Affinage

TRPC7

Short transient receptor potential channel 7 · UniProt Q9HCX4

Round 2 corrected
Length
862 aa
Mass
99.6 kDa
Annotated
2026-04-28
53 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRPC7 is a plasma membrane Ca²⁺-permeable non-selective cation channel of the TRPC3/6/7 subfamily that is directly activated by diacylglycerol (DAG) downstream of Gαq-coupled receptor–PLC signaling and assembles into homomeric or heteromeric complexes exclusively with TRPC3 and TRPC6 (PMID:12377790, PMID:16690880). Channel activity is negatively regulated by extracellular Ca²⁺ through voltage-dependent reductions in conductance and open probability, and by intracellular Ca²⁺ via calmodulin, while closely associated SERCA pumps protect the channel from Ca²⁺-CaM–mediated inactivation; at physiological expression levels, IP3 receptors are required as permissive cofactors for DAG-dependent gating (PMID:15579537, PMID:16401641, PMID:16822861). In cardiomyocytes, TRPC7-mediated Ca²⁺ entry drives both the intracellular Ca²⁺ clock (via RyR2 and phospholamban phosphorylation) and the membrane clock to regulate pacemaker automaticity (PMID:33941260). In skin, TRPC7 is the obligate mediator of UVB-induced Ca²⁺ influx and reactive oxygen species production, and its genetic ablation prevents UVB-driven epidermal thickening, DNA damage, and tumorigenesis in mice (PMID:31755176).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1998 High

    Identification of TRPC7 as a novel TRP-family member established the existence of a seventh human canonical TRP channel with predicted transmembrane topology consistent with a Ca²⁺-permeable pore.

    Evidence cDNA cloning from human fetal brain and caudate nucleus libraries with genomic mapping to 21q22.3

    PMID:9806837

    Open questions at the time
    • No functional electrophysiology performed
    • Expression pattern beyond Northern blot unknown
    • Activation mechanism not addressed
  2. 2001 Medium

    Discovery of conserved IP3R-binding and calmodulin-binding domains on the TRPC7 C-terminus, with competitive binding between the two, provided the first molecular framework for Ca²⁺-dependent channel regulation.

    Evidence GST pulldown and co-immunoprecipitation showing overlapping CaM and IP3R binding sites on TRPC C-termini

    PMID:11290752

    Open questions at the time
    • TRPC7 was studied alongside other TRPCs, not as primary target
    • Functional consequence of CaM vs. IP3R competition on TRPC7 currents not tested
    • Binding site residues not mapped
  3. 2002 High

    Demonstration that TRPC7 selectively co-assembles with TRPC3 and TRPC6 — but not with the TRPC1/4/5 subgroup — defined the combinatorial rules governing heteromeric TRP channel assembly.

    Evidence Reciprocal co-immunoprecipitation in Sf9 cells and native rat brain synaptosomes

    PMID:12377790

    Open questions at the time
    • Stoichiometry of heteromeric complexes unknown
    • No structural basis for subfamily-restricted assembly
  4. 2004 High

    Electrophysiological characterization established TRPC7 as a DAG-activated receptor-operated channel whose gating mode (receptor-operated vs. store-operated) depends on expression level, and revealed unique negative regulation by extracellular Ca²⁺ acting on unitary conductance and open probability via intracellular calmodulin.

    Evidence Patch-clamp comparison of stable vs. transient TRPC7 expression in HEK-293 cells; single-channel recordings with CaM mutants and pharmacological inhibitors

    PMID:15342342 PMID:15579537

    Open questions at the time
    • Molecular determinants of extracellular Ca²⁺ sensing not identified
    • Structural basis for DAG binding site unknown
  5. 2005 High

    Identification of an endogenous TRPC1–TRPC3–TRPC7 heteromeric complex mediating store-operated Ca²⁺ entry in HEK-293 cells showed that TRPC7 contributes to native SOCE channels, not only receptor-operated channels.

