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
- Sodium overload-induced necrotic cell death has been proposed as a stress-related cellular process potentially involved in tumor progression, but its relevance in pancreatic cancer remains poorly understood. TRPM4, a sodium-permeable ion channel, has been implicated in cellular stress responses; however, the prognostic significance of TRPM4 and its associated transcriptional features in pancreatic cancer has not been comprehensively evaluated. This study integrated multi-cohort transcriptomic datasets to construct a prognostic risk score model based on TRPM4-associated genes. - Source: PubMed
Publication date: 2026/03/24
Li QingchunZhou YongWu AndingLiang Yun - The effects of alpha-tocopherol on seizure parameters, locomotor-cognitive functions, inflammatory response, oxidative stress response, histopathological changes, immunohistochemical parameters, and miRNA fold changes were investigated in rats with traumatic brain injury (TBI) and pentylenetetrazol (PTZ)-induced seizures. Sprague-Dawley male rats were randomly divided into three groups: Control (n = 8), TBI + PTZ (n = 10), and TBI + PTZ + tocopherol (n = 10). After inducing TBI in animals using the weight-drop method, increased post-injury seizure susceptibility was achieved by administering subconvulsive doses of PTZ. Saline was administered intraperitoneally to the control and TBI + PTZ groups for 6 days, while 500 mg/kg alpha-tocopherol was administered intraperitoneally to the TBI + PTZ + tocopherol group. Seizure intensity, seizure frequency, and total seizure duration were significantly reduced in the TBI + PTZ + tocopherol group compared to the TBI + PTZ group (p < 0.05). No significant adverse effects related to TBI and PTZ were observed in the animals' locomotor activity, anxiety-like behaviors, or learning and memory test outcomes. In the TBI + PTZ + tocopherol group, significant reductions were observed in inflammatory cytokine response, oxidative stress, and SUR1-TRPM4 channel activity compared to the TBI + PTZ group (p < 0.001). While degenerative and apoptotic neurons and the number of 8-OHdG-positive cells in the CA1 and dentate gyrus regions were limited in the TBI + PTZ + tocopherol group, downregulated miR-324-5p increased (p < 0.05). Alpha-tocopherol reduced the severity and duration of seizures, reduced oxidative stress and inflammation, and stabilized the thiol-disulfide balance. It also reduced degenerative cell structures and DNA damage in the cortex, hippocampus, and dentate gyrus. In conclusion, the findings of this study suggest that alpha-tocopherol is a potential neuroprotective agent that modulates early epileptogenic network instability in TBI and seizure susceptibility through multiple pathways, including oxidative stress, inflammation, and ion channel regulation. - Source: PubMed
Publication date: 2026/05/19
Demirtas CumaaliYildirim HavaDemir HuseyinKiroglu SezinSevgin KubraBeyaztas HakanGuler Eray MetinHekimoglu GulamAykin UgurCoskunpinar Ender MehmetYildirim Mehmet - Atherosclerosis is a chronic inflammatory condition of the arterial wall in which endothelial dysfunction serves as a key driver of disease progression. Endothelial inflammation and pyroptosis are major contributors in this context; therefore, targeting these processes may confer therapeutic benefits. Transient receptor potential cation channel subfamily M member 4 (TRPM4) is a voltage-sensitive, non-selective cation channel belonging to the transient receptor potential family. Although TRPM4 contributes to the regulation of vascular endothelium, its precise role in endothelial inflammation remains poorly understood. Accordingly, this study aims to elucidate the function and molecular mechanisms of TRPM4 in vascular endothelial inflammation and pyroptosis. - Source: PubMed
Publication date: 2026/04/24
Shen MeimeiZhao YuZhang YuyaoTong TingtingCui YunfengGuo XinLiang WenMa ZiyueJin JingXiong LisiTang KeGao KaiyangZhang JunhaoLv HongzhaoHuo RongBan Tao - Osteoarthritis (OA) is a chronic, disabling condition whose pathogenesis remains unclear. TRPM4 is closely associated with OA, but its specific roles and regulatory networks within different cell subsets remain to be elucidated. This study integrates single-cell and transcriptomic sequencing data to systematically analyse the cell-specific expression patterns, key downstream molecules, and regulatory networks of TRPM4, with the aim of identifying new therapeutic targets for OA. OA-related datasets were obtained from public databases. Key cells were identified at the single-cell level, and analyses including enriched pathways and cell communication