Ask about this productRelated genes to: TMOD2 antibody
- Gene:
- TMOD2 NIH gene
- Name:
- tropomodulin 2
- Previous symbol:
- -
- Synonyms:
- NTMOD
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-16
- Date modifiied:
- 2015-11-16
Related products to: TMOD2 antibody
Related articles to: TMOD2 antibody
- Alzheimer's disease (AD) is a neurodegenerative disorder marked by cognitive decline, memory impairment, and functional deterioration. Its complex pathogenesis involves factors such as amyloid plaques, tau tangles, neuroinflammation, and synaptic dysfunction, but the precise mechanisms remain unclear, hindering effective treatment. Genetic, environmental, and lifestyle factors contribute to AD risk, yet their interactions are poorly understood. Recent advances in transcriptomics and metabolomics have shed light on the molecular underpinnings of AD, with gene expression alterations and metabolic disruptions implicated in disease progression. These multi-omics disruptions highlight the need for integrative analytical approaches to better characterize AD-relevant biology and advance biomarker discovery. - Source: PubMed
Publication date: 2026/03/03
Choi Jerome JEngelman Corinne DLu Tianyuan - Colorectal adenomas (CRA) represent critical precursors to colorectal cancer (CRC), yet reliable transcriptomic biomarkers for early detection and therapeutic targeting remain limited. Integration of gut microbiota (GM) genetics with transcriptomics offers a novel approach to identify disease-associated molecular signatures. We sought to identify GM-associated molecular signatures that could serve as early intervention targets. We integrated transcriptomic data with Mendelian randomization (MR) analysis to establish causal relationships between GM and CRA development. Machine learning algorithms identified robust biomarkers, which we validated through expression analysis and receiver operating characteristic (ROC) analysis to construct predictive nomogram models. Comprehensive molecular characterization included Gene Set Enrichment Analysis (GSEA), immune profiling, and regulatory network analysis. Single-cell RNA sequencing (scRNA-seq) analysis further validated biomarker expression patterns across distinct cell populations in the tumor microenvironment. We discovered 12 GM species with significant causal relationships to CRA risk. Two biomarkers, TMOD2 and DOCK4, emerged as powerful predictive indicators with strong correlation ( = 0.66, < 0.001). These biomarkers demonstrated excellent diagnostic performance in ROC analysis and revealed previously unrecognized connections to cell adhesion pathways critical for adenoma progression. Single-cell analysis revealed TMOD2 expression across multiple cell clusters with notable exclusion in mast cells, while DOCK4 expression was predominantly restricted to fibroblasts, myeloid, and epithelial cells. Notably, we identified distinct immune cell infiltration patterns, including altered naive B cells and macrophage populations, suggesting immune dysregulation as a key mechanism. GSEA revealed enrichment in cell adhesion molecule (CAM) pathways. Regulatory network analysis uncovered complex control by 18 microRNAs (miRNAs), 40 long noncoding RNAs (lncRNAs), and 10 transcription factors (TFs), with EIF3A emerging as a key m6A reader protein. Drug screening identified 22 potential therapeutic compounds, with trichostatin A showing optimal binding affinity. These findings establish TMOD2 and DOCK4 as novel biomarkers linking GM dysbiosis to CRA development, opening new avenues for microbiome-targeted early intervention strategies. - Source: PubMed
Publication date: 2025/12/02
Liu ChuangWang LiHuai JianguoHe SongSu QiangMin QiumingAn Zhenxiang - Tropomodulin-2 (TMOD2) is upregulated in the nuclear compartment of highly liver metastatic colorectal cancer (CRC) cells. Its role in cancer and CRC progression is functionally undefined, despite its analysis in COAD and READ TCGA datasets revealing a correlation between high TMOD2 expression, advanced disease stages, and poorer survival in CRC patients. We aimed here to explore the role of TMOD2 in CRC and liver metastasis using functional proteomics, tumour samples, bioinformatics, and in vitro and in vivo CRC models. Stable overexpression and stable depletion of TMOD2 in isogenic CRC cells revealed its impact on tumorigenic and metastatic properties. TMOD2 overexpression enhanced cell adhesion, anchorage-independent growth, and migration, while stably TMOD2 depletion reduced them. In vivo, TMOD2-overexpressing cells formed larger tumours and enhanced liver colonisation of CRC cells. Clinically, TMOD2 protein levels demonstrated strong discriminatory ability between metastatic and non-metastatic CRC patients. Proteomic analyses allowed the identification of TMOD2-associated proteins involved in cytoskeletal dynamics, secretion, and focal adhesions, with further validation implicating STAG1 and MARCKS as mediators of TMOD2-driven pathways. Our findings demonstrate that TMOD2 plays a role in CRC progression by modulating cytoskeletal dynamics, enhancing cell adhesion and promoting liver metastasis, positioning TMOD2 as a target for therapeutic intervention in CRC. - Source: PubMed
