Affinage

INPP5A

Inositol polyphosphate-5-phosphatase A · UniProt Q14642

Length
412 aa
Mass
47.8 kDa
Annotated
2026-04-28
78 papers in source corpus 14 papers cited in narrative 14 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

INPP5A is a type I inositol polyphosphate 5-phosphatase that hydrolyzes both IP3 and PI(3,4,5)P3, thereby terminating IP3 receptor–mediated calcium signaling and attenuating PI3K/Akt pathway activation (PMID:11706019, PMID:33976123). In cerebellar Purkinje cells, INPP5A is essential for survival: genetic deletion causes progressive Purkinje cell degeneration and ataxia, while overexpression rescues neurodegeneration in SCA2 and SCA17 mouse models by reducing IP3 levels and normalizing calcium dynamics (PMID:26051944, PMID:22973002, PMID:32107387). INPP5A is a farnesylated and palmitoylated protein whose dual lipid modifications direct it to the plasma membrane and endomembranes; loss of INPP5A triggers IP3-dependent calcium release from the ER that dissociates OSBP from ER–Golgi membrane contact sites, disrupting cholesterol and glycosphingolipid surface delivery (PMID:33976123, PMID:40812428). In GNAQ/GNA11-mutant uveal melanoma, INPP5A is a synthetic lethal dependency that buffers constitutive Gq-driven IP3 production, and its depletion causes calcium overload and p53-dependent apoptosis (PMID:38233483, PMID:40812428).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2001 High

    Establishing that INPP5A is not merely an IP3 phosphatase but also a high-affinity PI(3,4,5)P3 phosphatase that controls Akt signaling and apoptotic sensitivity answered the question of whether 5-phosphatases could directly regulate the PI3K/Akt axis.

    Evidence In vitro enzyme kinetics with purified substrates plus stable overexpression in HEK293 cells measuring phosphoinositide mass, Akt phosphorylation, and FAS-induced apoptosis

    PMID:11706019

    Open questions at the time
    • Endogenous loss-of-function data for PI(3,4,5)P3 regulation were not provided
    • Relative contribution of IP3 vs PI(3,4,5)P3 hydrolysis in physiological contexts unclear
    • No structural basis for substrate selectivity
  2. 2006 Medium

    Demonstrating that INPP5A is an insulin-responsive phosphatase in hypothalamic neurons whose knockdown reduces food intake established a role for INPP5A in central metabolic regulation beyond its known IP3 phosphatase activity.

    Evidence Antisense oligonucleotide knockdown in rat hypothalamus with inositol phosphate accumulation, food intake, and body weight measurements

    PMID:16916951

    Open questions at the time
    • Genetic loss-of-function model not used
    • Whether the metabolic effect is IP3- or PI(3,4,5)P3-dependent was not resolved
    • No independent replication
  3. 2007 High

    Showing that INPP5A is dynamically recruited to FcγR phagocytic cups to degrade PI(3,4,5)P3 and enable phagosome closure answered how PI(3,4,5)P3 is spatiotemporally resolved during receptor-specific phagocytosis.

    Evidence Live-cell PI(3,4,5)P3 biosensor imaging combined with dominant-negative expression and siRNA knockdown in macrophages

    PMID:17682126

    Open questions at the time
    • Whether INPP5A recruitment mechanism involves direct lipid or protein interactions at the cup is unknown
    • In vivo phagocytosis phenotype not tested
  4. 2011 Medium

    Identification of compensatory INPP5A upregulation at synapses upon loss of ITPKA linked INPP5A to fine-tuning of synaptic IP3/Ca²⁺ signal duration, addressing which phosphatases shape postsynaptic IP3 dynamics.

    Evidence ITPKA siRNA knockdown in neurons with synaptoneurosome fractionation, IP3 mass assay, and dendritic calcium imaging

    PMID:22120525

    Open questions at the time
    • Evidence is correlative from a compensatory context
    • Direct synaptic loss-of-function of INPP5A not performed
    • Mechanism of upregulation unknown
  5. 2012 High

    AAV-mediated Purkinje cell–specific overexpression of INPP5A rescuing SCA2 motor and electrophysiological phenotypes established INPP5A as a neuroprotective agent that counteracts IP3R-driven excitotoxic calcium signaling in cerebellar ataxia.

