Affinage

ITPR2

Inositol 1,4,5-trisphosphate-gated calcium channel ITPR2 · UniProt Q14571

Length
2701 aa
Mass
308.1 kDa
Annotated
2026-04-28
42 papers in source corpus 20 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ITPR2 is an endoplasmic reticulum-resident inositol 1,4,5-trisphosphate (IP3)-gated calcium release channel that couples ER calcium stores to mitochondrial and cytosolic signaling across diverse cell types. IP3 binds with high affinity to the IP3-binding core domain (residues 224–604; key residues R269, K508, R511), triggering conformational changes that gate calcium release (PMID:30244130); at mitochondria-associated ER membranes (MAMs), ITPR2 participates in an IP3R2–Grp75–VDAC1 complex that transfers calcium to mitochondria via MCU, and this ER-to-mitochondria calcium flux drives downstream outcomes including decreased mitochondrial membrane potential, ROS accumulation, and cellular senescence, pyroptosis, or apoptosis depending on context (PMID:24797322, PMID:33526781, PMID:38378646, PMID:40489543). In astrocytes, ITPR2 is the dominant IP3 receptor mediating GPCR-dependent somatic calcium transients and is required for experience-dependent synaptic depression and locomotion-evoked neuronal modulation (PMID:25894291, PMID:36090792, PMID:40710356), while in oligodendrocytes it governs calcium homeostasis necessary for OPC proliferation via the MAPK/ERK–CDK6 axis, differentiation, and proper myelination (PMID:34630045, PMID:38476116).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2013 High

    Establishing that IP3R2 is the specific isoform whose expression level determines pro-apoptotic calcium signaling upon disruption of the Bcl-2/IP3R complex answered whether individual IP3R isoforms have non-redundant roles in apoptosis.

    Evidence siRNA knockdown of IP3R1/2/3 individually and correlation of TAT-IDP(S)-induced apoptosis with IP3R2 levels across diffuse large B-cell lymphoma lines

    PMID:23681227

    Open questions at the time
    • Structural basis of Bcl-2 selectivity for IP3R2 over other isoforms unknown
    • Relevance beyond DLBCL not tested
  2. 2014 High

    Demonstrating that ITPR2-mediated ER-to-mitochondria calcium transfer via MCU drives ROS accumulation, mitochondrial depolarization, and oncogene-induced senescence established a direct mechanistic link between IP3R2 calcium flux and the senescence program.

    Evidence Loss-of-function screen, siRNA knockdown of ITPR2 and MCU, calcium imaging, ROS and mitochondrial membrane potential assays in OIS models

    PMID:24797322

    Open questions at the time
    • Identity of adaptor proteins mediating ER-mitochondria contact in this context not defined
    • Whether other IP3R isoforms can substitute under chronic conditions unknown
  3. 2014 High

    Identifying IP3R2 as the dominant astrocytic IP3 receptor for GPCR-dependent somatic calcium signals — while showing residual process-localized calcium is IP3R2-independent — defined the spatial selectivity of IP3R2 in glial calcium signaling.

    Evidence Ip3r2 knockout and conditional knockout mice with two-photon calcium imaging in vivo and in slices, behavioral battery

    PMID:25429263 PMID:25894291

    Open questions at the time
    • Molecular identity of calcium sources in astrocyte processes not resolved
    • Behavioral consequences under more complex cognitive demands remain uncertain
  4. 2018 Medium

    Biochemical characterization of the IP3-binding core domain (residues 224–604) with key ligand-coordinating residues R269, K508, R511 provided the first direct structural insight into how IP3R2 recognizes its ligand.

    Evidence Recombinant IBC domain purification, far-CD and intrinsic fluorescence spectroscopy upon IP3 binding

    PMID:30244130

    Open questions at the time
    • No mutagenesis validation of individual residue contributions
    • No high-resolution cryo-EM or crystal structure of IP3R2
    • Full-length channel gating mechanism not addressed
  5. 2021 High

    In vivo confirmation that Itpr2 knockout reduces ER-mitochondria contacts and that forced re-establishment of those contacts induces premature senescence provided causal evidence that the physical MAM architecture maintained by IP3R2 — not merely calcium flux — is integral to the senescence mechanism.

