Ask about this productRelated genes to: TMEM109 Blocking Peptide
- Gene:
- TMEM109 NIH gene
- Name:
- transmembrane protein 109
- Previous symbol:
- -
- Synonyms:
- MGC5508
- Chromosome:
- 11q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-22
- Date modifiied:
- 2014-11-19
Related products to: TMEM109 Blocking Peptide
Related articles to: TMEM109 Blocking Peptide
- - Source: PubMed
Long Zheng X - Thrombotic thrombocytopenic purpura (TTP) is a rare but life-threatening thrombotic microangiopathy, with a substantial risk of relapse despite advances in therapy. Robust biomarkers to predict relapse are urgently needed to inform risk-adapted management. This study represents the first application of bone marrow proteomic profiling in TTP to explore relapse-associated biomarkers. - Source: PubMed
Publication date: 2026/01/29
Wen QingChen JiaSun TingWang XiyanJu MankaiLiu XiaofanLi HuiyuanFu RongfengLiu WeiXue FengDong HuanDai XinyueWang WentianChi YingYang RenchiChen YunfeiZhang Lei - Mitsugumin 23 (MG23) is a transmembrane protein expressed in the nuclear membrane and endo/sarcoplasmic reticulum (ER/SR) of various tissues, including skeletal and cardiac muscle. MG23 is a non-selective cation channel that has been implicated in the leakage of calcium ions (Ca) under diverse pathophysiological conditions. SR Ca leak is considered to be a contributing factor of skeletal muscle weakness and is also implicated in the progression of heart failure. The absence of MG23 has been reported to alleviate negative outcomes associated with SR Ca leak. Targeting MG23 could represent a new therapeutic strategy against muscle disorders. This review discusses the potential role of MG23 in skeletal and cardiac muscle, and highlights MG23 as both a regulator of basal SR Ca-handling and a mediator of pathophysiological remodelling in muscle. - Source: PubMed
Publication date: 2025/12/10
Watanabe DaikiEdel Richard CNishi MiyukiTakeshima HiroshiPitt Samantha J - Ferroptosis is an iron‑dependent type of regulated cell death which is dysregulated in several tumors, including glioblastoma (GBM). Zinc finger and BTB domain‑containing protein 20 (), a transcription repressor, is expressed at low levels in GBM and suppresses GBM cell proliferation through the ERK signaling pathway. However, the effect of on ferroptosis has not been explored. The present study aimed to explore the role of ZBTB20 in ferroptosis of glioma cells and its underlying mechanism. The present study demonstrated that both expression and ferroptosis levels in GBM cells were lower than that in normal glial cells. Gain‑ and loss‑of‑function experiments revealed that overexpression promoted ferroptosis and knockdown inhibited ferroptosis in GBM cells. Moreover, the results demonstrated that transcriptionally repressed the expression of transmembrane protein 109 () in GBM cells, assessed using dual‑luciferase reporter and chromatin immunoprecipitation assays. TMEM109 is mainly localized on the endoplasmic reticulum (ER) membrane of cells and regulates calcium leakage at the ER or sarcoplasmic reticulum. The present study revealed that overexpression inhibited ferroptosis and knockdown promoted ferroptosis in GBM cells. Using co‑transfection experiments, it was further revealed that the promotive effect of can reverse the inhibitory effect of TMEM109 on ferroptosis. In conclusion, the findings indicated that promotes ferroptosis in GBM cells through transcriptionally repressing the expression of . - Source: PubMed
Publication date: 2025/09/26
Chen XuhaoLuo MingqiNiu XiaoyuWang WangCao HuanhuanZhang LiweiWei RuolunDuan Ping - Acute myeloid leukemia (AML) exhibits significant heterogeneity in disease progression and therapeutic response, highlighting the urgent need for novel biomarkers to improve risk stratification and therapeutic targeting. In this study, we integrated multi-omics data from The Cancer Genome Atlas (TCGA, n = 151) and Genotype-Tissue Expression (GTEx, n = 337) cohorts to systematically analyze dynamic expression patterns of exosome-related genes in AML. Using univariate Cox regression and least absolute shrinkage and selection operator (LASSO) algorithms, we identified 13 exosome-associated genes (EXOSC4, TMEM109, THBS1, MYH9, HLA-DRA, CAPZB, ITGA4, MYL6, CYB5R1, PSMA2, MPO, NDST2, and CANX) and constructed a prognostic risk model. The model demonstrated superior predictive accuracy compared to traditional clinical parameters, with area under the curve (AUC) values of 0.819, 0.825, and 0.832 for 1-, 2-, and 3-year survival predictions in the training set, and 0.909 in the independent GEO validation cohort (GSE71014). Kaplan-Meier analysis revealed significantly shorter overall survival in the high-risk group (log-rank P < 0.001, hazard ratio = 0.22, 95% CI = 0.13-0.36). Immune microenvironment characterization using CIBERSORTx identified increased infiltration of regulatory T cells (Tregs, P < 0.01) in high-risk patients. Functional enrichment analysis revealed enrichment of PI3K-Akt signaling pathways and TP53 transcriptional networks in high-risk groups. Molecular docking studies confirmed strong binding affinity of verteporfin (ITGA4 inhibitor, docking score=-16.0 kcal/mol) and ebselen (MPO inhibitor) to their respective targets, suggesting potential therapeutic strategies to overcome chemotherapy resistance. This study establishes a robust 13-gene exosome-based prognostic signature for AML risk stratification and identifies novel immunomodulatory mechanisms mediated by exosome-driven Treg polarization. - Source: PubMed
Publication date: 2025/09/01
Wang Min-XiaoLiao Chang-ShengXie Yu-QinWei Xue-QinHan Peng-FeiYu Yan-Hui