    Evidence AAV delivery to SCA2 transgenic mouse cerebellum with rotarod, Purkinje cell electrophysiology, and histological survival analysis

    PMID:22973002

    Open questions at the time
    • Endogenous INPP5A loss-of-function in cerebellum had not yet been reported
    • Whether rescue reflects IP3 or PI(3,4,5)P3 hydrolysis not distinguished
  6. 2013 Medium

    Antisense reduction of INPP5A in obese rats improving insulin sensitivity and glucose homeostasis established it as a negative regulator of peripheral insulin signaling, complementing the central metabolic role described earlier.

    Evidence Antisense knockdown in obese rodents with hyperinsulinemic-euglycemic clamp and insulin signaling immunoblots

    PMID:23349329

    Open questions at the time
    • Genetic knockout model for peripheral insulin action not available
    • Relative importance in muscle vs adipose not resolved
  7. 2015 High

    Gene-trap deletion of Inpp5a causing progressive Purkinje cell loss and ataxia in mice provided the first definitive loss-of-function genetic evidence that INPP5A is non-redundantly required for Purkinje cell survival.

    Evidence Gene-trap mouse model with rotarod, immunohistochemistry, and phosphatase activity assays

    PMID:26051944

    Open questions at the time
    • Cell-autonomous vs non-cell-autonomous contributions not fully dissected
    • Downstream calcium and IP3 levels not directly measured in knockout cerebellum
  8. 2020 High

    Discovery that mutant TBP in SCA17 represses INPP5A transcription via SP1, and that CRISPR deletion of Inpp5a in wild-type cerebellum recapitulates Purkinje cell degeneration, linked INPP5A deficiency to transcriptionally driven cerebellar neurodegeneration and identified the upstream regulatory axis.

    Evidence SCA17 knock-in mice; CRISPR/Cas9 cerebellar deletion; AAV overexpression rescue; IP3 measurement; SP1 transcription assays

    PMID:32107387

    Open questions at the time
    • Whether SP1-INPP5A axis is relevant in other polyglutamine ataxias beyond SCA2 and SCA17 not tested
    • Chromatin-level regulation of INPP5A promoter not fully characterized
  9. 2021 High

    Demonstration that INPP5A loss triggers an IP3→Ca²⁺→OSBP dissociation cascade that disrupts ER–Golgi membrane contact sites and depletes surface cholesterol/Gb3 revealed a previously unknown role for INPP5A in non-vesicular lipid transport.

    Evidence INPP5A loss-of-function with IP3 measurement, calcium imaging, OSBP localization, cholesterol/Gb3 staining, and Shiga toxin uptake

    PMID:33976123

    Open questions at the time
    • Whether this lipid transfer defect contributes to Purkinje cell degeneration is unknown
    • Direct physical interaction between INPP5A and OSBP/VAP not assessed
  10. 2024 High

    Genome-scale CRISPR screens identifying INPP5A as a selective synthetic lethal dependency in GNAQ/GNA11-mutant uveal melanoma established that oncogenic Gq signaling creates a critical reliance on INPP5A to buffer IP3/Ca²⁺ overload, with p53 as the apoptotic executor upon INPP5A loss.

    Evidence Genome-scale CRISPR screens in UM cell panels; xenograft models; IP3/IP4 mass measurements; calcium imaging; p53-dependent apoptosis assays

    PMID:38233483

    Open questions at the time
    • Therapeutic window for INPP5A inhibition in vivo not established
    • Whether other Gq-driven cancers share this dependency is untested
  11. 2025 High

    Structure-function analysis showing that farnesylation directs INPP5A away from the nucleus while palmitoylation targets it to the plasma membrane, where it controls Ca²⁺ oscillation frequency, resolved how dual lipid modifications govern INPP5A's subcellular localization and function in UM cells.

    Evidence GFP-tagged INPP5A with prenylation and palmitoylation site mutagenesis; single-cell calcium imaging; pharmacological inhibitor YU144369

    PMID:40812428

    Open questions at the time
    • Identity of the palmitoyl acyltransferase(s) modifying INPP5A unknown
    • Structural basis for membrane orientation not determined
    • Whether lipid modification state changes in cerebellar neurons is untested
  12. 2026 Medium

    Identification of MBD2 as a direct transcriptional repressor of INPP5A, stabilized by PKA-mediated phosphorylation and 14-3-3σ binding, revealed a second transcriptional axis (beyond SP1/TBP) that silences INPP5A to promote IP3/Akt-driven tumorigenesis in pituitary tumors.