    Evidence siRNA knockdown of individual subunits combined with co-immunoprecipitation and thapsigargin-stimulated Ba²⁺ entry

    PMID:15972814

    Open questions at the time
    • SOCE role not confirmed in primary cells
    • Relationship to Orai/STIM-mediated SOCE unclear
  6. 2006 High

    Multiple studies converged to show that (i) native TRPC7 gating by DAG requires IP3 receptors as permissive cofactors at physiological expression levels, (ii) SERCA pumps physically associated with TRPC7 protect the channel from Ca²⁺-CaM–mediated inactivation, and (iii) TRPC6–TRPC7 heteromers constitute the native receptor-operated channel in vascular smooth muscle.

    Evidence Genetic epistasis in TRPC7⁻/⁻ and IP3R⁻/⁻ DT40 cells with rescue; thapsigargin/cytochalasin D pharmacology in HEK cells; co-IP and dominant-negative electrophysiology in A7r5 cells and coronary myocytes

    PMID:16401641 PMID:16690880 PMID:16741513 PMID:16822861 PMID:17303636

    Open questions at the time
    • Mechanism by which IP3R licenses DAG gating is unknown
    • Identity of the SERCA isoform and mode of physical coupling not determined
    • Native stoichiometry of TRPC6/7 heteromers in vivo undefined
  7. 2008 Medium

    Dissection of TRPC7 inactivation showed that persistent Ca²⁺-dependent shutdown requires synergistic action of both DAG and IP3, revealing a dual-signal integration mechanism for channel silencing independent of IP3 receptor opening.

    Evidence Whole-cell patch clamp with intracellular dialysis of IP3, OAG, and Ca²⁺ chelators in HEK-293 cells

    PMID:18158870

    Open questions at the time
    • Molecular target of IP3's direct sensitizing action not identified
    • In vivo relevance of dual-signal inactivation not tested
  8. 2008 Medium

    Detection of TRPC7 at Golgi compartments and its ability to enhance constitutive secretion suggested a second site of action beyond the plasma membrane.

    Evidence Immunofluorescence co-localization with Golgi markers and alkaline phosphatase secretion assay in COS-7 cells

    PMID:18452405

    Open questions at the time
    • Golgi localization not confirmed in primary cells
    • Mechanism linking TRPC7 channel activity to vesicular secretion undefined
  9. 2009 High

    Demonstration that a disease-associated truncated polycystin-2 (TRPP2) mutant physically associates with TRPC7 and alters its pore properties linked TRPC7 to polycystic kidney disease-relevant signaling complexes.

    Evidence Co-IP, cross-linking, and single-channel recordings showing altered conductance and reversal potential of TRPC7 in complex with TRPP2-697fsX

    PMID:19812035

    Open questions at the time
    • Interaction with wild-type TRPP2 not equivalently characterized
    • Relevance to renal cyst formation in vivo not demonstrated
  10. 2016 Medium

    Localization of TRPC7 to sarcolemma and T-tubules in cardiomyocytes, with downregulation in hypertrophic hearts reversible by angiotensin receptor blockade, implicated TRPC7 in cardiac remodeling via Ang II/PKC signaling.

    Evidence Immunohistochemistry and Western blot in a 2K1C renovascular hypertension rat model with losartan rescue

    PMID:26371949

    Open questions at the time
    • PKC–TRPC7 regulatory mechanism is correlative, not causal
    • Direct TRPC7 phosphorylation by PKC not demonstrated in this model
  11. 2019 High

    Genetic ablation in mice established TRPC7 as the obligate initiator of UVB-induced Ca²⁺ influx, ROS production, and downstream photoaging/tumorigenesis in skin, revealing a physiological nociceptive-mechanoreceptor role.

