Affinage

TRPM4

Transient receptor potential cation channel subfamily M member 4 · UniProt Q8TD43

Length
1214 aa
Mass
134.3 kDa
Annotated
2026-04-28
100 papers in source corpus 48 papers cited in narrative 48 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRPM4 is a Ca²⁺-activated, voltage-dependent, monovalent cation-selective channel that depolarizes the plasma membrane to regulate Ca²⁺ entry driving force across diverse cell types, thereby shaping immune cell activation, vascular tone, cardiac action potentials, synaptic plasticity, and taste transduction. The channel is directly activated by intracellular Ca²⁺ (~400 nM KD), exhibits intrinsic voltage-dependent gating, and its Ca²⁺ sensitivity is positively modulated by PIP₂ binding at C-terminal and proximal N-terminal domains, PKC phosphorylation (particularly PKCδ-dependent membrane translocation), and calmodulin binding, while ATP binding at the N-terminal nucleotide-binding domain and the NO/cGMP/PKG/IRAG/IP₃R axis negatively regulate channel activity (PMID:12015988, PMID:12799367, PMID:15590641, PMID:16424899, PMID:34734188). Cryo-EM structures reveal a homotetrameric architecture with a Ca²⁺-binding site in the intracellular S1–S4 domain, a selectivity filter glutamine essential for monovalent selectivity, dual gates, and an ATP-binding nucleotide-binding domain (PMID:29217581, PMID:29211714, PMID:29211723). TRPM4 co-assembles with SUR1 to form SUR1-TRPM4 heteromers with enhanced Ca²⁺ sensitivity and sulfonylurea responsiveness that drive pathological cell swelling and inflammatory signaling in CNS injury, and physically couples with NMDARs through intracellular near-membrane domains to mediate excitotoxic neuronal death (PMID:23255597, PMID:33033186, PMID:37279286).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2002 High

    Establishing that TRPM4b is a Ca²⁺-activated channel selective for monovalent cations resolved the molecular identity of an endogenous depolarizing conductance that modulates Ca²⁺ entry driving force without itself conducting Ca²⁺.

    Evidence Cloning, heterologous expression, and patch-clamp electrophysiology in transfected cells

    PMID:12015988

    Open questions at the time
    • Structural basis for monovalent selectivity unknown
    • In vivo physiological role not yet demonstrated
  2. 2003 High

    Demonstrating intrinsic voltage-dependent gating independent of divalent block established that TRPM4 integrates both Ca²⁺ and voltage signals, explaining its outward rectification.

    Evidence Whole-cell and cell-free patch-clamp with Boltzmann analysis and tail currents

    PMID:12799367

    Open questions at the time
    • Molecular identity of the voltage sensor unknown
    • Coupling between Ca²⁺ binding and voltage gating unresolved
  3. 2004 High

    Identifying ATP, PKC phosphorylation, and calmodulin as modulators of TRPM4 Ca²⁺ sensitivity established a multi-input regulatory framework that controls channel activity under physiological conditions, while simultaneous demonstration of TRPM4's role in myogenic vasoconstriction provided the first native physiological function.

    Evidence Mutagenesis of ATP-binding/PKC/calmodulin sites with patch-clamp; antisense knockdown in cerebral arteries with pressure myography

    PMID:15472118 PMID:15590641

    Open questions at the time
    • Direct binding sites for ATP not structurally resolved
    • Identity of calmodulin binding mode at C-terminal sites not confirmed structurally
  4. 2006 High

    Establishing PIP₂ as a major positive modulator that shifts TRPM4 voltage dependence and increases Ca²⁺ sensitivity ~100-fold, acting through a C-terminal PH domain, revealed how membrane phosphoinositide metabolism tunes channel activity.

    Evidence Inside-out and whole-cell patch-clamp with PIP₂ application, PLC activation, and PH-domain mutagenesis

    PMID:16424899

    Open questions at the time
    • Structural basis for PIP₂ binding not resolved at atomic level
    • Relative contributions of PIP₂ vs PIP₃ not clarified
  5. 2007 High

    Trpm4 knockout mice revealed that TRPM4 is a negative regulator of Ca²⁺-dependent mast cell degranulation and that PKCδ drives TRPM4 membrane translocation in smooth muscle, establishing cell-type-specific roles for TRPM4 in immune and vascular contexts.

    Evidence Trpm4⁻/⁻ bone marrow-derived mast cells with degranulation assays; antisense/siRNA knockdown with surface biotinylation and pressure myography in smooth muscle

    PMID:17293488 PMID:17293867

    Open questions at the time
    • Trafficking mechanism for PKCδ-dependent TRPM4 insertion not molecularly defined
    • Whether TRPM4 regulates other immune cell types beyond mast cells not established
  6. 2009 High

    De novo TRPM4 upregulation after spinal cord injury drives oncotic capillary cell death and secondary hemorrhage, establishing TRPM4 as a pathological effector of Na⁺ overload-induced necrosis in CNS injury.

    Evidence Trpm4⁻/⁻ mice and in vivo antisense in rodent SCI models with capillary integrity and lesion volume readouts

    PMID:19169264

    Open questions at the time
    • Transcriptional mechanism of TRPM4 upregulation after injury not defined
    • Whether SUR1 co-assembly is required for pathological function not yet tested
  7. 2010 High

    Multiple studies established TRPM4 as a broad regulator of excitable and secretory cell physiology: it shapes catecholamine secretion from chromaffin cells, controls T helper cell Ca²⁺ signaling and NFAT localization, and is sensitized by H₂O₂ oxidation of Cys1093 to drive Na⁺ overload-dependent necrosis.

    Evidence Trpm4⁻/⁻ chromaffin cells with capacitance measurements; Trpm4 knockdown with Ca²⁺ imaging and NFAT assays in T cells; Cys1093 mutagenesis with patch-clamp and cell death assays

    PMID:20656926 PMID:20679729 PMID:20884614

    Open questions at the time
    • Structural basis for Cys1093 oxidation-dependent desensitization removal unknown
    • Mechanism linking TRPM4 to NFAT nuclear localization in T cells is indirect
  8. 2012 High

    Discovery that SUR1 and TRPM4 co-assemble into heteromeric channels with doubled Ca²⁺ sensitivity and sulfonylurea responsiveness, appearing de novo after CNS injury, established a pharmacologically targetable pathological channel complex distinct from TRPM4 homomers.