    Evidence ChIP for MBD2 at INPP5A promoter; co-IP of MBD2/14-3-3σ; PKA activation; INPP5A overexpression/knockdown in pituitary tumor cells

    PMID:41857481

    Open questions at the time
    • Whether MBD2-mediated INPP5A repression occurs in other tumor types is unknown
    • Epigenetic context (DNA methylation state of INPP5A promoter) not fully characterized
    • Single-lab finding awaits independent confirmation

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for INPP5A's dual substrate specificity toward IP3 and PI(3,4,5)P3, the identity of the palmitoyl acyltransferase(s) modifying INPP5A, whether the ER–Golgi lipid transfer function contributes to neurodegeneration, and whether INPP5A inhibition is therapeutically viable in GNAQ/GNA11-mutant cancers.
  • No crystal structure of INPP5A
  • Palmitoylation enzyme not identified
  • Causal link between lipid transfer defect and Purkinje cell death not tested
  • In vivo pharmacological INPP5A inhibition in cancer models not yet reported

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 7 GO:0098772 molecular function regulator activity 4
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005886 plasma membrane 2 GO:0005635 nuclear envelope 1 GO:0005764 lysosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1643685 Disease 5 R-HSA-112316 Neuronal System 4 R-HSA-5357801 Programmed Cell Death 2 R-HSA-382551 Transport of small molecules 1
Partners
GNA11GNAQMBD2OSBPSP1TP53YWHAS