    Evidence TRPC7 knockout mice with multi-parameter phenotyping including Ca²⁺ influx, ROS, histology, DNA damage, and tumor formation

    PMID:31755176

    Open questions at the time
    • Mechanism of UVB-induced TRPC7 activation (direct photomechanical vs. lipid-mediated) unknown
    • Cell-type specificity within the epidermis not resolved
  12. 2021 High

    TRPC7 was shown to regulate cardiomyocyte pacemaker automaticity by coupling Ca²⁺ entry to dual clocks: the intracellular Ca²⁺ clock (via RyR2-S2814 and PLB-T17 phosphorylation/SERCA activation) and the membrane clock (via NCX), while a C-terminal truncation mutation produced dominant-negative effects in vivo distinct from null.

    Evidence Adenoviral KD/OE and dominant-negative constructs in mESC-derived cardiomyocytes with Ca²⁺ imaging and electrophysiology; ENU mutagenesis mouse with C-terminal stop codon

    PMID:33941260 PMID:34828338

    Open questions at the time
    • Kinase(s) mediating TRPC7-dependent RyR2/PLB phosphorylation not identified
    • Dominant-negative mechanism of C-terminal truncation not molecularly defined
  13. 2022 Medium

    Detection of Gαq-induced intramolecular conformational changes in TRPC7 via BRET biosensors provided the first real-time evidence of receptor-triggered structural rearrangements in the intact channel.

    Evidence Intramolecular BRET (GFP10-TRPC7-RLucII) in HEK293 cells and primary rat cardiac fibroblasts upon AT1R stimulation

    PMID:35269644

    Open questions at the time
    • Nature and location of conformational change not resolved at atomic level
    • Relationship between BRET change and channel gating transitions not established
  14. 2023 Medium

    TRPC7-mediated Ca²⁺ entry was linked to lung adenocarcinoma proliferation and migration through CaMKII/AKT/ERK signaling, extending TRPC7's pathophysiological relevance beyond skin and heart.

    Evidence siRNA knockdown with cell cycle, migration, and phospho-signaling readouts in lung adenocarcinoma cell lines

    PMID:36817036

    Open questions at the time
    • No in vivo tumor model
    • Selectivity for TRPC7 vs. other DAG-activated TRPCs not addressed
    • Direct vs. indirect activation of CaMKII/AKT/ERK not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for DAG binding and extracellular Ca²⁺ sensing, the mechanism by which IP3 receptors license TRPC7 gating at physiological expression, the identity of kinases linking TRPC7-mediated Ca²⁺ entry to RyR2/PLB phosphorylation in cardiomyocytes, and the biophysical mechanism of UVB-induced channel activation in skin.
  • No high-resolution structure of TRPC7
  • DAG binding site not mapped
  • IP3R–TRPC7 coupling mechanism molecularly undefined
  • UVB activation mechanism unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0098772 molecular function regulator activity 1
Localization
GO:0005886 plasma membrane 4 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-382551 Transport of small molecules 5
Partners
CALM1ITPR1PKD2RYR2TRPC1TRPC3TRPC6
Complex memberships
TRPC1/TRPC3/TRPC7 heteromeric channelTRPC3/TRPC7 heteromeric channelTRPC6/TRPC7 heteromeric channel