    Evidence Itpr2 knockout mice, electron microscopy quantification of ER-mitochondria contacts, forced synthetic linker contacts

    PMID:33526781

    Open questions at the time
    • Molecular partners that tether IP3R2-dependent MAMs in senescence not fully catalogued
    • Whether MAM structural role is separable from channel activity not resolved
  6. 2021 Medium

    Showing that Itpr2 deficiency delays oligodendrocyte differentiation, shifts myelination toward small-caliber axons, and alters optic nerve conduction established a cell-autonomous role for IP3R2 calcium signaling in CNS myelination.

    Evidence Conventional and conditional Itpr2 mutant mice, immunostaining for CAII+ oligodendrocyte subtypes, compound action potential recordings

    PMID:34630045

    Open questions at the time
    • Downstream calcium effectors mediating differentiation not identified
    • Whether the phenotype persists into adulthood not fully characterized
  7. 2022 Medium

    Identification of the IP3R2–VDAC1–MICU1 complex at MAMs, assembled on detyrosinated α-tubulin scaffolds upon autophagy activation, revealed how cytoskeletal remodeling controls the composition of ER-mitochondria calcium transfer machinery.

    Evidence Co-immunoprecipitation, autophagy inhibitors, siRNA, calcium imaging in hepatocytes under PFOS exposure

    PMID:35192817

    Open questions at the time
    • Stoichiometry and direct versus indirect interactions within the complex not established
    • Generalizability beyond PFOS-induced model uncertain
  8. 2022 Medium

    Demonstrating that astrocytic IP3R2-mediated calcium is required for experience-dependent Hebbian LTD — and that its absence switches the same stimulation to LTP via a distinct NMDAR signaling mode — revealed that astrocytic IP3R2 calcium acts as a gatekeeper of synaptic plasticity polarity.

    Evidence IP3R2 knockout mice, in vivo/ex vivo electrophysiology in barrel cortex, BAPTA-mediated acute astrocyte calcium chelation, pharmacological dissection

    PMID:36090792

    Open questions at the time
    • Gliotransmitter identity mediating the plasticity switch not identified
    • Circuit-level consequences of altered plasticity polarity not tested
  9. 2024 Medium

    Linking IP3R2 to NLRP3/Caspase-1/GSDMD pyroptosis in cardiomyocytes and showing mutual regulation with ER stress expanded the downstream effector repertoire of IP3R2-mediated calcium from senescence/apoptosis to inflammatory cell death.

    Evidence siRNA and xestospongin C inhibition of IP3R2, western blot for pyroptosis markers, rat LPS model

    PMID:38378646

    Open questions at the time
    • Whether IP3R2 directly or indirectly activates NLRP3 not distinguished
    • Specificity relative to IP3R1/3 in cardiomyocytes not fully tested
  10. 2024 Medium

    Demonstrating that oligodendrocyte-specific Itpr2 deletion impairs OPC proliferation through the MAPK/ERK–CDK6/cyclin D1 axis and causes anxiety/depressive behaviors provided a mechanistic pathway from IP3R2 calcium to cell cycle control and behavioral phenotype.

    Evidence OL-specific Itpr2 conditional knockout, transcriptomics, MAPK/ERK inhibitor rescue, behavioral testing

    PMID:38476116

    Open questions at the time
    • Direct calcium sensor linking IP3R2 flux to ERK activation not identified
    • Whether behavioral phenotype is reversible with remyelination not tested
  11. 2025 Medium

    Identification of FMO2 and FUNDC1 as distinct IP3R2-binding partners at MAMs — FMO2 maintaining the IP3R2–Grp75–VDAC1 complex for physiological bioenergetics and FUNDC1 regulating IP3R2 stability through ubiquitination — expanded the molecular inventory controlling IP3R2-dependent mitochondrial calcium transfer in cardiomyocytes.

    Evidence Co-immunoprecipitation, MAM-targeted mass spectrometry, AAV9 rescue in cardiac hypertrophy model (FMO2); Co-IP, ubiquitination assay, Mito Tempo rescue (FUNDC1)

    PMID:40451326 PMID:40489543

    Open questions at the time
    • Whether FMO2 and FUNDC1 compete for the same IP3R2 binding site unknown
    • E3 ligase mediating IP3R2 ubiquitination upon FUNDC1 loss not identified
    • Reciprocal validation across independent labs pending
  12. 2025 Medium

    In vivo dual-color imaging in awake Itpr2 knockout mice showed that IP3R2-dependent astrocytic calcium transients are required for locomotion-evoked neuronal modulation, establishing a non-synaptic glial mechanism for state-dependent circuit modulation.

