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Transient receptor potential cation channel, subfamily M, member 4

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. [provided by RefSeq, Aug 2010] (from NCBI)
Top mentioned proteins: melastatin, TRPM5, CAN, TRPM7, Trp6
Papers on TRPM4
Shear stress activates monovalent cation channel TRPM4 in rat atrial myocytes via type 2 inositol 1,4,5-trisphosphate receptors and Ca(2+) release.
Woo et al., Taejŏn, South Korea. In J Physiol, Feb 2016
It was suppressed by intracellular Ca(2+) buffering at a fixed physiological level, inhibitors of transient receptor potential melastatin subfamily 4 (TRPM4), intracellular introduction of TRPM4 antibodies, or knock-down of TRPM4 expression, suggesting that TRPM4 carries most of this current.
Rho kinase activity governs arteriolar myogenic depolarization.
Brayden et al., Burlington, United States. In J Cereb Blood Flow Metab, Jan 2016
Because of the well-established role of TRPM4 in pressure-induced depolarization, possible modulatory effects of Rho-associated protein kinase on TRPM4 currents were explored using patch clamp electrophysiology.
TRPM4-dependent post-synaptic depolarization is essential for the induction of NMDA receptor-dependent LTP in CA1 hippocampal neurons.
Balschun et al., Leuven, Belgium. In Pflugers Arch, Jan 2016
UNASSIGNED: TRPM4 is a calcium-activated but calcium-impermeable non-selective cation (CAN) channel.
Heterologously-expressed and Liposome-reconstituted Human Transient Receptor Potential Melastatin 4 Channel (TRPM4) is a Functional Tetramer.
Martinac et al., Sydney, Australia. In Sci Rep, Dec 2015
Mutation, irregular expression and sustained activation of the Transient Receptor Potential Channel, type Melastatin 4 (TRPM4), have been linked to various cardiovascular diseases.
TRPM4 in cardiac electrical activity.
Sallé et al., Caen, France. In Cardiovasc Res, Nov 2015
TRPM4 forms a non-selective cation channel activated by internal Ca(2+).
Physiological functions of the TRPM4 channels via protein interactions.
Park et al., Seoul, South Korea. In Bmb Rep, 2015
Transient Receptor Potential, Melastatin-related, member 4 (TRPM4) channels are Ca2(+)-activated Ca2(+)-impermeable cation channels.
Inherited progressive cardiac conduction disorders.
Abriel et al., Bern, Switzerland. In Curr Opin Cardiol, 2015
RECENT FINDINGS: Inherited PCCD in structurally normal hearts has been found to be linked to genetic variants in the ion channel genes SCN5A, SCN1B, SCN10A, TRPM4, and KCNK17, as well as in genes coding for cardiac connexin proteins.
Evaluation of the Genetic Basis of Familial Aggregation of Pacemaker Implantation by a Large Next Generation Sequencing Panel.
Vatta et al., Indianapolis, United States. In Plos One, 2014
Three patients (33.3%) had heterozygous deleterious variants previously reported in autosomal dominant cardiac diseases including CCD: LDB3 (p.D117N) and TRPM4 (p.G844D) variants in patient 4; TRPM4 (p.G844D) and ABCC9 (p.V734I) variants in patient 6; and SCN5A (p.T220I) and APOB (p.R3527Q) variants in patient 7. CONCLUSION: FaPPM occurred in 8% of our PPM clinic population.
Glibenclamide for the treatment of ischemic and hemorrhagic stroke.
Simard et al., Baltimore, United States. In Int J Mol Sci, 2014
Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1-transient receptor potential melastatin 4 (Sur1-Trpm4) channels and, in some cases, microglial KATP (Sur1-Kir6.2) channels, with glibenclamide is protective in a variety of contexts.
Vascular TRP channels: performing under pressure and going with the flow.
Nelson et al., Burlington, United States. In Physiology (bethesda), 2014
In this review, we explore the role of TRP channels, particularly endothelial TRPV4 and smooth muscle TRPC6 and TRPM4 channels, in vascular mechanosensing circuits, placing their putative mechanosensitivity in context with other proposed upstream and downstream signaling pathways.
TRPM4 cation channel mediates axonal and neuronal degeneration in experimental autoimmune encephalomyelitis and multiple sclerosis.
Friese et al., Hamburg, Germany. In Nat Med, 2012
Here we show that the transient receptor potential melastatin 4 (TRPM4) cation channel is crucial in this process.
On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1.
Nichols et al., Saint Louis, United States. In J Biol Chem, 2012
SUR1 controls K(ATP) channel activity but not TRPM4 channels.
Mutational spectrum in the Ca(2+)--activated cation channel gene TRPM4 in patients with cardiac conductance disturbances.
Schulze-Bahr et al., Münster, Germany. In Hum Mutat, 2012
In eight probands with atrioventricular block or right bundle branch block-five familial cases and three sporadic cases-a total of six novel and two published TRPM4 mutations were identified.
Endogenous cytosolic Ca(2+) buffering is necessary for TRPM4 activity in cerebral artery smooth muscle cells.
Earley et al., Fort Collins, United States. In Cell Calcium, 2012
Endogenous Ca(2+) buffer proteins play a critical role in maintaining TRPM4 channel activity in native cerebral artery smooth muscle cells.
Transient receptor potential channel m4 and m5 in magnocellular cells in rat supraoptic and paraventricular nuclei.
Armstrong et al., United States. In J Neuroendocrinol, 2011
These channels may play an important role in determining the distinct firing properties of vasopressin neurones in the supraoptic nucleus.
Basal protein kinase Cδ activity is required for membrane localization and activity of TRPM4 channels in cerebral artery smooth muscle cells.
Earley et al., Fort Collins, United States. In Channels (austin), 2011
TRPM4 channels are mobile in native cerebral myocytes and that basal PKCdelta activity supports excitability of these cells by maintaining localization TRPM4 protein at the plasma membrane.
De novo expression of Trpm4 initiates secondary hemorrhage in spinal cord injury.
Simard et al., Baltimore, United States. In Nat Med, 2009
in vivo gene suppression in rats treated with Trpm4 antisense or in Trpm4(-/-) mice preserved capillary structural integrity, eliminated secondary hemorrhage, yielded a 3x to 5x reduction in lesion volume and produced improvement in neurological function
The calcium-activated nonselective cation channel TRPM4 is essential for the migration but not the maturation of dendritic cells.
Launay et al., Paris, France. In Nat Immunol, 2008
TRPM4-regulated Ca(2+) homeostasis is crucial for DC mobility but not maturation
Increased IgE-dependent mast cell activation and anaphylactic responses in mice lacking the calcium-activated nonselective cation channel TRPM4.
Freichel et al., Leuven, Belgium. In Nat Immunol, 2007
Here we show that transient receptor potential TRPM4 proteins acted as calcium-activated nonselective cation channels and critically determined the driving force for Ca(2+) influx in mast cells.
Heat activation of TRPM5 underlies thermal sensitivity of sweet taste.
Nilius et al., Leuven, Belgium. In Nature, 2006
Here we show that TRPM5 is a highly temperature-sensitive, heat-activated channel: inward TRPM5 currents increase steeply at temperatures between 15 and 35 degrees C. TRPM4, a close homologue of TRPM5, shows similar temperature sensitivity.
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