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Inositol polyphosphate 5-phosphatase IV (INPP5A/5ptase IV) hydrolyzes PI(3,4,5)P3 with ~10-fold higher affinity (Km = 0.65 µM) than other 5-phosphatases including SHIP, OCRL, and 5ptase II. Overexpression in 293 cells depleted both PI(4,5)P2 and PI(3,4,5)P3, increased PI(4)P and PI(3,4)P2, inhibited Akt phosphorylation (correlated with PI(3,4,5)P3 levels, not PI(3,4)P2), and sensitized cells to FAS-induced apoptosis, placing 5ptase IV as a regulator of the PI3K/Akt pathway. In vitro enzyme kinetics; stable cell lines overexpressing 5ptase IV alone or combined with inositol polyphosphate 4-phosphatase; phosphoinositide mass measurement; Akt phosphorylation immunoblot; FAS-induced apoptosis assay The Journal of biological chemistry High 11706019
2006 Inositol polyphosphate 5-phosphatase IV (INPP5A/5ptase IV) is highly expressed in arcuate and lateral hypothalamic neurons, undergoes time-dependent tyrosine phosphorylation following intracerebroventricular insulin, and its antisense-mediated knockdown (~80% reduction) increases basal inositol phosphate accumulation in the hypothalamus, reduces food intake, and causes body weight loss, demonstrating that it regulates PI3K signaling downstream of insulin in the hypothalamus. Antisense oligonucleotide knockdown in rat hypothalamus; immunoblotting for tyrosine phosphorylation; inositol phosphate accumulation assay; food intake and body weight measurement Endocrinology Medium 16916951
2007 The 72-kDa inositol polyphosphate 5-phosphatase (72-5ptase, i.e., INPP5A) is dynamically recruited to FcγR-stimulated phagocytic cups, where it degrades PI(3,4,5)P3; dominant-negative 72-5ptase or siRNA knockdown amplifies and prolongs PI(3,4,5)P3 at the FcγR phagocytic cup but not the CR3 cup, inhibiting pseudopod extension and phagosome closure specifically in FcγR-mediated phagocytosis. Time-lapse imaging of PI(3,4,5)P3 biosensors; dominant-negative expression; siRNA knockdown; co-localization to phagocytic cup Blood High 17682126
2012 AAV-mediated overexpression of Inpp5a (5PP) in Purkinje cells of SCA2 transgenic mice chronically reduces IP3 levels, alleviates age-dependent aberrant firing patterns of Purkinje cells, rescues motor incoordination, and prevents Purkinje cell death, demonstrating that INPP5A-mediated IP3 hydrolysis is neuroprotective against supranormal IP3R-driven calcium signaling in SCA2. AAV-mediated gene delivery; rotarod behavioral testing; electrophysiology of Purkinje cell firing; histological assessment of Purkinje cell survival The Journal of neuroscience High 22973002
2015 Gene-trap deletion of Inpp5a in mice causes early-onset, slowly progressive Purkinje cell degeneration and ataxia; homozygous mutants show reduced phosphatase activity toward phosphoinositol substrates, locomotor instability beginning at P16, and widespread Purkinje cell loss by P60, establishing a non-redundant, cell-autonomous requirement for INPP5A in 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 down-regulate INPP5A; CRISPR/Cas9-mediated deletion of Inpp5a in wild-type mouse cerebellum causes Purkinje cell degeneration, and Inpp5a overexpression decreases IP3 levels and ameliorates Purkinje cell degeneration in SCA17 mice, placing INPP5A as a downstream effector of TBP/SP1 transcription that protects Purkinje cells by hydrolyzing IP3. SCA17 knock-in mice; CRISPR/Cas9 cerebellar deletion; AAV-mediated Inpp5a overexpression; IP3 level measurement; Purkinje cell histology; SP1-mediated transcription assays Nature communications High 32107387
2021 Loss of INPP5A causes IP3 accumulation and calcium efflux from ER stores, which triggers dissociation of oxysterol binding protein (OSBP) from the Golgi and from VAP-containing ER-Golgi membrane contact sites, resulting in depletion of cholesterol and Gb3 from the cell surface and blockade of clathrin-independent endocytosis of Shiga toxin. INPP5A loss-of-function; IP3 measurement; calcium imaging; OSBP localization by confocal microscopy; cholesterol and Gb3 surface staining; Shiga toxin uptake assay Nature communications High 33976123
2024 Genome-scale CRISPR screens identified INPP5A as a selective synthetic lethal dependency in GNAQ/GNA11-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. GNAQ/GNA11-mutant cells and patient tumors exhibit elevated IP4 (a biomarker of enhanced IP3 production) that is abolished by GNAQ/GNA11 inhibition and correlates with sensitivity to INPP5A depletion. Genome-scale CRISPR screens; in vivo xenograft models; IP3/IP4 mass measurement; calcium imaging; p53-dependent apoptosis assays; GNAQ/GNA11 inhibitor experiments Nature cancer High 38233483
2025 INPP5A is a farnesylated and reversibly palmitoylated membrane-bound IP3 5-phosphatase that is upregulated in and required by CA-GNAQ/11-driven UM cells. Palmitoylation targets INPP5A to the plasma membrane (mutation of palmitoylation site reduces PM localization), while mutation of the prenylation site results in purely nucleoplasmic localization. INPP5A regulates low-frequency Ca2+ oscillations in UM cells driven by constitutive Gq/11 activity, and acute pharmacological inhibition of INPP5A augments Ca2+ oscillation rate, demonstrating that it safeguards UM cells from Ca2+ overload by controlling IP3-evoked Ca2+ dynamics. GFP-tagged INPP5A localization imaging; palmitoylation and prenylation site mutagenesis; single-cell calcium imaging; pharmacological INPP5A inhibitor (YU144369); UM cell survival assays The Journal of biological chemistry High 40812428
2024 INPP5A is targeted to plasma membrane, nuclear envelope, ER, and lysosomes through C-terminal farnesylation and palmitoylation; mutation of the palmitoylation site significantly reduces plasma membrane localization, and these distinct localizations regulate IP3 metabolism and Ca2+ mobilization in uveal melanoma cells. GFP-INPP5A subcellular localization imaging; palmitoylation and prenylation site mutagenesis; calcium mobilization assays in UM cells bioRxivpreprint Medium bio_10.1101_2024.09.18.613756
2013 In obese rodent models, 72k-5ptase (INPP5A) expression is increased in skeletal muscle and adipose tissue; antisense oligonucleotide reduction of 72k-5ptase catalytic activity in obese rats improves insulin signal transduction and restores glucose homeostasis, demonstrating its role as a negative regulator of peripheral insulin signaling. Antisense oligonucleotide knockdown; immunoblotting for insulin signaling components; hyperinsulinemic-euglycemic clamp; 72k-5ptase catalytic activity assay The Journal of endocrinology Medium 23349329
2011 In itpka-deficient neurons, the levels of Inpp5a protein are upregulated at synapses as a compensatory response, and this is associated with decreased duration of IP3 signals and shorter IP3-dependent Ca2+ transients, establishing that INPP5A is a synaptic regulator of IP3 and Ca2+ signal duration. siRNA knockdown of itpka; immunoblotting for Inpp5a at synaptoneurosomes; IP3 mass assay; dendritic Ca2+ imaging Cellular signalling Medium 22120525
2021 TRIM32 deficiency in mice decreases INPP5A protein levels in the cerebellum, associated with impaired motor balance and Purkinje cell dendritic/synaptic deficits, suggesting TRIM32 regulates INPP5A abundance in cerebellar neurons. TRIM32 knockout mice; immunohistochemistry; Golgi staining; rotarod; immunoblotting for INPP5A Frontiers in aging neuroscience Low 34421574
2026 MBD2 directly binds the INPP5A promoter to repress its transcription; PKA-mediated phosphorylation of MBD2 at S99 recruits 14-3-3σ to stabilize MBD2, enhancing transcriptional repression of INPP5A; reduced INPP5A promotes IP3 accumulation and PI3K/Akt pathway activation, driving pituitary tumor malignant progression. ChIP assay (MBD2 binding to INPP5A promoter); PKA pharmacological activation; co-immunoprecipitation (MBD2/14-3-3σ); INPP5A overexpression and knockdown in pituitary tumor cells; IP3 measurement; PI3K/Akt pathway immunoblotting CNS neuroscience & therapeutics Medium 41857481

