Ask about this productRelated genes to: TRPM4 antibody
- Gene:
- TRPM4 NIH gene
- Name:
- transient receptor potential cation channel subfamily M member 4
- Previous symbol:
- -
- Synonyms:
- FLJ20041
- Chromosome:
- 19q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-11
- Date modifiied:
- 2016-01-28
Related products to: TRPM4 antibody
Related articles to: TRPM4 antibody
- Osteoporosis is the leading cause of fractures, characterized by reduced bone formation and increased bone resorption. Exploring the potential mechanisms of antidiabetic drugs in the treatment of OP provides valuable clinical insights for the future pharmacological management of osteoporosis patients. - Source: PubMed
Publication date: 2026/04/21
Jing Yu-LongZhu Xiao-YangGong Shen-AoSun TaoLin Xiao-Yan - Advanced and treatment-refractory prostate cancer, including castration-resistant disease, require new therapeutic strategies. TRPM4, a calcium-activated monovalent cation channel, regulates cell volume and promotes cancer progression. Acetalax induces oncosis-like death in TRPM4-positive triple-negative breast cancers, suggesting a TRPM4-dependent vulnerability. Here, we investigated whether TRPM4 expression defines Acetalax sensitivity in prostate cancer. We compared Acetalax sensitivity in TRPM4-high and -low prostate cancer cell lines, including androgen-dependent (LNCaP), castration-resistant (22Rv1), and androgen-independent (PC3, DU145) models. We evaluated TRPM4 dynamics and oncosis-associated phenotypes by Western blotting and immunofluorescence. Resistant clones were developed through continuous drug exposure. TRPM4 expression in patient samples was analyzed using prostate cancer tissue microarray and The Cancer Genome Atlas (TCGA). Transcriptional changes following TRPM4 loss were examined by RNA sequencing (RNA-seq). Antitumor activity and tolerability were evaluated in TRPM4-positive patient-derived xenograft (PDX) models. TRPM4-high cells (PC3, LNCaP and 22Rv1) underwent oncosis-like swelling and TRPM4 degradation upon Acetalax exposure, whereas TRPM4-low cell and resistant clones (DU145 and chronic exposure cells) remained insensitive and lacked TRPM4 expression. RNA-seq revealed transcriptomic remodeling associated with TRPM4 loss. TRPM4 was significantly elevated in tumors versus normal tissues and was unchanged across stages or Gleason scores. In TRPM4-positive PDX models, Acetalax (300 mg/kg) significantly suppressed tumor growth without body-weight loss, indicating antitumor efficacy without overt toxicity. TRPM4 is a mechanistic driver and predictive biomarker of Acetalax response in prostate cancer, supporting TRPM4-dependent targeting and providing a rationale for the clinical development of Acetalax for TRPM4-expressing and treatment-refractory prostate cancer. - Source: PubMed
Publication date: 2026/04/22
Hoshi-Kadonosawa YukaReinhold William CTaniyama DaikiInoue YoshitakaLuna AugustinKumar SureshSun Nai-YunKim Yoo SunYin Juan JuanRoper NitinSowalsky Adam GFigg William DTakebe NaokoPommier Yves - Large-core anterior circulation ischemic stroke (LCIS) complicated by malignant cerebral edema (MCE) remains a leading cause of early death and profound disability even in the era of endovascular thrombectomy (EVT). As EVT indications have expanded to include patients with large ischemic cores, more patients survive the initial ischemic insult but continue to face substantial risk of space-occupying edema, underscoring the need for standardized neurocritical care pathways. This narrative review summarizes evidence published between 2015 and 2025 from PubMed and Web of Science, emphasizing randomized trials, meta-analyses, high-quality observational cohorts, and major guidelines. Contemporary neurocritical care guidance increasingly treats LCIS as a distinct syndrome and recommends structured surveillance, timely osmotherapy, and consideration of decompressive hemicraniectomy (DHC). Recent large-core EVT trials show that, in carefully selected patients, EVT can improve functional outcomes, but it does not eliminate mortality or severe disability and is associated with higher risks of hemorrhage, while edema-related deterioration remains common after reperfusion. For patients who develop space-occupying middle cerebral artery infarction, early DHC consistently lowers mortality and increases the proportion of survivors with moderate disability. Meanwhile, predictive models and emerging deep-learning approaches are enhancing early risk stratification for MCE, supporting earlier escalation of monitoring and intervention. Overall, LCIS with MCE should be approached as a dynamic, time-sensitive condition that benefits from early recognition and a pragmatic, sequenced pathway integrating risk prediction, medical management, and surgical decompression when indicated. Future work should refine multimodal prediction tools, clarify DHC thresholds in reperfused patients, and develop more effective anti-edema therapies. An American Heart Association science advisory (published online 17 December 2024) synthesized the randomized evidence supporting EVT in selected large-core strokes and highlighted key implementation considerations. - Source: PubMed
Publication date: 2026/04/15
Qu Hui-LingSun Xiao-YuXu Xi-MengZhang Xiao-Bin - We report the discovery of novel anthranilic anilide-based compound PBA (), an inhibitor of Ca-activated monovalent cation channel TRPM4. PBA exhibits increased potency, ligand efficiency, aqueous solubility, and lipophilic ligand efficiency, as well as lower cytotoxicity compared to reference inhibitor NBA. The phenyl ring of the 4-chloro-2-(2-phenoxyacetamido)benzoic acid scaffold was found to be essential for activity, and PBA resulted from a focused SAR study conducted on this ring. The -position proved to be favorable for substitutions, where lipophilic groups generally led to more potent inhibitors compared to polar substituents. X-ray structures and NMR studies of anthranilic anilides revealed bifurcated intramolecular hydrogen bonds stabilizing a "bent" conformation that might be important for their mode of action. The discovery of TRPM4 inhibitor PBA, together with other findings from our SAR study, will benefit future TRPM4 drug development efforts and research. - Source: PubMed
Publication date: 2026/04/13
Gerber Christian EAugustynek Bartlomiej SGrossenbacher PhilippHauert BarbaraSinger Simon APeinelt ChristineLochner Martin - Traumatic brain injury (TBI) is a significant concern, with millions sustaining a TBI each year. The vast majority are categorized as mild, in which diffuse pathologies are the hallmark and multiple cell types are affected, including astrocytes. Buprenorphine (bup), a semi-synthetic opioid, is a common human and veterinary analgesic. Previous studies from our group showed that a single dose of slow-release bup administered acutely following TBI alters astrocyte morphology at 1 day and 4 weeks post-injury in a region-specific manner. The current study expands on these findings by examining how four major astrocyte-associated proteins, GFAP, SWELL1/LRRC8A, TRPM4, and AQP4, are affected by such a dose of bup. Adult male rats received either sham or TBI via a central fluid percussion injury model, followed by saline or bup 15 min following injury. Protein quantification at 1 day and 4 weeks post-injury revealed region- and time-dependent effects of acute bup administration. Specifically, bup reduced hippocampal GFAP, increased cortical TRPM4, and elevated thalamic AQP4 and SWELL1 at 4 weeks following TBI. Taken together, these findings indicate that a single post-injury dose of bup can alter major astrocytic protein expression beyond the acute phase in a region- and time-dependent manner. - Source: PubMed
Publication date: 2026/03/30
Lilova Radina LBernas TytusRyu JaneKelliher CorrinaLafrenaye Audrey