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
- Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide, and effective biomarkers for prognosis and therapeutic guidance are still lacking. TRPM4, a sodium-related ion channel, has been implicated in tumor progression; however, its role in LUAD, particularly at the single-cell level, remains unclear. Single-cell RNA sequencing data were used to analyze the cellular distribution of TRPM4 in LUAD. TRPM4-related genes were identified through correlation analysis in the TCGA cohort, followed by construction of a prognostic model using Cox and LASSO regression analyses. The model was validated in an independent GEO dataset. Functional enrichment and drug sensitivity analyses were performed to explore the underlying mechanisms and therapeutic implications. Random forest analysis was applied to identify key genes, and in vitro experiments were conducted to validate their biological functions. A TRPM4-related prognostic signature was established, demonstrating robust predictive performance in both training and validation cohorts. High-risk patients were characterized by activation of cell cycle and DNA replication pathways, showing differences in computationally predicted sensitivity to multiple chemotherapeutic and targeted agents. Furthermore, RNPEPL1 was identified as a key gene and experimentally validated to promote LUAD cell proliferation, migration, and invasion. The TRPM4-related signature and RNPEPL1 may provide novel insights for risk stratification and personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/08/16
Xia WenjiaLi MingXu YoutaoFeng DongjieOuyang WenhaoXu Lin - Prostate cancer (PCa) remains a prevalent male malignancy, imposing significant health burdens and socio-economic challenges globally. While early diagnosis is critical for effective intervention, current clinical strategies lack precision in risk stratification and treatment response prediction. This study aimed to identify key machine learning-derived biomarkers for PCa and to comprehensively evaluate the diagnostic, prognostic, and immune-related significance of . - Source: PubMed
Publication date: 2026/06/27
Zhu WanliWang JunyingZhou YizhiSong SainanLi ChunpingXue QingjieZhang Hui - A new type of regulated cell death known as Necrosis by Sodium Overload (NECSO) has been discovered recently. There is growing evidence indicating that NECSO is essential in both anti-tumor immune responses and the proliferation of cancer cells. Nonetheless, the underlying mechanisms and clinical relevance of NECSO are still not well understood, especially regarding its prognostic significance in kidney renal clear cell carcinoma (KIRC). - Source: PubMed
Publication date: 2026/07/28
Pan YitongWu RuiZhu XueyiHu XiaodiCheng JunKong Lingwen - Ovarian cancer is the most lethal malignancy of the female reproductive system worldwide. Chemoresistance, particularly platinum resistance, is a major factor limiting improvement in prognosis, and its underlying mechanisms involve complex regulation of and escape from multiple programmed cell death pathways in cancer cells. Disulfidptosis is triggered by high expression of solute carrier family 7 member 11 (SLC7A11) under glucose starvation and shares upstream regulatory nodes with ferroptosis. Necrosis by sodium overload is driven by sodium ion overload mediated by transient receptor potential cation channel subfamily M member 4 (TRPM4), but its role remains to be further investigated. Other programmed cell death pathways are interwoven into a dynamic regulatory network through key regulatory molecules such as tumor protein p53, the caspase family, cysteine-aspartic proteases, and glutathione. Autophagy can inhibit pyroptosis; ferroptosis and pyroptosis can synergistically amplify cell-killing effects through the reactive oxygen species/NOD-like receptor thermal protein domain-associated protein 3 axis; ferroptosis and cuproptosis share the glutathione metabolic axis; and the interaction between ferroptosis and disulfidptosis can shift from antagonism to synergy under specific metabolic stress. Ferroptosis and necrosis by sodium overload mutually promote each other through cascades involving adenosine triphosphate depletion, reactive oxygen species accumulation, and mitochondrial damage. PANoptosis can overcome cancer-cell resistance to a single mode of cell death through the simultaneous activation of multiple cell death pathways. A comprehensive review of the roles and interactive networks of various programmed cell death modalities, including disulfidptosis, necrosis by sodium overload, apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis, cuproptosis, and PANoptosis, in platinum resistance in ovarian cancer is expected to provide a solid theoretical basis and potential translational directions for reversing platinum resistance and optimizing clinical treatment strategies. - Source: PubMed
Xu JuanZhou XuanLuo Chenhui - - Source: PubMed
Publication date: 2026/07/14
Yan TengZhang ZeqiaoZhao SisiYang ChaoWang HuijunLin Zhimiao