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 TRPC7 was cloned as a novel human protein of 1503 amino acids from fetal brain and caudate nucleus cDNA libraries. It has seven putative transmembrane domains consistent with a Ca2+ channel and shows significant homology with Drosophila TRP proteins. The TRPC7 gene consists of 32 exons spanning ~90 kb and maps to human chromosome 21q22.3. cDNA cloning, Northern blot, genomic sequencing, chromosomal mapping Genomics High 9806837
2002 TRPC7 selectively assembles into homo- or heteromeric channel complexes exclusively within the TRPC3/6/7 subfamily. Co-immunoprecipitation in Sf9 cells and rat brain synaptosomes demonstrated that TRPC3, TRPC6, and TRPC7 co-associate with each other but do not cross-associate with the TRPC1/4/5 subgroup. TRPC3/6/7 subunits also did not interact with the PDZ-containing scaffold protein INAD. Reciprocal co-immunoprecipitation in heterologous (Sf9) cells and native rat brain synaptosomes The Journal of biological chemistry High 12377790
2001 TRPC7 (and other TRPC family members) possess a conserved IP3 receptor-binding domain and a calmodulin (CaM)-binding domain on their carboxyl termini. In the presence of Ca2+, CaM competes with IP3R for binding to TRPC7, suggesting that CaM and IP3R regulate TRPC7 gating through overlapping binding sites. GST pulldown, co-immunoprecipitation, gel shift assay, inside-out patch clamp with synthetic peptides The Journal of biological chemistry Medium 11290752
2004 TRPC7 functions as a receptor-operated, diacylglycerol (DAG)-activated non-selective cation channel when transiently expressed in HEK-293 cells (activated by PLC-stimulating agonists but not by Ca2+ store depletion). When stably expressed in HEK-293 cells, TRPC7 can be activated by either Ca2+ store depletion or PLC activation, demonstrating that expression level/environment determines the mode of TRPC7 gating. Stable and transient transfection in HEK-293 cells, patch clamp, thapsigargin-based store depletion, agonist stimulation American journal of physiology. Cell physiology High 15342342
2004 TRPC7 currents are inhibited by extracellular Ca2+ (IC50 ~0.4 mM) through voltage-dependent reductions in unitary conductance and open probability at the single-channel level. Single TRPC7 channel activity is concentration-dependently suppressed by nanomolar intracellular Ca2+ via calmodulin (CaM), and is conversely enhanced by IP3. This contrasts with TRPC6, which is potentiated by Ca2+ through a CaMKII-dependent mechanism. Nystatin-perforated patch clamp, conventional whole-cell clamp, single-channel recording, CaM mutant co-expression, pharmacological inhibitors (calmidazolium, AMP-PNP, CaMKII inhibitory peptide) The Journal of physiology High 15579537
2005 Endogenous TRPC1, TRPC3, and TRPC7 form a heteromeric complex in HEK-293 cells that mediates store-operated Ca2+ entry (SOCE). siRNA knockdown of each individually suppressed SOCE by 52–68%, and co-immunoprecipitation confirmed the existence of a TRPC1-TRPC3-TRPC7 heteromeric complex. TRPC3 and TRPC7 (but not TRPC1) also participate in receptor-operated channels. siRNA knockdown, co-immunoprecipitation, thapsigargin-stimulated Ba2+ entry measurements, 2-APB/SKF96365 pharmacology The Journal of biological chemistry High 15972814
2006 Native TRPC7 channel activity (75 pS single channels) in DT40 B lymphocytes requires inositol trisphosphate receptors (IP3Rs) for activation by DAG (OAG). TRPC7-null DT40 cells show no OAG-induced single-channel activity, restored by TRPC7 re-expression; IP3R-null cells similarly lack OAG-induced activity, restored by IP3R re-expression. At high TRPC7 expression levels, channel activity becomes IP3R-independent. Cell-attached patch clamp in TRPC7-/- and IP3R-/- DT40 B lymphocyte cell lines, genetic rescue experiments The Journal of biological chemistry High 16822861