    Evidence Simultaneous two-photon calcium imaging of astrocytes and neurons in somatosensory cortex of behaving Itpr2-/- mice

    PMID:40710356

    Open questions at the time
    • Molecular mediator released by astrocytes to modulate neurons not identified
    • Whether other behavioral states engage the same mechanism not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Critical open questions include: the high-resolution structure of full-length IP3R2 and the gating mechanism distinguishing it from IP3R1/3; the identity of gliotransmitters downstream of astrocytic IP3R2 calcium that control synaptic plasticity; the E3 ubiquitin ligase(s) governing IP3R2 turnover; and whether the MAM-structural and channel-gating functions of IP3R2 are separable in senescence and cell death pathways.
  • No full-length IP3R2 cryo-EM structure published
  • Gliotransmitter identity downstream of IP3R2 unknown
  • Separability of MAM tethering versus calcium flux functions unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0008289 lipid binding 1
Localization
GO:0005783 endoplasmic reticulum 8 GO:0005739 mitochondrion 6
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-382551 Transport of small molecules 4 R-HSA-112316 Neuronal System 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-8953897 Cellular responses to stimuli 3
Partners
BCL2ERP29ERP44FMO2FUNDC1GRP75MICU1VDAC1
Complex memberships
IP3R2-Bcl-2IP3R2-Grp75-VDAC1 (MAM tethering complex)IP3R2-VDAC1-MICU1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 ITPR2 mediates calcium release from the endoplasmic reticulum (ER), and this calcium is subsequently taken up by mitochondria via the mitochondrial calcium uniporter (MCU). During oncogene-induced senescence (OIS), this ER-to-mitochondria calcium transfer leads to decreased mitochondrial membrane potential, reactive oxygen species accumulation, and cellular senescence. Loss-of-function of either ITPR2 or MCU allows escape from OIS. Loss-of-function genetic screen, siRNA knockdown, calcium imaging, mitochondrial membrane potential assays, ROS measurements Nature communications High 24797322
2021 ITPR2 calcium-release channel and calcium fluxes from ER to mitochondria drive cellular senescence. Itpr2 knockout mice show decreased mitochondria-ER contacts, and forced ER-mitochondria contacts induce premature senescence, establishing that ITPR2-facilitated ER-mitochondria contacts are mechanistically required for senescence induction. Itpr2 knockout mice, electron microscopy of ER-mitochondria contacts, forced contact induction, aging phenotype characterization Nature communications High 33526781
2013 IP3R2 forms complexes with Bcl-2, and disruption of the IP3R2/Bcl-2 complex using a BH4-domain-targeting peptide (TAT-IDP(S)) promotes IP3R2-mediated pro-apoptotic Ca2+ signaling. The apoptotic sensitivity of diffuse large B-cell lymphoma cells to this peptide correlates specifically with IP3R2 protein levels, not IP3R1 or IP3R3 levels. Knockdown of IP3R2 reduces TAT-IDP(S)-induced apoptosis. siRNA knockdown, Ca2+ imaging, apoptosis assays, IP3R inhibitor, correlation analysis across cell lines Cell death & disease High 23681227
2015 IP3R2 is the primary mediator of GPCR-dependent somatic Ca2+ signaling in astrocytes. Ip3r2-/- mice lack somatic astrocyte Ca2+ responses but retain diverse Ca2+ fluctuations in astrocyte processes and end feet, indicating that IP3R2 specifically underlies somatic but not process-localized Ca2+ signaling. Ip3r2-/- mouse model, two-photon Ca2+ imaging in brain slices and in vivo, GPCR stimulation, startle response paradigm Nature neuroscience High 25894291
2014 IP3R2 is the dominant IP3 receptor isoform in astrocytes mediating GPCR-dependent Ca2+ fluxes from the ER. IP3R2 conditional knockout in astrocytes abolishes GPCR-dependent astrocytic Ca2+ responses, but this loss does not affect a broad range of mouse behaviors including anxiety, motor function, or Morris water maze performance. IP3R2 conditional knockout mouse, Ca2+ imaging, behavioral battery testing Frontiers in behavioral neuroscience High 25429263