    Evidence Co-immunoprecipitation, FRET, and patch-clamp in heterologous expression; in vivo SCI and EAE models with Trpm4⁻/⁻ mice

    PMID:23160238 PMID:23255597

    Open questions at the time
    • Structural basis for SUR1-TRPM4 co-assembly not resolved
    • Stoichiometry of SUR1:TRPM4 subunits in the heteromer unknown
  9. 2013 High

    Demonstrating that TRPM4 shapes ventricular action potential duration and β-adrenergic inotropy established its functional role in the cardiac conduction and contractility system.

    Evidence Trpm4⁻/⁻ mice with patch-clamp, pressure-volume loops, and membrane potential measurements

    PMID:24226423

    Open questions at the time
    • Relative contribution of TRPM4 vs TRPM5 in cardiac AP not dissected
    • Subcellular targeting mechanism in cardiomyocytes not defined
  10. 2015 High

    TRPM4 was identified as an essential co-activator of NMDARs during hippocampal LTP, generating a feed-forward depolarization necessary for full NMDAR activation, while cardiac-specific deletion revealed TRPM4 as a negative regulator of calcineurin-NFAT hypertrophic signaling.

    Evidence Trpm4⁻/⁻ mice with LTP/LTD electrophysiology and pairing-protocol rescue; cardiac-specific Trpm4 KO with AngII treatment and calcineurin assays

    PMID:26043922 PMID:26631168

    Open questions at the time
    • Physical basis for TRPM4-NMDAR functional coupling not yet demonstrated
    • Whether TRPM4-dependent LTP operates in brain regions beyond CA1 unknown
  11. 2017 High

    Cryo-EM structures at ~3 Å resolution defined the homotetrameric architecture, identified the Ca²⁺-binding site in the S1–S4 domain, the ATP-binding nucleotide-binding domain, and the selectivity filter glutamine responsible for monovalent selectivity, providing an atomic framework for decades of functional data.

    Evidence Single-particle cryo-EM of human and mouse TRPM4 in lipid nanodiscs/detergent with and without Ca²⁺/ATP; mutagenesis validation of filter residue

    PMID:29211714 PMID:29211723 PMID:29217581

    Open questions at the time
    • Open-state structure not captured
    • PIP₂-bound structure not available at high resolution
    • Conformational transition pathway from Ca²⁺-primed to voltage-activated state unresolved
  12. 2018 High

    Multiple discoveries expanded TRPM4's physiological scope: it cooperates with TRPM5 for sweet/bitter/umami taste transduction, contributes to SUR1-TRPM4-AQP4 tripartite complex-driven brain edema, and gain-of-function S6 domain mutations cause progressive symmetric erythrokeratodermia.

    Evidence Trpm4⁻/⁻ and double-KO mice with taste behavioral assays; co-IP/FRET of SUR1-TRPM4-AQP4 with in vivo edema models; human genetics with mutant channel electrophysiology

    PMID:28906027 PMID:29311301 PMID:30528822

    Open questions at the time
    • How TRPM4 and TRPM5 divide labor in taste cells not molecularly resolved
    • Structural basis for gain-of-function erythrokeratodermia mutations at the gate not fully modeled
  13. 2020 High

    Establishing that NMDARs physically couple to TRPM4 via intracellular near-membrane domains, and that disrupting this interface blocks excitotoxicity while preserving NMDAR Ca²⁺ signaling, provided a druggable mechanism separating physiological from pathological NMDAR function.

    Evidence Co-immunoprecipitation, structure-based computational screening, small molecule interface disruptors validated in stroke and retinal degeneration mouse models

    PMID:33033186

    Open questions at the time
    • Exact binding interface residues on TRPM4 side not mapped
    • Whether NMDAR-TRPM4 coupling exists in all neuronal subtypes unknown
  14. 2021 High

    Identification of NO/cGMP/PKG/IRAG/IP₃R as an upstream inhibitory axis for TRPM4 in smooth muscle connected canonical vasodilatory signaling directly to TRPM4 channel gating, while cardiomyocyte-specific deletion showed TRPM4 contributes to pressure overload-induced hypertrophy.

    Evidence Patch-clamp with superresolution microscopy and IRAG knockdown; cardiomyocyte-specific Trpm4 KO with transverse aortic constriction

    PMID:34190686 PMID:34734188

    Open questions at the time
    • Whether IRAG-IP₃R complex acts as a direct TRPM4 regulatory scaffold is unknown
    • Downstream effectors linking TRPM4-mediated depolarization to hypertrophic gene expression not fully defined
  15. 2022 High

    TRPM4 contributes to arrhythmogenic triggered activity via Ca²⁺ overload-induced background current, and meclofenamate was identified as a TRPM4 antagonist that suppresses arrhythmias in a TRPM4-dependent manner, opening a therapeutic avenue for CPVT.

    Evidence Trpm4⁻/⁻ mice with telemetric ECG, patch-clamp, and compound screening with pharmacological validation

    PMID:35822895

    Open questions at the time
    • Meclofenamate binding site on TRPM4 unknown
    • Selectivity of meclofenamate across TRP channels not fully characterized
  16. 2023 High

    A genome-wide CRISPR screen identified TRPM4 as essential for necrosis-inducing anticancer therapy by sustaining lethal UPR hyperactivation through Na⁺ influx-driven cell swelling, while astrocytic SUR1-TRPM4/NCX1/AQP4 signaling was shown to drive post-ischemic brain edema via reverse-mode NCX1 Ca²⁺ entry.

    Evidence CRISPR screen with TRPM4 KO in tumor models; astrocyte-specific SUR1-TRPM4 KO in ischemic stroke model with Ca²⁺ imaging and AQP4 translocation assays

    PMID:37279286 PMID:37522838

    Open questions at the time
    • Whether TRPM4 function in immunogenic cell death is generalizable across cancer types unknown
    • Calmodulin-dependent AQP4 translocation mechanism downstream of TRPM4-NCX1 not structurally resolved
  17. 2025 High

    Species-specific TRPM4 activation by compound NC1 induces necrotic cell death through sustained Na⁺ overload (NECSO), with domain-swapping experiments mapping species selectivity to a transmembrane region and cardiac gain-of-function mutations increasing NECSO vulnerability.