Source papers

Stage 0 corpus · 78 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 297 17088424
2011 Myo-inositol and beyond--emerging networks under stress. Plant science : an international journal of experimental plant biology 205 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
2008 Transgenic Arabidopsis plants expressing the type 1 inositol 5-phosphatase exhibit increased drought tolerance and altered abscisic acid signaling. The Plant cell 113 18849493
2004 Cotyledon vascular pattern2-mediated inositol (1,4,5) triphosphate signal transduction is essential for closed venation patterns of Arabidopsis foliar organs. The Plant cell 109 15100402
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 94 22973002
2004 FRAGILE FIBER3, an Arabidopsis gene encoding a type II inositol polyphosphate 5-phosphatase, is required for secondary wall synthesis and actin organization in fiber cells. The Plant cell 83 15539468
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 69 11402208
2018 Meta-analysis of epigenome-wide association studies of cognitive abilities. Molecular psychiatry 66 29311653
2008 Phosphoinositide and inositolpolyphosphate signalling in defense responses of Arabidopsis thaliana challenged by mechanical wounding. Molecular plant 61 19825537
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) 52 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 43 24966862
2004 Molecular characterization of an Arabidopsis gene encoding a phospholipid-specific inositol polyphosphate 5-phosphatase. Plant physiology 41 15181205
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 37 33976123
2013 Inositol polyphosphate phosphatidylinositol 5-phosphatase9 (At5ptase9) controls plant salt tolerance by regulating endocytosis. Molecular plant 37 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 34 24358143
2020 Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17. Nature communications 32 32107387
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
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 32 17682126
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 26 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 24 18392779
2024 Human skeletal muscle possesses an epigenetic memory of high-intensity interval training. American journal of physiology. Cell physiology 19 39570634
2021 DNA methylome in visceral adipose tissue can discriminate patients with and without colorectal cancer. Epigenetics 19 34311674
2020 Genome-wide DNA methylation analysis of cognitive function in middle and old-aged Chinese monozygotic twins. Journal of psychiatric research 16 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 12 32033113
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
2012 DWARF50 (D50), a rice (Oryza sativa L.) gene encoding inositol polyphosphate 5-phosphatase, is required for proper development of intercalary meristem. Plant, cell & environment 11 22574770
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 10 36012439
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 7 39302972
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
2016 Reversible Chemical Dimerization by rCD1. Methods in enzymology 7 28063490
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
2020 A putative tomato inositol polyphosphate 5-phosphatase, Le5PT1, is involved in plant growth and abiotic stress responses. 3 Biotech 5 31950007
2025 Functional-proteomics-based investigation of the cellular response to farnesyltransferase inhibition in lung cancer. iScience 4 39995872
2015 Genetic reduction of inositol triphosphate (InsP₃) increases tolerance of tomato plants to oxidative stress. Planta 4 25893866
2025 Soybean Inositol Polyphosphate 5-Phosphatase 8 Confers Salt Tolerance by Reducing Sodium Influx Through Inositol 1,4,5-Trisphosphate Signalling. Plant, cell & environment 3 40735769
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 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
2025 MTS1 regulates rice plant architecture by mediating phosphoinositide metabolism. Plant biotechnology journal 1 40627726
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
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
2021 Characterization of the ERP gene family in Arabidopsis thaliana. Plant signaling & behavior 0 33906568
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