2016 ERP44 (ER protein 44) inhibits IP3R2-mediated Ca2+ release from the ER in lung cancer cells. ERP44 overexpression reduces intracellular Ca2+ release, alters cell morphology, and inhibits migration of A549 cells specifically via IP3R2, as knockdown of IP3R2 (but not IP3R1 or IP3R3) mimics the migration-inhibiting effect. ERP44 overexpression, IP3R2/1/3 siRNA knockdown, wound healing assay, Ca2+ imaging, cell morphology analysis Aging Medium 27347718
2018 The IP3-binding core (IBC) domain of human ITPR2 (residues 224–604) binds IP3 with high affinity. IP3 binding induces conformational changes in both secondary and tertiary structure of the IBC domain. Key conserved residues R269, K508, and R511 are implicated in the ligand-binding site. Molecular cloning, bacterial expression, protein purification, far-CD spectroscopy, intrinsic fluorescence spectroscopy, bioinformatics International journal of biological macromolecules Medium 30244130
2022 BMAL1 (core circadian clock component) directly regulates transcription of ITPR2 (and ITPR3) in secretory gland acinar cells. Loss of BMAL1 downregulates ITPR2 expression, impairs secretory function, and causes vacuolation and apoptosis; restoration of ITPR2 and ITPR3 expression in Bmal1-deficient rats rescues lacrimal and parotid gland secretory dysfunction. Bmal1 knockout rats, viral rescue of ITPR2/ITPR3 expression, secretion functional assays, ChIP/transcription analysis implied The ocular surface Medium 39343166
2022 Autophagy-dependent increases in detyrosinated α-tubulin enhance formation of an IP3R2-VDAC1-MICU1 complex at ER-mitochondria contact sites, which mediates transfer of extracellular (plasma membrane-localized) Ca2+ from IP3R2 to mitochondria, causing mitochondrial Ca2+ overload and insulin resistance in hepatocytes. Co-immunoprecipitation, autophagy inhibitors, siRNA, Ca2+ imaging, mitochondrial fractionation, mouse model of PFOS exposure The Science of the total environment Medium 35192817
2024 IP3R2-mediated Ca2+ release activates the NLRP3/Caspase-1/GSDMD pyroptosis pathway in cardiomyocytes. LPS increases IP3R2 expression and ATP-induced intracellular Ca2+ release; inhibiting IP3R2 with xestospongin C or siRNA knockdown reverses LPS-induced pyroptosis. Additionally, ER stress and IP3R2-mediated Ca2+ release mutually regulate each other. siRNA knockdown, pharmacological inhibition (xestospongin C, MCC950), Ca2+ imaging, western blot, ELISA, rat LPS model Cell death discovery Medium 38378646
2024 miR-129 directly targets ITPR2 mRNA and represses its expression, controlling a cascade of intracellular Ca2+ signaling from ER to mitochondria. Reduced miR-129 in senescent cells allows increased ITPR2-mediated Ca2+ transfer to mitochondria via MCU, decreasing mitochondrial membrane potential, increasing ROS and DNA damage, promoting cellular senescence. miRNA overexpression/inhibition, luciferase reporter assay (implied direct targeting), Ca2+ imaging, MMP assay, ROS measurement, mouse intraperitoneal injection of miR-129 Mechanisms of ageing and development Medium 38218462
2021 ITPR2-mediated calcium release in oligodendrocytes regulates the development of CAII+ type I/II oligodendrocytes and determines myelin fiber sizes. Itpr2 deficiency causes developmental delay of oligodendrocyte differentiation, increasing the proportion of small-caliber myelinated axons and leading to abnormal compound action potentials in optic nerves. Conventional and conditional Itpr2 mutant mice, immunostaining, electrophysiology (compound action potential recordings) Frontiers in cellular neuroscience Medium 34630045
2024 Loss of ITPR2 in oligodendrocytes disturbs Ca2+ homeostasis, increases resting [Ca2+]i (compensated by upregulation of plasma membrane Ca2+ channels), inhibits OPC proliferation via MAPK/ERK-CDK6/cyclin D1 axis, and impairs myelination in adolescent mice, leading to anxiety/depressive-like behaviors. OL-specific Itpr2 conditional knockout, transcriptome profiling, MAPK/ERK inhibitor rescue, Ca2+ imaging, behavioral tests Advanced science Medium 38476116