    Evidence Domain swapping between human and mouse TRPM4, molecular docking, electrophysiology, and cell death assays

    PMID:39915626

    Open questions at the time
    • Exact NC1 binding pocket not resolved crystallographically
    • Whether NECSO pathway is relevant to human cardiac arrhythmia pathology in vivo unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of the open/conducting state and the voltage-gating conformational transition, the stoichiometry and atomic structure of SUR1-TRPM4 heteromers, identification of all post-translational modifications controlling trafficking and gating in vivo, and whether TRPM4-targeted therapeutics can be developed with sufficient selectivity for clinical translation.
  • No open-state cryo-EM structure available
  • SUR1-TRPM4 heteromer stoichiometry and structure unresolved
  • Comprehensive in vivo post-translational modification map lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0008289 lipid binding 2 GO:0140299 molecular sensor activity 2
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-382551 Transport of small molecules 4 R-HSA-112316 Neuronal System 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-397014 Muscle contraction 2 R-HSA-9709957 Sensory Perception 1
Complex memberships
SUR1-TRPM4SUR1-TRPM4-AQP4TRPM4 homotetramer

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 TRPM4b is a Ca2+-activated nonselective cation channel of 25 pS unitary conductance that conducts monovalent cations (Na+ and K+) without significant Ca2+ permeation, directly activated by intracellular Ca2+ with an apparent KD of ~400 nM, and functions to depolarize the plasma membrane thereby modulating the driving force for Ca2+ entry through other Ca2+-permeable pathways. Cloning, heterologous expression, patch-clamp electrophysiology Cell High 12015988
2003 TRPM4 exhibits intrinsic voltage-dependent gating (Boltzmann activation), with channel open probability increasing at positive potentials, producing outward rectification; this voltage dependence is not due to divalent cation block or voltage-dependent Ca2+ binding, indicating an intrinsic voltage-sensing mechanism. Whole-cell and cell-free patch-clamp electrophysiology, tail current analysis The Journal of biological chemistry High 12799367
2004 TRPM4 Ca2+ sensitivity is regulated by: (1) cytoplasmic ATP, which reverses desensitization via putative ATP-binding sites; (2) PKC-dependent phosphorylation at specific PKC phosphorylation sites that increases Ca2+ sensitivity; and (3) calmodulin binding at three C-terminal sites whose deletion strongly impairs current activation by reducing Ca2+ sensitivity and shifting voltage dependence. Mutagenesis of ATP-binding sites and PKC phosphorylation sites, calmodulin dominant-negative overexpression, patch-clamp electrophysiology The Journal of biological chemistry High 15590641
2004 TRPM4 mediates pressure-induced smooth muscle cell depolarization and myogenic vasoconstriction of cerebral arteries; TRPM4 antisense oligodeoxynucleotide-mediated knockdown attenuates pressure-induced depolarization and myogenic constriction without affecting KCl-induced constriction. Antisense oligodeoxynucleotide knockdown, patch-clamp electrophysiology, pressure myography Circulation research High 15472118
2006 PIP2 is a positive modulator of TRPM4 that counteracts Ca2+ desensitization, shifts voltage dependence toward negative potentials, and increases Ca2+ sensitivity ~100-fold; the C-terminal pleckstrin homology (PH) domain mediates PIP2 action, as neutralization of basic residues in this domain accelerated desensitization and attenuated PIP2 effects; PLC-mediated PIP2 depletion potently inhibits TRPM4 currents. Inside-out and whole-cell patch-clamp, PLC-coupled receptor activation, pharmacological PIP2 depletion, site-directed mutagenesis of PH domain The EMBO journal High 16424899
2007 TRPM4 channels act as Ca2+-activated nonselective cation channels in mast cells that critically limit the driving force for Ca2+ influx; Trpm4-/- mast cells show more Ca2+ entry after FcεRI stimulation, augmented degranulation, and increased release of histamine, leukotrienes, and TNF, establishing TRPM4 as a negative regulator of Ca2+ entry-dependent mast cell activation. Trpm4 knockout mice, bone marrow-derived mast cell cultures, Ca2+ imaging, degranulation assays Nature immunology High 17293867
2007 PKC activation increases TRPM4 Ca2+ sensitivity in vascular smooth muscle cells and promotes translocation of TRPM4 to the plasma membrane, contributing to pressure-induced depolarization and myogenic vasoconstriction; PKCδ specifically mediates TRPM4 membrane translocation. Antisense knockdown, patch-clamp electrophysiology, phorbol ester stimulation, pressure myography American journal of physiology. Heart and circulatory physiology High 17293488
2008 9-Phenanthrol selectively inhibits human TRPM4 but not TRPM5 in a voltage-independent manner, with similar IC50 in whole-cell and inside-out configurations suggesting direct channel block. Whole-cell and inside-out patch-clamp in HEK293 cells stably expressing TRPM4 or TRPM5 British journal of pharmacology High 18297105
2009 De novo upregulation of Trpm4 in capillaries after spinal cord injury renders cells susceptible to oncotic swelling and death following ATP depletion; in vivo Trpm4 antisense suppression or Trpm4-/- mice preserved capillary integrity, eliminated secondary hemorrhage, and reduced lesion volume. Rodent SCI models, Trpm4 antisense in vivo, Trpm4 knockout mice, COS-7 cell oncotic swelling assay Nature medicine High 19169264
