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Compound heterozygous TRPM4 null mutations were identified in a patient with Brugada type 1 electrocardiogram.
Differentiated normal bronchial epithelial (NHBE) cells and tracheal cells from patients with cystic fibrosis (CFT1-LC3) expressed only TRPM4 and all three isoforms of NCXs. Blocking the activity of TRPM4 or NCX proteins abrogated MUC5AC secretion from NHBE and CFT1-LC3 cells.
This study presents further evidence to show that TRPM4 regulates beta-catenin signaling and enhances the proliferation of prostate cancer cell lines, through a calcium-dependent regulation of Akt1 and GSK-3beta activity.
Data suggest that TRPM4 exhibits binding sites for calmodulin (CaM) and S100 calcium-binding protein A1 (S100A1) located in very distal part of TRPM4 N-terminus.
Here, we report the functional effects of previously uncharacterized variants of uncertain significance (VUS) that we have found while performing a "genetic autopsy" in individuals who have suffered sudden unexpected death. We have identified thirteen uncommon missense VUS in TRPM4 by testing 95 targeted genes implicated in channelopathy and cardiomyopathy in 330 cases
We identified a double heterozygosity for pathogenic mutations in SCN5A and TRPM4 in a Brugada syndrome patient.
The electron cryomicroscopy structure of human transient receptor potential melastatin subfamily member 4 (TRPM4) in a closed, Na(+)-bound, apo state at pH 7.5 to an overall resolution of 3.7 A is reported.
electron cryo-microscopy structure of the most widespread CAN channel, human TRPM4, bound to the agonist Ca(2+) and the modulator decavanadate
TRPM4 protein expression is up-regulated in diffuse large B cell lymphoma
study presents 2 structures of TRPM4 embedded in lipid nanodiscs at ~3-angstrom resolution, as determined by single-particle cryo-electron microscopy; these structures, with and without calcium bound, reveal a general architecture for this major subfamily of TRP channels and a well-defined calcium-binding site within the intracellular side of the S1-S4 domain
The loss-of-function variants A432T/G582S found in 2 unrelated patients with atrioventricular block are most likely caused by misfolding-dependent altered trafficking.
Study supports the view that TRPM4 variants could be responsible for about 2% of LQT syndrome cases. The impact of these variants results in electrophysical disturbances.
A large pedigree diagnosed with progressive familial heart block type I was linked to a mutation of the TRPM4 ion channel.
Identify TRPM4 as a regulator of store operated calcium entry in prostate tumor cells, and demonstrate a role for TRPM4 in cancer cell migration.
TRPM4 channels regulate human detrusor smooth muscle excitability and contractility and are critical determinants of human urinary bladder function
TRPM4 protein expression is widely expressed in benign and cancerous prostate tissue
new insight into the ligand binding domains of the TRPM4 channel
Casein kinase 1 phosphorylates S839 and is responsible for the basolateral localization of TRPM4.
TRPM4 acts to maintain endothelial features and its loss promotes fibrotic conversion via TGF-beta production.
we demonstrate that the inhibition of TRPM4 activity alters cellular contractility in vivo, affecting cutaneous wound healing.
TRPM4 protein and mRNA are upregulated in experimental autoimmune encephalomyelitis, and that their upregulation correlated with disease progression.
Pharmacologically attenuating endogenous activation of TRPM4, TRPC3, or Ca(2+)-activated nonselective cation current in vitro similarly reduced the amplitude of inspiratory motoneuronal activity without significant perturbations of inspiratory frequency or variability of the rhythm. Amplitude perturbations were correlated with reduced inspiratory glutamatergic pre-Botzinger complex neuronal activity.
The activation of TRPM4 during ischemia-reperfusion injury involves the increase in both, intracellular calcium and H2O2, which may act together to produce a sustained activation of the channel.
Both TRPM4 and TRPM5 are required for normal responses to bitter, sweet, and umami stimuli.
The findings of this study demonstrated a novel molecular mechanism involving the SUR1-TRPM4-AQP4 complex to account for bulk water influx during astrocyte swelling.
Calcium studies demonstrated that TRPM4 channel negatively regulates calcium entry providing support for activation of the Cn-NFAT pathway in Trpm4 (-/-) mice. Authors provide evidence for the functional expression of TRPM4 channel in response to endurance training.
Study demonstrates that TRPM4 functions as a limiting factor for antigen evoked calcium rise in connective tissue type mast cells and concurrent translocation of TRPM4 into the plasma membrane is part of this mechanism.
Atrial TRPM4 channel is activated by a physiological range of Ca2+ concentrations and its excessive activity can cause arrhythmic changes.
electron cryo-microscopy structures of the mouse TRPM4 channel with and without ATP
Disrupting the Trpm4 gene in mice specifically eliminates NMDAR-dependent LTP.
observations are consistent with a model in which TRPM4 is a regulator of calcium homeostasis in cardiomyocytes after AngII stimulation
The PKC-dependent effect of GLP-1 on membrane potential and electrical activity was mediated by activation of Na(+)-permeable TRPM4 and TRPM5 channels by mobilization of intracellular Ca(2+) from thapsigargin-sensitive Ca(2+) stores
The function of TRPM4 in renal primary cilia is not yet known, but it is likely to influence the apical Ca(2) dynamics of the cell
Deletion of the Trpm4 gene in mice improved survival and significantly enhanced beta-adrenergic cardiac reserve after inducing ischaemic heart failure.
TRPM4 has pleiotropic roles in the heart, including the regulation of conduction and cellular electrical activity which impact heart development.
The present study demonstrates that robust TRPM4-IR is localized specifically in the soma of Inner Auditory Hair Cells in the organ of Corti.
These results showed that the cell surface expression of TRPM4 channels is mediated by 14-3-3gamma binding.
Adenylyl cyclase-mediated effects contribute to increased isoprenaline-induced cardiac contractility in TRPM4-deficient mice.
Results show that functional TRPM4 proteins are novel determinants of the inotropic effect of beta-adrenergic stimulation on the ventricular heart muscle.
N-Glycosylation is not required for surface expression, but complex N-glycosylation stabilizes Trpm4b surface expression.
The protein encoded by this gene is a calcium-activated nonselective ion channel that mediates transport of monovalent cations across membranes, thereby depolarizing the membrane. The activity of the encoded protein increases with increasing intracellular calcium concentration, but this channel does not transport calcium. Two transcript variants encoding different isoforms have been found for this gene.
, calcium-activated non-selective cation channel 1
, long transient receptor potential channel 4
, transient receptor potential cation channel subfamily M member 4
, melastatin like 2 protein
, melastatin-like 2
, transient receptor potential ion channel melastatin subgroup member 4
, transient receptor potential cation channel, subfamily M, member 4
, LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily M member 4