2022 Astrocyte IP3R2-mediated Ca2+ signaling is required for experience-dependent Hebbian depression (LTD) in mouse barrel cortex. In IP3R2-/- mice or upon acute astrocytic Ca2+ buffering, 1 Hz stimulation that normally induces LTD instead produces NMDAR-dependent LTP, revealing a mechanistic switch. Both WT LTD and IP3R2-/- 1 Hz LTP involve non-ionotropic NMDAR signaling, but only WT LTD is P38 MAPK-dependent. IP3R2-/- mice, in vivo and ex vivo electrophysiology, acute astrocytic Ca2+ chelation (BAPTA), pharmacological dissection of LTP/LTD pathways Frontiers in cellular neuroscience Medium 36090792
2025 FMO2 localizes to mitochondria-associated ER membranes (MAMs) and binds IP3R2 as a component of the IP3R2-Grp75-VDAC1 complex, maintaining ER-mitochondria contact and regulating mitochondrial Ca2+ signaling for bioenergetics. FMO2 deletion worsens and overexpression prevents pathological cardiac hypertrophy in vivo. Co-immunoprecipitation, MAM-targeted mass spectrometry, AAV9-mediated overexpression, cardiomyocyte-specific genetic mouse models, synthetic peptide rescue Circulation Medium 40489543
2025 FUNDC1 binds IP3R2 at MAMs to regulate ER-to-mitochondria Ca2+ transfer. FUNDC1 knockdown reduces mitochondrial Ca2+ concentration and increases IP3R2 ubiquitination (promoting its degradation), while FUNDC1 overexpression promotes mitochondrial dysfunction and pyroptosis in cardiomyocytes in a mitochondrial ROS-dependent manner. Co-immunoprecipitation (FUNDC1-IP3R2 interaction), siRNA knockdown, overexpression, ubiquitination assay, mitochondrial Ca2+ measurement, Mito Tempo rescue Life sciences Medium 40451326
2024 DPP4 binding to IGF2-R on Treg cell surface activates PKA/SP1 signaling, which upregulates ERp29 expression; ERp29 binds to IP3R2, inhibiting its degradation and promoting MAM formation and mitochondrial Ca2+ overload in Tregs, thereby impairing Treg function. Co-immunoprecipitation (ERp29-IP3R2 binding), siRNA knockdown of pathway components, Ca2+ imaging, mouse model Metabolism: clinical and experimental Medium 36302455
2024 IP3R2-MAM-mediated mitochondrial Ca2+ overload drives mitochondrial dysfunction and apoptosis in photoreceptors under hypoxia. IP3R2 knockdown limits MAM formation, reduces mitochondrial Ca2+ overload, improves mitochondrial morphology and function, and attenuates apoptosis. siRNA knockdown, transmission electron microscopy, ER-mitochondria colocalization, MAM reporter, flow cytometry, western blot, in vivo subretinal injection model Experimental eye research Medium 38851477
2020 Tcirg1/V-ATPase knockdown reduces IP3R2 expression in osteoclast precursors, which decreases intracellular calcium levels and limits nuclear translocation of NFATc1, thereby inhibiting large osteoclast generation during RANKL-induced differentiation. Lentiviral knockdown of Tcirg1, IP3R2 expression analysis, intracellular Ca2+ measurement, NFATc1 nuclear localization assay, bone marrow-derived monocyte differentiation PloS one Low 32790690
2025 Astrocytic IP3R2-mediated Ca2+ transients are required for the modulatory effect of locomotion on neurons in mouse somatosensory cortex. In Itpr2-/- mice, locomotion-induced modulation of neuronal Ca2+ activity is absent despite preserved astrocytic Ca2+ activity, suggesting a non-synaptic mechanism by which IP3R2-dependent astrocytic Ca2+ transients modulate local neuronal circuits. Dual-color two-photon Ca2+ imaging of astrocytes and neurons simultaneously in awake-behaving Itpr2-/- mice Cells Medium 40710356
2025 IP3R2 is a negative regulator of melanophagy. IP3R2 knockdown decreases mitochondrial Ca2+ uptake, augments ADP/ATP ratio, activates AMPK-ULK1 pathway to induce melanophagy. Simultaneously, IP3R2 knockdown increases ER-lysosome proximity, elevates lysosomal Ca2+, reduces lysosomal pH, activates TRPML1, and promotes nuclear translocation of TFEB to transcriptionally upregulate autophagy and melanophagy genes. This function is specific to IP3R2 and not IP3R1 or IP3R3. siRNA knockdown, novel ratiometric live-cell imaging probes for melanophagy, biochemical assays, confocal microscopy, Ca2+ imaging, zebrafish in vivo model bioRxivpreprint Medium