2010 PKCδ activity causes smooth muscle depolarization and vasoconstriction by increasing the number of TRPM4 channels in the sarcolemma; PKC activation with PMA increases cell surface TRPM4 levels ~3-fold within 10 min, and this translocation requires PKCδ but not PKCα or PKCβ. Live-cell confocal imaging with GFP-tagged TRPM4, FRAP, cell surface biotinylation, TIRF microscopy, siRNA knockdown, pressure myography American journal of physiology. Cell physiology High 20610768
2010 H2O2 eliminates TRPM4 desensitization in a dose-dependent manner through oxidation of Cys1093, sustaining TRPM4 activity and causing Na+ overload-dependent necrotic cell death; TRPM4 knockdown prevents H2O2-induced necrosis but not apoptosis. Site-directed mutagenesis (Cys1093), patch-clamp, TRPM4 shRNA knockdown, cell death assays The Journal of biological chemistry High 20884614
2010 TRPM4 deficiency in chromaffin cells causes increased acetylcholine-induced exocytotic release events, leading to elevated plasma epinephrine and hypertension; TRPM4 normally limits catecholamine release by regulating membrane potential and Ca2+ entry driving force. Trpm4-/- mice, capacitance measurements of exocytosis in chromaffin cells, pharmacological ganglionic blockade, plasma catecholamine measurements The Journal of clinical investigation High 20679729
2010 Trpm4 deficiency alters Th1 and Th2 Ca2+ signaling divergently and controls nuclear localization of NFATc1; higher TRPM4 expression in Th2 cells limits Ca2+ influx and oscillations, while lower expression in Th1 cells has the opposite effect. Trpm4 knockdown, Ca2+ imaging, NFAT nuclear localization assay, cytokine production measurement Journal of immunology Medium 20656926
2011 TRPM4 enhances cell proliferation through upregulation of β-catenin signaling; TRPM4 silencing promotes GSK-3β-dependent degradation of β-catenin and reduces β-catenin/Tcf/Lef-dependent transcription, while TRPM4 overexpression increases proliferation and β-catenin levels. TRPM4 shRNA knockdown, TRPM4 overexpression, luciferase reporter assays for β-catenin/Tcf/Lef, Western blotting Journal of cellular physiology Medium 20625999
2012 SUR1 and TRPM4 co-assemble into heteromeric Sur1-Trpm4 channels in CNS injury; co-expression yields channels with biophysical properties of TRPM4 and pharmacological properties (sulfonylurea sensitivity) of SUR1; co-assembly doubles TRPM4 affinity for calmodulin and doubles Ca2+ sensitivity; Sur1-Trpm4 heteromers appear de novo after spinal cord injury. FRET, co-immunoprecipitation, patch-clamp electrophysiology, in vivo spinal cord injury model The Journal of biological chemistry High 23255597
2012 TRPM4 mediates axonal and neuronal degeneration in inflammatory CNS lesions; TRPM4 is expressed in neuronal somata and in axons in EAE/MS lesions; TRPM4 deficiency or glibenclamide treatment reduces axonal/neuronal degeneration; electrophysiology reveals TRPM4-dependent ion influx and oncotic swelling upon excitotoxic stimulation. Trpm4-/- mice, EAE model, pharmacological inhibition, electrophysiology, in vitro excitotoxicity Nature medicine High 23160238
2012 TRPM4 channel controls Ca2+ signaling in monocytes/macrophages; TRPM4 deficiency impairs Ca2+ mobilization in macrophages, downregulates AKT signaling, and reduces phagocytic activity leading to bacterial overgrowth in sepsis; neutrophil Ca2+ signaling and function are unaffected by TRPM4 loss. Trpm4-/- mice, cecal ligation and puncture sepsis model, Ca2+ imaging, phagocytosis assays, AKT signaling analysis Journal of immunology High 22933633
2013 TRPM4 is functionally present in mouse ventricular myocytes and is activated by Ca2+-induced Ca2+ release; loss of TRPM4 shortens action potential duration (APD50/APD90), increases driving force for L-type Ca2+ current, and augments β-adrenergic inotropic response in vitro and in vivo. Trpm4-/- mice, patch-clamp, membrane potential measurements, microfluorometry, pressure-volume loop analysis Circulation research High 24226423
2014 TRPM4 localizes to focal adhesions and interacts with focal adhesion-related proteins; TRPM4 suppression in MEFs impairs focal adhesion turnover, FAK and Rac activities, serum-induced Ca2+ influx, and reduces cellular spreading, migration, and contractility; TRPM4 inhibition also impairs cutaneous wound healing in vivo. Mass spectrometry proteomics, immunofluorescence co-localization, TRPM4 siRNA/shRNA, FAK and Rac activity assays, Ca2+ imaging, migration assays, in vivo wound healing PloS one High 26110647
2014 Negatively charged residues Asp1049 and Glu1062 in and near the TRP domain of TRPM4 C-terminal tail are required for normal Ca2+ sensitivity; mutation of these residues deteriorates Ca2+ sensitivity in the presence of Co2+ or PIP2, identifying the TRP domain as a site responsible for Ca2+ sensitivity regulation. Site-directed mutagenesis, patch-clamp electrophysiology, divalent cation application The Journal of biological chemistry High 25378404
2014 TRPM4 is N-linked glycosylated at Asn992; abolishment of glycosylation by N992Q mutation decreases current density without altering plasma membrane channel number, whereas tunicamycin treatment increases TRPM4 current, suggesting glycosylation primarily modulates channel function rather than trafficking. Site-directed mutagenesis (N992Q), Western blot, surface biotinylation, patch-clamp electrophysiology, tunicamycin treatment Frontiers in cellular neuroscience Medium 24605085
2015 TRPM4 acts as an essential co-activator of NMDA receptors during LTP induction in CA1 hippocampal neurons; Trpm4-/- mice lack NMDAR-dependent LTP, which is rescued by facilitating NMDAR activation or post-synaptic membrane depolarization in a pairing protocol; TRPM4 generates post-synaptic depolarization in a feed-forward loop necessary for full NMDAR activation. Trpm4-/- mice, in vitro electrophysiology (LTP/LTD protocols), pairing protocol rescue Pflugers Archiv High 26631168