were conducted. Candidate genes were screened by cross-referencing differentially expressed genes (DEGs), key module genes from high-dimensional weighted gene co-expression network analysis (hdWGCNA) analysis related to key cells, and TRPM4-related DEGs. We then employed machine learning algorithms and expression levels to screen key genes. Subsequently, analyses such as functional enrichment, immune infiltration analysis, construction of molecular regulatory networks, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were executed. Human Leukocyte Antigen-DR Alpha Chain (HLA-DRA) cells were the key cells, and the enriched pathways they participated in mainly included "FMO oxidizes nucleophiles", and frequent cell-cell interactions were observed between HLA-DRA cells and synovial subintimal fibroblasts (SSF) in OA. Later, 2 key genes (FOSL2 and S100A11) were obtained. S100A11 was up-regulated, while FOSL2 was down-regulated in the OA group, and RT-qPCR showed consistent results (p < 0.05). In addition, FOSL2 and S100A11 shared 14 enriched pathways, such as the p53 pathway and oxidative phosphorylation, and there were infiltration differences of 8 types of immune cells between OA and control samples (p < 0.05). The miRNA-mRNA network (e.g., has-miR-6134-S100A11) was constructed. This study suggested that TRPM4-associated HLA-DRA antigen-presenting cells may be associated with osteoarthritis, and, based on transcriptomic correlation analysis and limited qPCR validation, identified S100A11 and FOSL2 as candidate biomarkers associated with TRPM4. These findings provided preliminary, hypothesis-generating clues regarding the cellular heterogeneity and immunometabolic pathways in which TRPM4 may be involved in osteoarthritis; however, its specific role remained to be validated by subsequent functional experiments. - Source: PubMed
Publication date: 2026/05/09
Chen YunxiuGuo DaxinZhu JiawangWang Zhiqiang - Neonatal bacterial sepsis (NBS) remains a major global burden. Although immune dysfunction is central to its pathogenesis, the causal contribution of specific immune cell phenotypes and their upstream genetic regulation is unclear. This study aimed to test whether genetically predicted gene expression influences NBS risk through immune cell traits using an integrative two-step Mendelian randomization (MR) mediation framework. We combined eQTLGen whole-blood expression quantitative trait loci (n ≈ 30,000), genome-wide association study of 731 immune traits (Sardinian cohort, n ≈ 3757), and FinnGen R12 NBS summary statistics (P16_BACTERIAL_SEPSIS_NEWBO; 203 cases, 499,933 controls). Instruments met genome-wide significance, stringent linkage disequilibrium clumping, and F-statistic >10. Primary analyses used inverse-variance weighted MR, with MR-Egger and weighted median as sensitivity analyses. Mediation was estimated as the product of effects. Colocalization (coloc; summary-data-based Mendelian randomization-heterogeneity in dependent instruments) was used to evaluate shared causal variants. Heterogeneity (Cochran Q), MR-Egger intercepts, leave-one-out, and reverse MR were performed. We identified 147 gene expressions and 23 immune traits associated with NBS after false discovery rate correction. Two-step MR yielded multiple gene-immune-NBS mediation chains, with CD28-related T-cell phenotypes consistently prominent. The TRPM4 → CD28 on double-negative T cells → NBS pathway showed the largest mediation proportion (~40.54%) and remained directionally consistent across sensitivity tests. Several colocalized signals (e.g., DBF4B, SNCA, SYCE1L) supported shared variants with immune traits; however, not all corresponding mediation paths passed heterogeneity/sensitivity checks, and are therefore interpreted as suggestive rather than definitive. Associations involving CD64 on monocyte subsets were not robust across sensitivity analyses and were not retained as primary findings. Reverse MR did not indicate feedback from NBS liability to the immune traits prioritized in forward analyses. Genetically informed immune phenotypes (particularly CD28-related T-cell features and the broader CD8bright/regulatory T cell axis) appear to partly mediate the effect of gene expression on NBS susceptibility. Colocalized mediation signals provide supportive, hypothesis-generating evidence but require cautious interpretation given sensitivity/heterogeneity findings. These results motivate neonatal-specific validation and functional studies to refine mechanistic targets for risk stratification. - Source: PubMed
Liang JingWei RongYi WeiChen JunchangLi DongxiaoXiao LinLai QiuruFang QiutingLü JibaoWei YingcaiYuan JiaquanGan Junhong