Publication date: 2025/09/17
Montero-Calle AnaJiménez de Ocaña SofíaRejas-González RaquelBenavente-Naranjo RuthSanz-López RodrigoDziaková JanaMartínez-Useros JavierPeláez-García Albertode Los Ríos VivianBartolomé Rubén ACasal J IgnacioFernández-Aceñero María JesúsBarderas Rodrigo - Prostate cancer (PCa) is a major cause of cancer-related mortality in men worldwide. PCa mortality is expected to almost double by 2040 which is probably associated with the increase in obesity rates, a global health problem linked to an increased risk of developing multiple cancer types. Therefore, the identification of improved, personalized, therapeutic and diagnostic/prognostic tools is urgently needed. MicroRNAs have emerged as promising diagnostic/therapeutic tools for various metabolic/tumoral pathologies but the clinical utility and pathophysiological role of different miRNAs in the interplay between obesity-PCa have been poorly studied. Herein, miR-191-5p levels (plasma and tissue) were analyzed in control and PCa patients by quantitative-PCR and microarrays using one internal (n = 202) and two external (n = 1600) cohorts, and its diagnostic/prognostic/therapeutic potential and functional role was assessed through bioinformatic and clinical association analyses, and in vitro assays (e.g. proliferation/migration/colony-formation, phenotype-rescue). Plasma miR-191-5p was significantly altered in independent PCa cohorts (p < 0.0001), showing a better ability than Prostate Specific Antigen (PSA) to discriminate between patients with and without PCa, especially in the 'grey zone' of PSA (3-10 ng/mL; wherein sensitivity/specificity for diagnosing PCa is significantly compromised). Remarkably, the diagnostic capacity of miR-191-5p drastically increased when obese PCa patients were considered, allowing a strong discriminatory capacity between obese patients with PCa or significant-PCa vs. control-patients and, most importantly, between obese patients with significant-PCa vs. nonsignificant-PCa, thus representing a potential personalized diagnostic/prognostic biomarker in obesity-PCa interplay. Additionally, miR-191-5p act as a tumour-suppressor in PCa cells by regulating critical PCa hallmarks (including proliferation/migration/colony-formation and key oncogenic molecular markers expression) through the posttranscriptional downregulation of TMOD2 (member of the tropomodulin-family). Altogether, our results provide new, compelling evidence supporting the contention that miR-191-5p represents a promising diagnostic/prognostic biomarker and a novel therapeutic tool, especially in the pathological association between PCa and obesity. - Source: PubMed
Publication date: 2025/07/05
Porcel-Pastrana FranciscoMontero-Hidalgo Antonio JHerrero-Aguayo VicenteSáez-Martínez PrudencioPerez-Gómez Jesús MSarmento-Cabral AndréCampos-Hernández Juan PRangel-Zuñiga Oriol ACarrasco-Valiente JuliaMartínez-Fuentes Antonio JGahete Manuel DGómez-Gómez EnriqueLuque Raúl M - Actin dynamics are crucial for the morphogenesis and function of neurons in the brain. Tropomodulins (Tmods) belong to a family of actin-binding proteins that cap the pointed-end of actin filaments. There are four Tmod isoforms, and three of which, Tmod1, Tmod2 and Tmod3, are expressed in the brain, with Tmod2 exhibiting neuronal specific expression. By regulating actin filament dynamics, Tmods participate in neurite outgrowth, dendritic spine formation, and synaptic morphology, thereby contributing to structural and functional neural plasticity. Dysregulation of Tmods has been demonstrated in several neurodegenerative and neuropsychiatric diseases, such as Alzheimer's disease, epilepsy, Down syndrome, and addictive behaviors. Currently, compared to cancer and cardiovascular diseases, the roles and mechanisms of altered Tmod expression in neurological diseases remain poorly understood. In this article, we provided an overview on the physiological roles and crucial functions of Tmods in the brain, summarized the recent advances in alterations of Tmods in neurodegenerative and neuropsychiatric diseases, and discussed their implications and potential contributions to disease pathology and treatment. This review may expedite future studies to delineate the roles and molecular mechanisms of Tmods in brain physiology and pathology, ultimately promoting the development of novel diagnostic and therapeutic strategies for related neurological diseases. - Source: PubMed
Publication date: 2025/06/13
Hong ChuanLiu XiaopengZhou ZhouXing YuanCao ZixuanChang Yan-ZhongGao Guofen