2006 TRPC7 channels are subject to negative feedback regulation by Ca2+ entering through the channels themselves. Thapsigargin-mediated inhibition of SERCA pumps blocks DAG-activated TRPC7, an effect dependent on extracellular Ca2+, the driving force for Ca2+ entry, and calmodulin. Pharmacological disruption of the actin cytoskeleton mimics the effect of thapsigargin. This suggests that closely associated SERCA pumps protect TRPC7 from Ca2+-calmodulin-mediated inhibition under physiological conditions. Whole-cell patch clamp, thapsigargin, calmodulin inhibition, cytochalasin D actin disruption, extracellular Ca2+ manipulation FASEB journal High 16401641
2006 TRPC7 is the molecular substrate for DAG-activated receptor-operated Ca2+ entry in human keratinocytes (HaCaT cells). CCh- and ATP-induced cation currents were inhibited by a PLC blocker and mimicked by the DAG analog OAG, but were insensitive to IP3 and to PKC inhibitors, indicating direct DAG activation. Antisense knockdown of TRPC7 reduced ATP- and CCh-induced Ca2+ entry and OAG-evoked current. Patch clamp, antisense oligonucleotide knockdown, pharmacological dissection (PLC inhibitor, PKC inhibitor, OAG, IP3) The Journal of investigative dermatology Medium 16741513
2006 In rabbit coronary artery myocytes, ET-1 activates a Ca2+-permeable non-selective cation channel with TRPC3 and TRPC7 properties via ETA receptor and PLC. Anti-TRPC3 and anti-TRPC7 antibodies applied to inside-out patches inhibited ET-1-evoked currents; antibodies to TRPC1, C4, C5, C6 had no effect. Immunocytochemistry revealed preferential TRPC7 plasma membrane localization and co-localization of TRPC3 and TRPC7 at or near the plasma membrane. Cell-attached and inside-out patch clamp with channel-blocking antibodies, immunocytochemistry The Journal of physiology Medium 17303636
2006 TRPC7 protein exhibits constitutive activity and is directly activated by DAG downstream of PLC signaling. TRPC7 is uniquely susceptible to negative regulation by extracellular Ca2+, distinguishing it from closely related TRPC3 and TRPC6. Review synthesizing patch-clamp and molecular biological data from multiple studies Handbook of experimental pharmacology Low 17217055
2006 TRPC6 and TRPC7 form heteromeric receptor-operated channels in A7r5 vascular smooth muscle cells that mediate arginine vasopressin (AVP)-induced non-selective cation current. Co-immunoprecipitation confirmed physical TRPC6-TRPC7 association. Dominant-negative TRPC6 (but not TRPC5) suppressed AVP-induced currents. Extracellular Ca2+ suppressed native, TRPC7, and TRPC6-TRPC7 heteromeric currents, but the Ca2+ sensitivity matched the native channel only for the heteromeric TRPC6-TRPC7 construct. Co-immunoprecipitation, dominant-negative expression, whole-cell patch clamp, extracellular Ca2+ titration Circulation research High 16690880
2008 Ca2+-dependent inactivation of TRPC7 requires the synergistic actions of both DAG and IP3. OAG-induced TRPC7 currents alone do not undergo persistent Ca2+-mediated inhibition, but co-application of intracellular IP3 renders them susceptible to persistent Ca2+-mediated inactivation independently of IP3 receptors (not blocked by heparin or thapsigargin). Carbachol- and GTPγS-activated TRPC7 currents undergo persistent Ca2+-dependent inhibition that requires strong intracellular Ca2+ buffering (BAPTA) for recovery. Whole-cell patch clamp, intracellular dialysis with IP3, OAG, GTPγS, BAPTA, heparin, thapsigargin Acta pharmacologica Sinica Medium 18158870
2008 Heterologously expressed TRPC3 and TRPC7 localize not only to the plasma membrane but also to intracellular Golgi (both cis-Golgi and trans-Golgi network) compartments in COS-7 cells, as shown by co-localization with Golgi markers and Brefeldin A redistribution. Expression of TRPC3 or TRPC7 (but not TRPC1) increased constitutive secretion of alkaline phosphatase 2–4-fold, suggesting these channels enhance vesicular transport/secretion. Immunofluorescence microscopy, Brefeldin A treatment, alkaline phosphatase secretion assay The Biochemical journal Medium 18452405