2015 PIP2 and PIP3 interact with the proximal N-terminal region (E733–W772) of TRPM4; R755 and R767 are important for PIP2/PIP3 binding specificity as their mutation reduces binding; PIP3-TRPM4 interaction is a novel finding. Biophysical binding assays, molecular modeling, mutagenesis of R755 and R767 Biophysical chemistry Medium 26071843
2015 Selective cardiac TRPM4 deletion results in increased hypertrophic growth after chronic angiotensin II treatment; TRPM4-deficient cardiomyocytes show increased store-operated Ca2+ entry upon AngII treatment, elevated calcineurin activity and NFAT pathway activation, establishing TRPM4 as a negative regulator of calcineurin-NFAT-dependent cardiac hypertrophy. Cardiac-specific Trpm4 knockout mice, AngII treatment, Ca2+ measurements, calcineurin activity assays, gene expression Basic research in cardiology High 26043922
2016 Sur1-Trpm4 channels in TLR4-activated microglia regulate NOS2 transcription via a Ca2+-sensitive calcineurin/NFAT pathway; inhibiting or silencing Sur1 or Trpm4 paradoxically increases intracellular Ca2+, activating CaMKII phosphorylation of calcineurin, reducing NFAT nuclear translocation, and decreasing Nos2 expression and NO production. In vivo microglia, primary cultures from KO mice, co-immunoprecipitation, patch-clamp, Ca2+ imaging, chromatin immunoprecipitation, Griess assay Journal of neuroinflammation High 27246103
2016 The PLC inhibitor U73122 is a potent agonist of TRPM4 channels through covalent modification, directly activating TRPM4 independently of PLC, PIP2, and Ca2+; TRPM5 is insensitive while TRPM3 is inhibited, demonstrating specificity within the TRPM family. Patch-clamp electrophysiology in CHO, HEK293T, Jurkat cells with endogenous and recombinant TRPM4 British journal of pharmacology High 27328745
2017 Cryo-EM structure of full-length human TRPM4 in lipid nanodiscs at ~3 Å resolution reveals a well-defined Ca2+-binding site within the intracellular S1-S4 domain; two structures (with and without Ca2+) represent closed states; Ca2+ binding induces conformational changes that prime the channel for voltage-dependent opening. Single-particle cryo-EM in lipid nanodiscs Science High 29217581
2017 Cryo-EM structure of mouse TRPM4 reveals three-tiered architecture; ATP binds at the N-terminal nucleotide-binding domain and inhibits channel activity; filter residue Gln973 is essential for monovalent cation selectivity; PtdIns(4,5)P2 and Ca2+-binding sites are located in the S1-S4 domain and TRP domain. Cryo-EM structure determination with and without ATP; functional validation of filter mutants Nature High 29211714
2017 Cryo-EM structure of human TRPM4 bound to Ca2+ and decavanadate reveals an umbrella-like cytosolic architecture with coiled-coil pole and MHR helical ribs; two decavanadate-binding sites identified; Gln in selectivity filter is an important determinant of monovalent selectivity. Single-particle cryo-EM Nature High 29211723
2017 AQP4 physically co-assembles with SUR1-TRPM4 to form a tripartite SUR1-TRPM4-AQP4 heteromultimeric complex that drives fast, high-capacity water transport and astrocyte swelling; the full tripartite complex is required for cell swelling, and genetic inactivation of the SUR1-TRPM4 solute pore blocks in vivo astrocyte swelling in brain edema. Co-immunoprecipitation, FRET, calcein fluorescence cell-swelling assays in COS-7 cells, primary astrocytes, and in vivo mouse brain edema model Glia High 28906027
2018 Cryo-EM structure of full-length human TRPM4 in apo state at 3.7 Å identifies an upper gate in the selectivity filter and a lower gate at the entrance to the cytoplasmic coiled-coil; intramolecular interactions exist between TRP domain and S4-S5 linker; 24 lipid binding sites, one pore-loop disulfide bond, and N-linked glycosylation at an extracellular site are identified; five partially hydrated Na+ ions occupy the pore. Single-particle cryo-EM Proceedings of the National Academy of Sciences High 29463718
2018 Gain-of-function mutations in the S6 transmembrane domain of TRPM4 (p.Ile1033Met, p.Ile1040Thr) cause progressive symmetric erythrokeratodermia; mutants show enhanced baseline activity, increased Ca2+ sensitivity, and elevated resting membrane potential; these substitutions affect activation gating as predicted by cryo-EM structures. Human genetic analysis, electrophysiology of mutant channels, in vitro keratinocyte overexpression studies The Journal of investigative dermatology High 30528822
2018 TRPM4 and TRPM5 are both required for taste transduction; loss of either channel significantly impairs sweet, bitter, and umami detection, and combined loss of both channels completely abolishes detection of these stimuli, placing both channels as downstream components of multiple taste signaling pathways. Trpm4-/- and double-KO mice, live cell Ca2+ imaging of taste receptor cells, behavioral taste preference assays Proceedings of the National Academy of Sciences High 29311301
2018 tPA induces PAR1-mediated, SUR1-TRPM4-dependent phasic secretion of MMP-9 from activated brain endothelial cells; tPA causes SUR1-TRPM4 channel opening via plasmin-, PAR1-, TRPC3- and Ca2+-dependent manner; inhibition of SUR1 decreases tPA-induced phasic but not tonic MMP-9 secretion. Patch-clamp electrophysiology, Ca2+ imaging, immunoblot, ELISA, zymography, genetic and pharmacological manipulations in brain endothelial cells, in vivo stroke model PloS one High 29617457
2018 TRPM4 is expressed in soma and proximal dendrites but not the axon initial segment of mPFC pyramidal neurons; a 9-phenanthrol-sensitive current is active at resting membrane potential in soma but not distal dendrites, indicating subcellular compartment-specific TRPM4 function. Multiplex immunofluorescence labeling, perforated patch-clamp with local perfusion Frontiers in cellular neuroscience Medium 29440991
