosphate levels influence multiple regulatory functions of the lipid in intact living cells. The Journal of cell biology 298 17088424
2011 Myo-inositol and beyond--emerging networks under stress. Plant science : an international journal of experimental plant biology 208 21889044
2009 The role of the inositol polyphosphate 5-phosphatases in cellular function and human disease. The Biochemical journal 186 19272022
2018 DNA methylation analysis on purified neurons and glia dissects age and Alzheimer's disease-specific changes in the human cortex. Epigenetics & chromatin 167 30045751
2005 A universal role for inositol 1,4,5-trisphosphate-mediated signaling in plant gravitropism. Plant physiology 101 16384898
2012 Chronic suppression of inositol 1,4,5-triphosphate receptor-mediated calcium signaling in cerebellar purkinje cells alleviates pathological phenotype in spinocerebellar ataxia 2 mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 96 22973002
2001 Phosphoinositide-specific inositol polyphosphate 5-phosphatase IV inhibits Akt/protein kinase B phosphorylation and leads to apoptotic cell death. The Journal of biological chemistry 82 11706019
2001 Molecular characterization of At5PTase1, an inositol phosphatase capable of terminating inositol trisphosphate signaling. Plant physiology 70 11402208
2018 Meta-analysis of epigenome-wide association studies of cognitive abilities. Molecular psychiatry 69 29311653
1998 Multiple forms of the SH2-containing inositol phosphatase, SHIP, are generated by C-terminal truncation. Blood 54 9694708
2017 Atxn2 Knockout and CAG42-Knock-in Cerebellum Shows Similarly Dysregulated Expression in Calcium Homeostasis Pathway. Cerebellum (London, England) 53 26868665
2007 Inositol polyphosphate 5-phosphatases 1 and 2 are required for regulating seedling growth. Plant physiology 52 17237190
2017 miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). Oncology research 51 28653606
2008 An inositol polyphosphate 5-phosphatase functions in PHOTOTROPIN1 signaling in Arabidopis by altering cytosolic Ca2+. The Plant cell 46 18252844
2006 Phosphatidylinositol 3-phosphate [PtdIns3P] is generated at the plasma membrane by an inositol polyphosphate 5-phosphatase: endogenous PtdIns3P can promote GLUT4 translocation to the plasma membrane. Molecular and cellular biology 46 16880518
1997 SHIP, a new player in cytokine-induced signalling. Leukemia 45 9009077
2014 Phosphoinositide-signaling is one component of a robust plant defense response. Frontiers in plant science 44 24966862
2002 Up-regulation of phosphoinositide metabolism in tobacco cells constitutively expressing the human type I inositol polyphosphate 5-phosphatase. Plant physiology 41 12177493
2021 Inositol triphosphate-triggered calcium release blocks lipid exchange at endoplasmic reticulum-Golgi contact sites. Nature communications 39 33976123
2013 Inositol polyphosphate phosphatidylinositol 5-phosphatase9 (At5ptase9) controls plant salt tolerance by regulating endocytosis. Molecular plant 38 23658066
2009 Increasing inositol (1,4,5)-trisphosphate metabolism affects drought tolerance, carbohydrate metabolism and phosphate-sensitive biomass increases in tomato. Plant biotechnology journal 37 20040061
2013 Identification of novel genetic alterations in samples of malignant glioma patients. PloS one 36 24358143
2020 Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17. Nature communications 33 32107387
2007 Regulation of FcgammaR-stimulated phagocytosis by the 72-kDa inositol polyphosphate 5-phosphatase: SHIP1, but not the 72-kDa 5-phosphatase, regulates complement receptor 3 mediated phagocytosis by differential recruitment of these 5-phosphatases to the phagocytic cup. Blood 33 17682126
2010 Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. Cancer prevention research (Philadelphia, Pa.) 32 20876729
2009 Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. Nucleic acids research 32 19875416
2014 Chromosomal Instability and Phosphoinositide Pathway Gene Signatures in Glioblastoma Multiforme. Molecular neurobiology 31 25502460
2015 Canine Mammary Tumours Are Affected by Frequent Copy Number Aberrations, including Amplification of MYC and Loss of PTEN. PloS one 29 25955013
2020 Mouse Ataxin-2 Expansion Downregulates CamKII and Other Calcium Signaling Factors, Impairing Granule-Purkinje Neuron Synaptic Strength. International journal of molecular sciences 28 32932600
2011 Inositol-1,4,5-trisphosphate 3-kinase A regulates dendritic morphology and shapes synaptic Ca2+ transients. Cellular signalling 28 22120525
2015 Deletion of Inpp5a causes ataxia and cerebellar degeneration in mice. Neurogenetics 27 26051944
2006 Phosphoinositide-specific inositol polyphosphate 5-phosphatase IV inhibits inositide trisphosphate accumulation in hypothalamus and regulates food intake and body weight. Endocrinology 26 16916951
2008 A phosphatidylinositol phosphate-specific myo-inositol polyphosphate 5-phosphatase required for seedling growth. Plant molecular biology 25 18392779
2021 DNA methylome in visceral adipose tissue can discriminate patients with and without colorectal cancer. Epigenetics 24 34311674
2024 Human skeletal muscle possesses an epigenetic memory of high-intensity interval training. American journal of physiology. Cell physiology 20 39570634
2020 Genome-wide DNA methylation analysis of cognitive function in middle and old-aged Chinese monozygotic twins. Journal of psychiatric research 17 33131831
2008 Transcriptional changes in U343 MG-a glioblastoma cell line exposed to ionizing radiation. Human & experimental toxicology 16 19273547