2009 A pathogenic C-terminus-truncated polycystin-2 (TRPP2) mutant (697fsX) physically associates with TRPC3 and TRPC7 at the plasma membrane, and this association enhances muscarinic receptor-activated Ca2+ influx and alters ion-permeating pore properties (depolarizing shift in reversal potential, enhanced single-channel conductance) of the mAChR-activated current. Co-immunoprecipitation, pulldown, and cross-linking confirmed the TRPP2 mutant-TRPC7 interaction. Co-immunoprecipitation, pulldown assay, cross-linking, whole-cell patch clamp, single-channel recording, immunofluorescence The Journal of biological chemistry High 19812035
2019 TRPC7 acts as a nociceptive mechanoreceptor that specifically mediates UVB-induced Ca2+ influx and subsequent reactive oxygen species production in skin cells within 30 minutes of irradiation. In TRPC7 knockout mice, UVB-associated epidermal thickening, abnormal keratinocyte differentiation, DNA damage response activation, p53 family mutations, and tumor formation were all prevented, establishing TRPC7 as a required initiator of UVB-induced skin aging and tumorigenesis. TRPC7 knockout mice, Ca2+ influx assays, ROS measurements, histology, immunostaining, mutation analysis Aging cell High 31755176
2021 TRPC7 regulates the automaticity (spontaneous action potential firing) of mouse embryonic stem cell-derived cardiomyocytes via two mechanisms: (1) positively regulating the intracellular Ca2+ clock by enhancing RyR2 phosphorylation at S2814 and SERCA activity (via phospholamban phosphorylation at T17); (2) positively regulating the membrane clock via NCX activity. These effects are Ca2+-dependent, as a dominant-negative N-terminal TRPC7 construct that abolishes Ca2+ permeability reduces AP frequency. Adenoviral TRPC7 knockdown/overexpression, confocal Ca2+ imaging, whole-cell patch clamp, Western blot for phosphorylation, dominant-negative TRPC7 N-terminus construct Stem cell research & therapy High 33941260
2021 A truncation mutation in the Trpc7 cytoplasmic C-terminus (stop codon at amino acid 810, affecting the conserved C-terminal domain) produces a dominant-negative effect in heterozygous mice, causing distinct morphological and behavioral alterations not seen in Trpc7 knockout mice, demonstrating that the C-terminus is critical for normal TRPC7 function. ENU mutagenesis mouse model, Sanger sequencing, phenotypic characterization of heterozygous mutants Genes Medium 34828338
2022 TRPC7 undergoes conformational changes upon activation by Gαq-coupled receptors, as detected by intramolecular BRET biosensors (GFP10-TRPC7-RLucII). Activation of Gαq-coupled receptors (including the angiotensin II AT1R) induces a Gαq-dependent BRET response in both HEK293 cells and rat neonatal cardiac fibroblasts expressing endogenous AT1R and TRPC7, confirming receptor-induced structural rearrangements in TRPC7. Intramolecular BRET biosensors in HEK293 cells and primary rat cardiac fibroblasts, GPCR agonist stimulation, Gαq pathway pharmacology International journal of molecular sciences Medium 35269644
2023 TRPC7 facilitates lung adenocarcinoma cell growth and migration via Ca2+-dependent activation of CaMKII, AKT, and ERK signaling pathways. TRPC7 knockdown restrained cell cycle progression and migration by interrupting TRPC7-mediated Ca2+ signaling, upstream of AKT and MAPK pathway activation. TRPC7 siRNA knockdown, cell cycle analysis, invasion assay, Ca2+ response assay, immunoblot for phospho-CaMKII/AKT/ERK Oncology letters Medium 36817036
2016 In normal rat cardiomyocytes, TRPC7 localizes to the surface sarcolemma and striated subcellular (T-tubule) regions. In renovascular hypertrophic hearts, TRPC7 expression is significantly downregulated while PKC expression is upregulated, with a negative correlation between TRPC7 and PKC levels. Losartan (angiotensin II receptor blocker) reverses TRPC7 downregulation, implicating Ang II/PKC signaling in the suppression of TRPC7 in cardiac hypertrophy. Immunohistochemistry, immunocytochemistry, Western blot, 2K1C renovascular hypertension model, losartan treatment Journal of cardiovascular pharmacology Medium 26371949

