ArticleMolecular brain2014
Depletion of 14-3-3γ reduces the surface expression of Transient Receptor Potential Melastatin 4b (TRPM4b) channels and attenuates TRPM4b-mediated glutamate-induced neuronal cell death.
Article in Molecular brain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- TRP Channels Interactome as a Novel Therapeutic Target in Breast Cancer.Frontiers in oncology · 2021Pooled it
- Identification of 14-3-3 Proteins as Binding Partners of TRP Channels.Journal of chemical information and modeling · 2026Article
- The TRP channels serving as chemical-to-electrical signal converter.Physiological reviews · 2025Review
- TRPM4 contributes to cell death in prostate cancer tumor spheroids, and to extravasation and metastasis in a zebrafish xenograft model system.Molecular oncology · 2025Article
- Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy.Frontiers in neuroscience · 2025Review
- Case Report: Loss-of-function TRPM4 mutation p.L91Δ implicated in progressive cardiac conduction defect.Frontiers in physiology · 2025Article
- Cholinergic stimulation stabilizes TRPM4 in the plasma membrane of cortical pyramidal neurons.Frontiers in cell and developmental biology · 2024Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- 14-3-3 proteins regulate cullin 7-mediated Eag1 degradation.Cell & bioscience · 2023Article
- TRPM4 in Cancer-A New Potential Drug Target.Biomolecules · 2021Review
- A Rationale for Hypoxic and Chemical Conditioning in Huntington's Disease.International journal of molecular sciences · 2021Review
- PPI-MASS: An Interactive Web Server to Identify Protein-Protein Interactions From Mass Spectrometry-Based Proteomics Data.Frontiers in molecular biosciences · 2021Article
- TRPM4 non-selective cation channel in human atrial fibroblast growth.Pflugers Archiv : European journal of physiology · 2020Article
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Inherited Cardiac Arrhythmia Syndromes: Focus on Molecular Mechanisms Underlying TRPM4 Channelopathies.Cardiovascular therapeutics · 2020Review
- 14-3-3γ Haploinsufficient Mice Display Hyperactive and Stress-sensitive Behaviors.Experimental neurobiology · 2019Article
- PTPN6 regulates the cell-surface expression of TRPM4 channels in HEK293 cells.Pflugers Archiv : European journal of physiology · 2018Article
- The kinase activity of the channel-kinase protein TRPM7 regulates stability and localization of the TRPM7 channel in polarized epithelial cells.The Journal of biological chemistry · 2018Article
- The ion channel TRPM4 in murine experimental autoimmune encephalomyelitis and in a model of glutamate-induced neuronal degeneration.Molecular brain · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTRPM4 channels are Ca2+-activated nonselective cation channels which are deeply involved in physiological and pathological conditions. However, their trafficking mechanism and binding partners are still elusive.
resultsWe have found the 14-3-3γ as a binding partner for TRPM4b using its N-terminal fragment from the yeast-two hybrid screening. Ser88 at the N-terminus of TRPM4b is critical for 14-3-3γ binding by showing GST pull-down and co-immunoprecipitation. Heterologous overexpression of 14-3-3γ in HEK293T cells increased TRPM4b expression on the plasma membrane which was measured by whole-cell recordings and cell surface biotinylation experiment. Surface expression of TRPM4b was greatly reduced by short hairpin RNA (shRNA) against 14-3-3γ. Next, endogenous TRPM4b-mediated currents were electrophysiologically characterized by application of glutamate and 9-phenanthrol, a TRPM4b specific antagonist in HT-22 cells which originated from mouse hippocampal neurons. Glutamate-induced TRPM4b currents were significantly attenuated by shRNAs against 14-3-3γ or TRPM4b in these cells. Finally, glutamate-induced cell death was greatly prevented by treatment of 9-phenanthrol or 14-3-3γ shRNA.
conclusionThese results showed that the cell surface expression of TRPM4 channels is mediated by 14-3-3γ binding, and the specific inhibition of this trafficking process can be a potential therapeutic target for glutamate-induced neuronal cell death.
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