2018 Deletion of Trpm4 unexpectedly reduces peak Na+ currents (Nav1.5-mediated) in cardiac myocytes, consistent with slower intraventricular conduction, suggesting TRPM4 regulates Nav1.5 function in murine cardiomyocytes. Trpm4-/- mice, perforated-patch clamp, immunoblotting, in vivo and Langendorff ECG International journal of molecular sciences Medium 33810249
2020 NMDAR-mediated excitotoxicity requires physical coupling of NMDARs to TRPM4 via intracellular near-membrane domains; disruption of the NMDAR/TRPM4 interaction interface by small molecules spares NMDAR-induced Ca2+ signaling but blocks excitotoxicity, mitochondrial dysfunction, and CREB shutoff, and reduces neuronal loss in stroke and retinal degeneration models. Co-immunoprecipitation, structure-based computational drug screening, small molecule interface inhibitors, mouse models of stroke and retinal degeneration Science High 33033186
2021 Selective deletion of TRPM4 in cardiomyocytes results in ~50% reduction in LVH induced by transverse aortic constriction, identifying TRPM4 as a component of the mechanosensory signaling pathway that induces pressure overload-dependent hypertrophy. Cardiomyocyte-specific Trpm4 knockout mice, transverse aortic constriction, cardiac morphometry and function eLife High 34190686
2021 NO/cGMP/PKG signaling causes vasodilation by inhibiting TRPM4 channels in smooth muscle cells via IRAG; phosphorylation of IRAG by PKG inhibits IP3R-mediated Ca2+ release from the SR, thereby blocking Ca2+-dependent TRPM4 activation; IRAG, PKG, and IP3Rs form a nanoscale signaling complex on the SR. Patch-clamp electrophysiology, superresolution microscopy, IRAG knockdown, pharmacological inhibition of PKG/sGC Function (Oxford, England) High 34734188
2022 TRPM4 contributes to a long-lasting Ca2+ overload-induced background current regulating cardiomyocyte excitability; Trpm4-/- mice show reduced Ca2+-dependent triggered arrhythmias; meclofenamate is identified as a potent TRPM4 antagonist that suppresses catecholaminergic polymorphic ventricular tachycardia-associated arrhythmias in a TRPM4-dependent manner. Trpm4-/- mice, patch-clamp, in vivo telemetric ECG, compound screening, drug validation European heart journal High 35822895
2022 SUR1-TRPM4 activation in microglia triggers K+ efflux via Na+ influx-driven opening of K+ channels, which activates NLRP3 inflammasome; this process requires P2X7 receptor-mediated Ca2+ influx to activate SUR1-TRPM4; GLB or 9-phenanthrol block this pathway. In vivo rat cardiac arrest model, BV2 microglial cells, siRNA knockdown, pharmacological inhibition, inflammasome assays Molecular neurobiology Medium 35972671
2023 Na+ influx through SUR1-TRPM4 in perivascular astrocyte endfeet induces Ca2+ transport via NCX1 in reverse mode, raising intra-endfoot Ca2+, which stimulates calmodulin-dependent translocation of AQP4 to the plasma membrane and water influx causing brain swelling after ischemic stroke. Mouse ischemic stroke model, pharmacological inhibition, astrocyte-specific KO of SUR1-TRPM4, Ca2+ imaging, AQP4 surface localization assays Science signaling High 37279286
2023 A genome-wide CRISPR screen identifies TRPM4 as essential for necrosis-inducing anticancer therapy; TRPM4-mediated Na+ influx and cell swelling sustains lethal unfolded protein response (a-UPR) hyperactivation; TRPM4 knockout abolishes therapy-induced tumor regression in vivo and blocks immunogenic cell death signals. Genome-wide CRISPR-Cas9 screen, TRPM4 KO, in vivo tumor models, UPR assays, cell volume measurements, ATP depletion assays, macrophage activation assays Cancer research High 37522838
2025 Persistent TRPM4 activation by compound NC1 induces necrotic cell death through Na+ overload (NECSO); NC1 specifically activates human but not mouse TRPM4 due to differences in a transmembrane region identified by domain swapping and molecular docking; gain-of-function cardiac arrhythmia mutations in TRPM4 increase vulnerability to NECSO. Domain swapping, molecular docking, TRPM4-deficient cells, electrophysiology, cell death assays, chemical screening Nature chemical biology High 39915626
2016 TRPM4 is a functional tetramer in detergent micelles and can be reconstituted into liposomes as a functional channel; single-channel recordings from proteoliposomes show inhibition by flufenamic acid. Crosslinking, native gel electrophoresis, multi-angle laser light scattering, electron microscopy, electrophysiology of proteoliposomes Scientific reports High 26785754
2023 Piezo1 activation functionally couples to TRPM4 in atrial myocyte-like cells; Yoda1-induced Piezo1 activation changes action potential frequency, and this effect is significantly reduced by TRPM4 knockdown or pharmacological inhibition, demonstrating a Piezo1→Ca2+→TRPM4 signaling axis in cardiomyocytes. siRNA knockdown, pharmacological inhibition, fluorescent voltage-sensitive dye action potential recording in HL-1 cells The Journal of physiology Medium 38098265
2022 p53 represses TRPM4 expression by acting on the TRPM4 promoter; loss of p53 or p63γ increases TRPM4 promoter activity, mRNA, protein, and Na+ currents; p53-mediated TRPM4 suppression increases store-operated Ca2+ entry and alters cell cycle distribution. CRISPR-Cas9 TRPM4 KO, p53 overexpression, promoter reporter assays, patch-clamp, Ca2+ imaging Cell calcium Medium 35500522
2018 TRPM4 inhibition in CA1 neurons and hippocampus contributes to synaptic plasticity; in Trpm4-/- rats, TRPM4 deletion impairs hippocampus-dependent spatial working and reference memory and affects LTP kinetics, with enhanced initial BOLD fMRI response in the stimulated hippocampus. Trpm4-/- rats, chronic in vivo electrophysiology, behavioral testing (Barnes maze, T-maze, Morris water maze), fMRI Brain structure & function Medium 29571504