Source papers

Stage 0 corpus · 53 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2000 The DNA sequence of human chromosome 21. Nature 808 10830953
2001 ADP-ribose gating of the calcium-permeable LTRPC2 channel revealed by Nudix motif homology. Nature 783 11385575
2002 LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death. Molecular cell 684 11804595
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2002 Subunit composition of mammalian transient receptor potential channels in living cells. Proceedings of the National Academy of Sciences of the United States of America 612 12032305
2008 TRPM2-mediated Ca2+influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration. Nature medicine 508 18542050
2001 Immunocyte Ca2+ influx system mediated by LTRPC2. Science (New York, N.Y.) 389 11509734
2006 TRPM2 activation by cyclic ADP-ribose at body temperature is involved in insulin secretion. The EMBO journal 344 16601673
2005 International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels. Pharmacological reviews 313 16382100
2002 Activation of the cation channel long transient receptor potential channel 2 (LTRPC2) by hydrogen peroxide. A splice variant reveals a mode of activation independent of ADP-ribose. The Journal of biological chemistry 299 11960981
2004 Accumulation of free ADP-ribose from mitochondria mediates oxidative stress-induced gating of TRPM2 cation channels. The Journal of biological chemistry 289 15561722
2017 Genome-wide CRISPR screen identifies HNRNPL as a prostate cancer dependency regulating RNA splicing. Proceedings of the National Academy of Sciences of the United States of America 282 28611215
2005 Cyclic ADP-ribose and hydrogen peroxide synergize with ADP-ribose in the activation of TRPM2 channels. Molecular cell 270 15808509
2002 Selective association of TRPC channel subunits in rat brain synaptosomes. The Journal of biological chemistry 260 12377790
2003 Critical intracellular Ca2+ dependence of transient receptor potential melastatin 2 (TRPM2) cation channel activation. The Journal of biological chemistry 254 12529379
2001 Identification of common binding sites for calmodulin and inositol 1,4,5-trisphosphate receptors on the carboxyl termini of trp channels. The Journal of biological chemistry 253 11290752
2009 TRPM2 functions as a lysosomal Ca2+-release channel in beta cells. Science signaling 239 19454650
1998 Molecular cloning of a novel putative Ca2+ channel protein (TRPC7) highly expressed in brain. Genomics 220 9806837
2003 A novel TRPM2 isoform inhibits calcium influx and susceptibility to cell death. The Journal of biological chemistry 203 12594222
2007 Role of TRPM2 channel in mediating H2O2-induced Ca2+ entry and endothelial hyperpermeability. Circulation research 192 18048770
2005 Endogenous TRPC1, TRPC3, and TRPC7 proteins combine to form native store-operated channels in HEK-293 cells. The Journal of biological chemistry 172 15972814
2004 Multiple regulation by calcium of murine homologues of transient receptor potential proteins TRPC6 and TRPC7 expressed in HEK293 cells. The Journal of physiology 162 15579537
2003 Expression profile of the transient receptor potential (TRP) family in neutrophil granulocytes: evidence for currents through long TRP channel 2 induced by ADP-ribose and NAD. The Biochemical journal 158 12564954
2018 Structures and gating mechanism of human TRPM2. Science (New York, N.Y.) 149 30467180
2006 Nicotinic acid adenine dinucleotide phosphate and cyclic ADP-ribose regulate TRPM2 channels in T lymphocytes. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 148 16585058
2012 Redox signal-mediated sensitization of transient receptor potential melastatin 2 (TRPM2) to temperature affects macrophage functions. Proceedings of the National Academy of Sciences of the United States of America 147 22493272
