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Study supports the view that TRPM4 variants could be responsible for about 2% of LQT (显示 KCNQ1 ELISA试剂盒) 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 (显示 CSNK1A1 ELISA试剂盒) 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 (显示 TGFB1 ELISA试剂盒) production.
we demonstrate that the inhibition of TRPM4 activity alters cellular contractility in vivo, affecting cutaneous wound healing.
The PKC-dependent effect of GLP-1 (显示 GCG ELISA试剂盒) on membrane potential and electrical activity was mediated by activation of Na(+)-permeable TRPM4 and TRPM5 (显示 TRPM5 ELISA试剂盒) channels by mobilization of intracellular Ca(2 (显示 CA2 ELISA试剂盒)+) from thapsigargin-sensitive Ca(2 (显示 CA2 ELISA试剂盒)+) stores
Disrupting the Trpm4 gene in mice specifically eliminates NMDAR (显示 GRIN1 ELISA试剂盒)-dependent LTP (显示 SCP2 ELISA试剂盒).
observations are consistent with a model in which TRPM4 is a regulator of calcium homeostasis in cardiomyocytes after AngII stimulation
The PKC (显示 PKC ELISA试剂盒)-dependent effect of GLP-1 (显示 GCG ELISA试剂盒) on membrane potential and electrical activity was mediated by activation of Na(+)-permeable TRPM4 and TRPM5 (显示 TRPM5 ELISA试剂盒) channels by mobilization of intracellular Ca(2 (显示 CA2 ELISA试剂盒)+) from thapsigargin-sensitive Ca(2 (显示 CA2 ELISA试剂盒)+) stores
The function of TRPM4 in renal primary cilia is not yet known, but it is likely to influence the apical Ca(2 (显示 CA2 ELISA试剂盒)) 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 (显示 YWHAG ELISA试剂盒) 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.
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.
transient receptor potential cation channel, subfamily M, member 4
, 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