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 TRPM4 is a Ca2+-activated nonselective cation channel mediating cell membrane depolarization. Cell 594 12015988
2004 Critical role for transient receptor potential channel TRPM4 in myogenic constriction of cerebral arteries. Circulation research 312 15472118
2003 Voltage dependence of the Ca2+-activated cation channel TRPM4. The Journal of biological chemistry 292 12799367
2006 The Ca2+-activated cation channel TRPM4 is regulated by phosphatidylinositol 4,5-biphosphate. The EMBO journal 256 16424899
2004 Regulation of the Ca2+ sensitivity of the nonselective cation channel TRPM4. The Journal of biological chemistry 237 15590641
2007 Increased IgE-dependent mast cell activation and anaphylactic responses in mice lacking the calcium-activated nonselective cation channel TRPM4. Nature immunology 222 17293867
2017 Structure of the human TRPM4 ion channel in a lipid nanodisc. Science (New York, N.Y.) 208 29217581
2009 De novo expression of Trpm4 initiates secondary hemorrhage in spinal cord injury. Nature medicine 176 19169264
2012 TRPM4 cation channel mediates axonal and neuronal degeneration in experimental autoimmune encephalomyelitis and multiple sclerosis. Nature medicine 169 23160238
2017 Structures of the calcium-activated, non-selective cation channel TRPM4. Nature 159 29211714
2012 The sulfonylurea receptor 1 (Sur1)-transient receptor potential melastatin 4 (Trpm4) channel. The Journal of biological chemistry 150 23255597
2017 Electron cryo-microscopy structure of a human TRPM4 channel. Nature 144 29211723
2007 Protein kinase C regulates vascular myogenic tone through activation of TRPM4. American journal of physiology. Heart and circulatory physiology 137 17293488
2010 Increased catecholamine secretion contributes to hypertension in TRPM4-deficient mice. The Journal of clinical investigation 131 20679729
2008 9-phenanthrol inhibits human TRPM4 but not TRPM5 cationic channels. British journal of pharmacology 131 18297105
2011 Mutational spectrum in the Ca(2+)--activated cation channel gene TRPM4 in patients with cardiac conductance disturbances. Human mutation 122 21887725
2020 Coupling of NMDA receptors and TRPM4 guides discovery of unconventional neuroprotectants. Science (New York, N.Y.) 115 33033186
2018 TRPM4 and TRPM5 are both required for normal signaling in taste receptor cells. Proceedings of the National Academy of Sciences of the United States of America 112 29311301
2017 SUR1-TRPM4 and AQP4 form a heteromultimeric complex that amplifies ion/water osmotic coupling and drives astrocyte swelling. Glia 112 28906027
2007 Insights into TRPM4 function, regulation and physiological role. Handbook of experimental pharmacology 106 17217063
2010 Pharmacological inhibition of TRPM4 hyperpolarizes vascular smooth muscle. American journal of physiology. Cell physiology 94 20826763
2010 Trpm4 differentially regulates Th1 and Th2 function by altering calcium signaling and NFAT localization. Journal of immunology (Baltimore, Md. : 1950) 84 20656926
2015 Sur1-Trpm4 Cation Channel Expression in Human Cerebral Infarcts. Journal of neuropathology and experimental neurology 82 26172285
2014 The TRPM4 channel inhibitor 9-phenanthrol. British journal of pharmacology 82 24433510
2012 The TRPM4 channel controls monocyte and macrophage, but not neutrophil, function for survival in sepsis. Journal of immunology (Baltimore, Md. : 1950) 81 22933633
2018 Structure of full-length human TRPM4. Proceedings of the National Academy of Sciences of the United States of America 79 29463718
2011 The non-selective monovalent cationic channels TRPM4 and TRPM5. Advances in experimental medicine and biology 75 21290294
2016 The Sur1-Trpm4 channel regulates NOS2 transcription in TLR4-activated microglia. Journal of neuroinflammation 72 27246103
2013 Increased β-adrenergic inotropy in ventricular myocardium from Trpm4-/- mice. Circulation research 68 24226423
2012 TRPM4 channels in the cardiovascular system: physiology, pathophysiology, and pharmacology. Biochemical pharmacology 67 22750058
2014 Trpm4 gene invalidation leads to cardiac hypertrophy and electrophysiological alterations. PloS one 66 25531103
2010 Hydrogen peroxide removes TRPM4 current desensitization conferring increased vulnerability to necrotic cell death. The Journal of biological chemistry 63 20884614
2018 Identification of potent and selective small molecule inhibitors of the cation channel TRPM4. British journal of pharmacology 62 29579323
2015 TRPM4 in cardiac electrical activity. Cardiovascular research 62 26272755
2011 TRPM4 enhances cell proliferation through up-regulation of the β-catenin signaling pathway. Journal of cellular physiology 62 20625999
2015 TRPM4 Is a Novel Component of the Adhesome Required for Focal Adhesion Disassembly, Migration and Contractility. PloS one 58 26110647
2015 Silencing of Abcc8 or inhibition of newly upregulated Sur1-Trpm4 reduce inflammation and disease progression in experimental autoimmune encephalomyelitis. Journal of neuroinflammation 57 26581714
2014 TRPM4. Handbook of experimental pharmacology 57 24756717
2010 Vasoconstriction resulting from dynamic membrane trafficking of TRPM4 in vascular smooth muscle cells. American journal of physiology. Cell physiology 57 20610768
2018 TRPM4 channel is involved in regulating epithelial to mesenchymal transition, migration, and invasion of prostate cancer cell lines. Journal of cellular physiology 54 30343491
2015 The Ca(2+)-activated cation channel TRPM4 is a negative regulator of angiotensin II-induced cardiac hypertrophy. Basic research in cardiology 54 26043922
2019 TRPM4 channel and cancer. Cancer letters 51 30980865
2003 Identification and characterization of the murine TRPM4 channel. Biochemical and biophysical research communications 50 12893253
2016 Direct modulation of TRPM4 and TRPM3 channels by the phospholipase C inhibitor U73122. British journal of pharmacology 49 27328745
2021 TRPM4 in Cancer-A New Potential Drug Target. Biomolecules 48 33562811
2025 Persistent activation of TRPM4 triggers necrotic cell death characterized by sodium overload. Nature chemical biology 45 39915626
2018 SUR1-TRPM4 channel activation and phasic secretion of MMP-9 induced by tPA in brain endothelial cells. PloS one 45 29617457
2018 MicroRNA-150 suppresses epithelial-mesenchymal transition, invasion, and metastasis in prostate cancer through the TRPM4-mediated β-catenin signaling pathway. American journal of physiology. Cell physiology 45 30566393
2016 Targeted resequencing identifies TRPM4 as a major gene predisposing to progressive familial heart block type I. International journal of cardiology 45 26820365
2006 From cardiac cation channels to the molecular dissection of the transient receptor potential channel TRPM4. Pflugers Archiv : European journal of physiology 44 16680483
2018 Gain-of-Function Mutations in TRPM4 Activation Gate Cause Progressive Symmetric Erythrokeratodermia. The Journal of investigative dermatology 43 30528822
2014 TRPM4 channels couple purinergic receptor mechanoactivation and myogenic tone development in cerebral parenchymal arterioles. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 43 25099756