2006 Metabolite of SIR2 reaction modulates TRPM2 ion channel. The Journal of biological chemistry 130 16565078
2008 The Poly(ADP-ribose) polymerase PARP-1 is required for oxidative stress-induced TRPM2 activation in lymphocytes. The Journal of biological chemistry 124 18599483
2018 Structure of a TRPM2 channel in complex with Ca2+ explains unique gating regulation. eLife 123 29745897
2015 The Transient Receptor Potential Melastatin 2 (TRPM2) Channel Contributes to β-Amyloid Oligomer-Related Neurotoxicity and Memory Impairment. The Journal of neuroscience : the official journal of the Society for Neuroscience 120 26558786
2010 Transient receptor potential melastatin 2 is required for lipopolysaccharide-induced cytokine production in human monocytes. Journal of immunology (Baltimore, Md. : 1950) 116 20107186
2006 Regulation of the transient receptor potential channel TRPM2 by the Ca2+ sensor calmodulin. The Journal of biological chemistry 107 16461353
2006 Heteromultimeric TRPC6-TRPC7 channels contribute to arginine vasopressin-induced cation current of A7r5 vascular smooth muscle cells. Circulation research 73 16690880
2007 Endothelin-1 activates a Ca2+-permeable cation channel with TRPC3 and TRPC7 properties in rabbit coronary artery myocytes. The Journal of physiology 67 17303636
2004 Canonical transient receptor potential TRPC7 can function as both a receptor- and store-operated channel in HEK-293 cells. American journal of physiology. Cell physiology 64 15342342
2006 TRPC7 is a receptor-operated DAG-activated channel in human keratinocytes. The Journal of investigative dermatology 48 16741513
2006 Native TRPC7 channel activation by an inositol trisphosphate receptor-dependent mechanism. The Journal of biological chemistry 30 16822861
2006 Protection of TRPC7 cation channels from calcium inhibition by closely associated SERCA pumps. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 29 16401641
2009 A pathogenic C terminus-truncated polycystin-2 mutant enhances receptor-activated Ca2+ entry via association with TRPC3 and TRPC7. The Journal of biological chemistry 27 19812035
2020 LncRNA TRPC7-AS1 regulates nucleus pulposus cellular senescence and ECM synthesis via competing with HPN for miR-4769-5p binding. Mechanisms of ageing and development 25 32585234
2019 Nociceptive transient receptor potential canonical 7 (TRPC7) mediates aging-associated tumorigenesis induced by ultraviolet B. Aging cell 19 31755176
2007 TRPC7. Handbook of experimental pharmacology 14 17217055
2021 TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes. Stem cell research & therapy 13 33941260
2021 Involvement of TRPC7-AS1 Expression in Hepatitis B Virus-Related Hepatocellular Carcinoma. Journal of oncology 12 34512754
2008 Increasing the expression of calcium-permeable TRPC3 and TRPC7 channels enhances constitutive secretion. The Biochemical journal 11 18452405
2024 The IGF2BP2-lncRNA TRPC7-AS1 axis promotes hepatocellular carcinoma cell proliferation and invasion. Cellular signalling 10 38320625
2023 TRPC7 facilitates cell growth and migration by regulating intracellular Ca2+ mobilization in lung adenocarcinoma cells. Oncology letters 8 36817036
2016 Transient Receptor Potential Canonical 7 (TRPC7), a Calcium (Ca(2+)) Permeable Non-selective Cation Channel. Advances in experimental medicine and biology 6 27161232
2022 Monitoring TRPC7 Conformational Changes by BRET Following GPCR Activation. International journal of molecular sciences 3 35269644
2008 Synergistic actions of diacylglycerol and inositol 1,4,5 trisphosphate for Ca2+-dependent inactivation of TRPC7 channel. Acta pharmacologica Sinica 3 18158870
2016 Morphological Identification of TRPC7 in Cardiomyocytes From Normal and Renovascular Hypertensive Rats. Journal of cardiovascular pharmacology 2 26371949
2021 Distinct Morphological and Behavioural Alterations in ENU-Induced Heterozygous Trpc7 Mutant Mice. Genes 0 34828338