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo. Nature neuroscience 387 25894291
2014 Endoplasmic reticulum calcium release through ITPR2 channels leads to mitochondrial calcium accumulation and senescence. Nature communications 185 24797322
2007 ITPR2 as a susceptibility gene in sporadic amyotrophic lateral sclerosis: a genome-wide association study. The Lancet. Neurology 170 17827064
2021 Calcium channel ITPR2 and mitochondria-ER contacts promote cellular senescence and aging. Nature communications 148 33526781
2013 IP3R2 levels dictate the apoptotic sensitivity of diffuse large B-cell lymphoma cells to an IP3R-derived peptide targeting the BH4 domain of Bcl-2. Cell death & disease 97 23681227
2014 Astrocyte IP3R2-dependent Ca(2+) signaling is not a major modulator of neuronal pathways governing behavior. Frontiers in behavioral neuroscience 95 25429263
2015 Disruption of IP₃R2-mediated Ca²⁺ signaling pathway in astrocytes ameliorates neuronal death and brain damage while reducing behavioral deficits after focal ischemic stroke. Cell calcium 61 26433454
2021 Astrocytic IP3Rs: Beyond IP3R2. Frontiers in cellular neuroscience 49 34393726
2022 Nonenzymatic function of DPP4 promotes diabetes-associated cognitive dysfunction through IGF-2R/PKA/SP1/ERp29/IP3R2 pathway-mediated impairment of Treg function and M1 microglia polarization. Metabolism: clinical and experimental 38 36302455
2022 Perfluorooctane sulfonate induces mitochondrial calcium overload and early hepatic insulin resistance via autophagy/detyrosinated alpha-tubulin-regulated IP3R2-VDAC1-MICU1 interaction. The Science of the total environment 32 35192817
2024 IP3R2-mediated Ca2+ release promotes LPS-induced cardiomyocyte pyroptosis via the activation of NLRP3/Caspase-1/GSDMD pathway. Cell death discovery 28 38378646
2015 Genome-wide association study identifies ITPR2 as a susceptibility gene for Kashin-Beck disease in Han Chinese. Arthritis & rheumatology (Hoboken, N.J.) 28 25303641
2022 Ferulic acid attenuates high glucose-induced MAM alterations via PACS2/IP3R2/FUNDC1/VDAC1 pathway activating proapoptotic proteins and ameliorates cardiomyopathy in diabetic rats. International journal of cardiology 27 36481261
2016 ERP44 inhibits human lung cancer cell migration mainly via IP3R2. Aging 27 27347718
2009 No evidence of association of FLJ10986 and ITPR2 with ALS in a large German cohort. Neurobiology of aging 22 19464757
2012 No contribution of IP3-R(2) to disease phenotype in models of dilated cardiomyopathy or pressure overload hypertrophy. Circulation. Heart failure 17 23258573
2023 Proteomic analysis of ITPR2 as a new therapeutic target for curcumin protection against AFB1-induced pyroptosis. Ecotoxicology and environmental safety 14 37257342
2024 ITPR2 Mediated Calcium Homeostasis in Oligodendrocytes is Essential for Myelination and Involved in Depressive-Like Behavior in Adolescent Mice. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 12 38476116
2020 Knockdown of Tcirg1 inhibits large-osteoclast generation by down-regulating NFATc1 and IP3R2 expression. PloS one 12 32790690
2021 Evidence That ITPR2-Mediated Intracellular Calcium Release in Oligodendrocytes Regulates the Development of Carbonic Anhydrase II + Type I/II Oligodendrocytes and the Sizes of Myelin Fibers. Frontiers in cellular neuroscience 9 34630045
2022 A requirement for astrocyte IP3R2 signaling for whisker experience-dependent depression and homeostatic upregulation in the mouse barrel cortex. Frontiers in cellular neuroscience 8 36090792