2018 Four TRPM4 Cation Channel Mutations Found in Cardiac Conduction Diseases Lead to Altered Protein Stability. Frontiers in physiology 41 29568272
2018 Role of the TRPM4 Channel in Cardiovascular Physiology and Pathophysiology. Cells 41 29914130
2015 TRPM4-dependent post-synaptic depolarization is essential for the induction of NMDA receptor-dependent LTP in CA1 hippocampal neurons. Pflugers Archiv : European journal of physiology 40 26631168
2023 Cation flux through SUR1-TRPM4 and NCX1 in astrocyte endfeet induces water influx through AQP4 and brain swelling after ischemic stroke. Science signaling 38 37279286
2013 Biochemical, single-channel, whole-cell patch clamp, and pharmacological analyses of endogenous TRPM4 channels in HEK293 cells. Neuroscience letters 37 23428507
2014 TRPM4 inhibitor 9-phenanthrol activates endothelial cell intermediate conductance calcium-activated potassium channels in rat isolated mesenteric artery. British journal of pharmacology 36 25323322
2020 TRPM4 is overexpressed in breast cancer associated with estrogen response and epithelial-mesenchymal transition gene sets. PloS one 35 32484822
2018 Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury. Translational stroke research 35 29569041
2018 Sodium channel TRPM4 and sodium/calcium exchangers (NCX) cooperate in the control of Ca2+-induced mucin secretion from goblet cells. The Journal of biological chemistry 34 30482841
2014 Glycosylation of TRPM4 and TRPM5 channels: molecular determinants and functional aspects. Frontiers in cellular neuroscience 34 24605085
2019 Downstream TRPM4 Polymorphisms Are Associated with Intracranial Hypertension and Statistically Interact with ABCC8 Polymorphisms in a Prospective Cohort of Severe Traumatic Brain Injury. Journal of neurotrauma 33 30484364
2013 The Sur1-Trpm4 Channel in Spinal Cord Injury. Journal of spine 32 24834370
2011 Stimulation of bursting in pre-Bötzinger neurons by Epac through calcium release and modulation of TRPM4 and K-ATP channels. Journal of neurochemistry 32 21281309
2020 HIV-1 Vpr-Induced Proinflammatory Response and Apoptosis Are Mediated through the Sur1-Trpm4 Channel in Astrocytes. mBio 30 33293383
2015 Enhanced β-adrenergic cardiac reserve in Trpm4⁻/⁻ mice with ischaemic heart failure. Cardiovascular research 30 25600961
2021 The Ca2+-activated cation channel TRPM4 is a positive regulator of pressure overload-induced cardiac hypertrophy. eLife 29 34190686
2018 Transient Receptor Potential Channels TRPM4 and TRPC3 Critically Contribute to Respiratory Motor Pattern Formation but not Rhythmogenesis in Rodent Brainstem Circuits. eNeuro 28 29435486
2015 PIP2 and PIP3 interact with N-terminus region of TRPM4 channel. Biophysical chemistry 28 26071843
2022 Glibenclamide Directly Prevents Neuroinflammation by Targeting SUR1-TRPM4-Mediated NLRP3 Inflammasome Activation In Microglia. Molecular neurobiology 27 35972671
2023 Plasma Membrane Channel TRPM4 Mediates Immunogenic Therapy-Induced Necrosis. Cancer research 26 37522838
2022 TRPM4 inhibition by meclofenamate suppresses Ca2+-dependent triggered arrhythmias. European heart journal 26 35822895
2021 Species-Specific Effects of Cation Channel TRPM4 Small-Molecule Inhibitors. Frontiers in pharmacology 26 34335274
2020 Inherited Cardiac Arrhythmia Syndromes: Focus on Molecular Mechanisms Underlying TRPM4 Channelopathies. Cardiovascular therapeutics 26 33381229
2022 A novel methylated cation channel TRPM4 inhibited colorectal cancer metastasis through Ca2+/Calpain-mediated proteolysis of FAK and suppression of PI3K/Akt/mTOR signaling pathway. International journal of biological sciences 24 36147460
2021 Nitric Oxide Signals Through IRAG to Inhibit TRPM4 Channels and Dilate Cerebral Arteries. Function (Oxford, England) 24 34734188
2018 The ion channel TRPM4 in murine experimental autoimmune encephalomyelitis and in a model of glutamate-induced neuronal degeneration. Molecular brain 24 29996905
2014 Negatively charged amino acids near and in transient receptor potential (TRP) domain of TRPM4 channel are one determinant of its Ca2+ sensitivity. The Journal of biological chemistry 24 25378404
2012 On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1. The Journal of biological chemistry 24 22291026
2022 Emergent Temporal Signaling in Human Trabecular Meshwork Cells: Role of TRPV4-TRPM4 Interactions. Frontiers in immunology 23 35432302
2015 Physiological functions of the TRPM4 channels via protein interactions. BMB reports 23 25441424
2020 Small Molecular Inhibitors Block TRPM4 Currents in Prostate Cancer Cells, with Limited Impact on Cancer Hallmark Functions. Journal of molecular biology 22 33058873
2014 Histamine-induced Ca²⁺ signalling is mediated by TRPM4 channels in human adipose-derived stem cells. The Biochemical journal 22 25001294
2021 Upregulation of transient receptor potential melastatin 4 (TRPM4) in ventricular fibroblasts from heart failure patients. Pflugers Archiv : European journal of physiology 21 33594499
2021 Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2: TRPM4 in Health and Disease. Pharmaceuticals (Basel, Switzerland) 21 35056097
2020 Comparison of Anti-oncotic Effect of TRPM4 Blocking Antibody in Neuron, Astrocyte and Vascular Endothelial Cell Under Hypoxia. Frontiers in cell and developmental biology 21 33195194
2020 TRPM4 inhibition improves spatial memory impairment and hippocampal long-term potentiation deficit in chronic cerebral hypoperfused rats. Behavioural brain research 20 32619565
2022 Germline Variants of CYBA and TRPM4 Predispose to Familial Colorectal Cancer. Cancers 19 35158942
2022 p53 alters intracellular Ca2+ signaling through regulation of TRPM4. Cell calcium 19 35500522
2021 Deletion of Trpm4 Alters the Function of the Nav1.5 Channel in Murine Cardiac Myocytes. International journal of molecular sciences 19 33810249
2019 Glibenclamide, a Sur1-Trpm4 antagonist, does not improve outcome after collagenase-induced intracerebral hemorrhage. PloS one 19 31042750
2018 Disentangling the role of TRPM4 in hippocampus-dependent plasticity and learning: an electrophysiological, behavioral and FMRI approach. Brain structure & function 19 29971514
2018 Subcellular Localization and Activity of TRPM4 in Medial Prefrontal Cortex Layer 2/3. Frontiers in cellular neuroscience 18 29440991
2009 Cloning and characterization of rat transient receptor potential-melastatin 4 (TRPM4). Biochemical and biophysical research communications 18 19945433
2023 Functional coupling between Piezo1 and TRPM4 influences the electrical activity of HL-1 atrial myocytes. The Journal of physiology 17 38098265
2018 Involvement of TRPM4 in detrusor overactivity following spinal cord transection in mice. Naunyn-Schmiedeberg's archives of pharmacology 17 30054681
2017 Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 17 28214884
2016 Heterologously-expressed and Liposome-reconstituted Human Transient Receptor Potential Melastatin 4 Channel (TRPM4) is a Functional Tetramer. Scientific reports 16 26785754
2020 Genetic background influences expression and function of the cation channel TRPM4 in the mouse heart. Basic research in cardiology 15 33205255