2015 Coordinated Expression of Phosphoinositide Metabolic Genes during Development and Aging of Human Dorsolateral Prefrontal Cortex. PloS one 15 26168237
2011 Silencer of death domains (SODD) inhibits skeletal muscle and kidney enriched inositol 5-phosphatase (SKIP) and regulates phosphoinositide 3-kinase (PI3K)/Akt signaling to the actin cytoskeleton. The Journal of biological chemistry 15 21712384
1996 A novel phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase associates with the interleukin-3 receptor. The Journal of biological chemistry 15 8939907
2021 Optogenetic Modulation of Intraocular Pressure in a Glucocorticoid-Induced Ocular Hypertension Mouse Model. Translational vision science & technology 14 34111256
2011 Reduction of inositol (1,4,5)-trisphosphate affects the overall phosphoinositol pathway and leads to modifications in light signalling and secondary metabolism in tomato plants. Journal of experimental botany 14 21994174
2022 Identification of Methylation Signatures and Rules for Sarcoma Subtypes by Machine Learning Methods. BioMed research international 13 36619306
2020 Ectopic Expression of Gs5PTase8, a Soybean Inositol Polyphosphate 5-Phosphatase, Enhances Salt Tolerance in Plants. International journal of molecular sciences 13 32033113
2022 The Emerging Key Role of the mGluR1-PKCγ Signaling Pathway in the Pathogenesis of Spinocerebellar Ataxias: A Neurodevelopmental Viewpoint. International journal of molecular sciences 12 36012439
2024 INPP5A phosphatase is a synthetic lethal target in GNAQ and GNA11-mutant melanomas. Nature cancer 11 38233483
2021 Identification of Novel Autoantibodies Based on the Human Proteomic Chips and Evaluation of Their Performance in the Detection of Gastric Cancer. Frontiers in oncology 11 33718231
2019 Expansion and Functional Divergence of Inositol Polyphosphate 5-Phosphatases in Angiosperms. Genes 11 31121965
2021 Deficiency of TRIM32 Impairs Motor Function and Purkinje Cells in Mid-Aged Mice. Frontiers in aging neuroscience 10 34421574
2024 KRN5b regulates maize kernel row number through mediating phosphoinositol signalling. Plant biotechnology journal 8 39302972
2016 Reversible Chemical Dimerization by rCD1. Methods in enzymology 8 28063490
2023 MARCKS and PI(4,5)P2 reciprocally regulate actin-based dendritic spine morphology. Molecular biology of the cell 7 38088877
2022 INPP5A/HLA-G1/IL-10/MMP-21 Axis in Progression of Esophageal Squamous Cell Carcinoma. Iranian biomedical journal 7 36437782
2015 A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh. Cancer 7 25759212
2013 Inhibition of 72 kDa inositol polyphosphate 5-phosphatase E improves insulin signal transduction in diet-induced obesity. The Journal of endocrinology 7 23349329
2017 Polyphenolic extract of InsP 5-ptase expressing tomato plants reduce the proliferation of MCF-7 breast cancer cells. PloS one 6 28448505
2025 Functional-proteomics-based investigation of the cellular response to farnesyltransferase inhibition in lung cancer. iScience 5 39995872
2025 Soybean Inositol Polyphosphate 5-Phosphatase 8 Confers Salt Tolerance by Reducing Sodium Influx Through Inositol 1,4,5-Trisphosphate Signalling. Plant, cell & environment 5 40735769
2020 A putative tomato inositol polyphosphate 5-phosphatase, Le5PT1, is involved in plant growth and abiotic stress responses. 3 Biotech 5 31950007
2015 Genetic reduction of inositol triphosphate (InsP₃) increases tolerance of tomato plants to oxidative stress. Planta 4 25893866
2021 A novel microduplication in INPP5A segregates with schizophrenia spectrum disorder in the family of a patient with both childhood onset schizophrenia and autism spectrum disorder. American journal of medical genetics. Part A 3 33720513
2025 MTS1 regulates rice plant architecture by mediating phosphoinositide metabolism. Plant biotechnology journal 2 40627726
2025 The genetics of TDP43-Type-C neurodegeneration: a whole genome sequencing study. medRxiv : the preprint server for health sciences 1 39973992
2025 Genome-wide characterization of the inositol polyphosphate 5-phosphatase gene family in cotton revealed Gh5PTase34 as a key regulator of Pi starvation response and rhizosphere acidification. Plant physiology and biochemistry : PPB 1 40239257
2024 [Prokaryotic expression, purification, and activity of the inositol polyphosphate 5-phosphatase Gs5PTase8 from wild soybean]. Sheng wu gong cheng xue bao = Chinese journal of biotechnology 1 39467752
2026 The PKA/MBD2 Axis Transcriptionally Represses INPP5A to Modulate PI3K/Akt Signaling and Accelerate Pituitary Tumorigenesis. CNS neuroscience & therapeutics 0 41857481
2026 Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs. The FEBS journal 0 41909920
2026 Genome-Wide Discovery Reveals Adipose-Specific and Systemic Regulators of Insulin Resistance. medRxiv : the preprint server for health sciences 0 41959785
2026 Identification of key genes and immune mechanisms in atrial fibrillation: An observational bioinformatics and single-cell transcriptome study. Medicine 0 42071886
2025 MicroRNA analysis of porcine muscle tissue involved in phosphoinositol metabolism. Frontiers in veterinary science 0 40777826
2025 Inositol (1,4,5)-trisphosphate 5-phosphatase promotes survival of uveal melanoma by regulating oncogenic G protein-driven calcium oscillations. The Journal of biological chemistry 0 40812428
2019 [Screening of interacting proteins of SHIP2 in human gastric mucosal epithelium by yeast two-hybrid system]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 0 31878996

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