2020 Minimal contribution of IP3R2 in cardiac differentiation and derived ventricular-like myocytes from human embryonic stem cells. Acta pharmacologica Sinica 8 33037404
2017 Germline genetic variations in PDZD2 and ITPR2 genes are associated with clear cell renal cell carcinoma in Chinese population. Oncotarget 8 26918600
2024 BMAL1 deficiency provokes dry mouth and eyes by down-regulating ITPR2/3. The ocular surface 7 39343166
2025 FMO2 Prevents Pathological Cardiac Hypertrophy by Maintaining the ER-Mitochondria Association Through Interaction With IP3R2-Grp75-VDAC1. Circulation 6 40489543
2024 Calcium transferring from ER to mitochondria via miR-129/ITPR2 axis controls cellular senescence in vitro and in vivo. Mechanisms of ageing and development 6 38218462
2024 IP3R2 regulates apoptosis by Ca2+ transfer through mitochondria-ER contacts in hypoxic photoreceptor injury. Experimental eye research 6 38851477
2018 Experimental and theoretical study of IBC domain from human IP3R2; molecular cloning, bacterial expression and protein purification. International journal of biological macromolecules 6 30244130
2025 The IP3R2 Knockout Mice in Behavior: A Blessing or a Curse? Journal of neurochemistry 5 40172184
2020 In Vivo Structural and Functional Abnormalities of the Striatums Is Related to Decreased Astrocytic BDNF in Itpr2 Mice Exhibiting Depressive-Like Behavior. Neural plasticity 4 32952549
2015 Effects of IP3R2 Receptor Deletion in the Ischemic Mouse Retina. Neurochemical research 3 26446037
2025 Role of IP3R2-Mediated mitochondrial calcium homeostasis in early hypoxic stress injury of retinal pigment epithelial cells. Biochemical and biophysical research communications 2 40267840
2025 METTL3-mediated m6A modification of FUNDC1/IP3R2 pathway facilitates cardiac hypertrophy in obesity hypertension. Life sciences 2 40451326
2025 IP3R2-Mediated Astrocytic Ca2+ Transients Are Critical to Sustain Modulatory Effects of Locomotion on Neurons in Mouse Somatosensory Cortex. Cells 2 40710356
2019 Genetic variants in the ITPR2 gene are associated with Kashin-Beck Disease in Tibetan. Molecular genetics & genomic medicine 2 31066235
2024 Expression of ITPR2 regulated by lncRNA-NONMMUT020270.2 in LPS-stimulated HT22 cells. Heliyon 1 39040287
2023 Genetic Ablation of Inositol 1,4,5-Trisphosphate Receptor Type 2 (IP3R2) Fails to Modify Disease Progression in a Mouse Model of Spinocerebellar Ataxia Type 3. International journal of molecular sciences 1 37445783
2020 [Changes in three-dimensional arterial spin labeling perfusion imaging of the hippocampus in depressive Itpr-/- mice]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 1 32376566
2026 ITPR2 Promotes Acute Myeloid Leukemia Progression Through Calcium-Mediated Mitochondrial Dysfunction. Frontiers in bioscience (Landmark edition) 0 41761959
2026 Discovery of a novel ITPR2::KRAS fusion in large cell neuroendocrine lung cancer: a case report. Translational lung cancer research 0 41808705
2026 Validation of ITPR2, DPF3, EPAS1, and PVT1-associated SNPs as biomarkers for RCC in an independent case-control cohort. Frontiers in medicine 0 41889506
2025 Discovery metabolomics and genetic analysis reveal lipid pathway alterations associated with malignant phenotype acquisition in pleomorphic adenoma and a novel NTF3::ITPR2 fusion in carcinoma ex pleomorphic adenoma. Virchows Archiv : an international journal of pathology 0 41081890