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
- 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 - Overactive bladder (OAB) is a prevalent syndrome whose first-line pharmacotherapy with antimuscarinics and β-adrenoceptor agonists is limited by suboptimal efficacy and poor tolerability, underscoring the unmet need for novel molecular targets. As key regulators of detrusor smooth muscle excitability and bladder afferent signaling, ion channels have emerged as a compelling target class capable of modulating bladder function with high spatial precision. This review summarizes current evidence on the role of cation and anion channels in OAB pathophysiology and critically appraises their therapeutic potential, covering the principal channel families implicated in detrusor and afferent dysfunction, including voltage-gated Ca and Na channels, K channel subfamilies, HCN, TRP, and PIEZO channels, ligand-gated cation channels, ENaC/ASIC, and Cl channels, with preclinical and clinical evidence integrated throughout. Despite this strong mechanistic rationale, clinical translation has been hampered by ubiquitous channel expression, patient heterogeneity, and the absence of stratifying biomarkers. Although the supporting evidence remains uneven, spanning genetic, ex vivo, and early-phase clinical studies, future progress will likely depend on tissue-selective compounds, biomarker-defined subphenotypes, and emerging targets such as TMEM16A, TRPM4, and PIEZO channels, which represent particularly promising avenues for next-generation OAB pharmacotherapy. - Source: PubMed
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