TMOD3, 1-352aa, Recombinant Protein
- Known as:
- TMOD3, 1-352aa, Recombinant Protein
- Catalog number:
- GWB-P0391A
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- TMOD3 1-352aa Recombinant Protein
Related genes to: TMOD3, 1-352aa, Recombinant Protein
- Gene:
- TMOD3 NIH gene
- Name:
- tropomodulin 3
- Previous symbol:
- -
- Synonyms:
- UTMOD
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-16
- Date modifiied:
- 2015-11-16
Related products to: TMOD3, 1-352aa, Recombinant Protein
Related articles to: TMOD3, 1-352aa, Recombinant Protein
- Pancreatic cancer is a highly aggressive malignancy with a 5-year relative survival rate of only 13%. Current treatment options have limited efficacy, and mRNA vaccines offer a new direction for its treatment. However, how to accurately identify antigen targets that possess tumor specificity, functional relevance, and immunogenicity remains the key bottleneck restricting the clinical translation of mRNA vaccines for pancreatic cancer. Recent clinical studies have advanced KRAS mutant vaccines and personalized neoantigen mRNA vaccines, yet most rely on single antigens or highly individualized designs, limiting scalability and broader clinical applicability. In this systematic review, we integrated evidence from public databases and experimental studies to identify and evaluate 16 potential pancreatic cancer mRNA vaccine antigens (ADAM9, WNT7A, TMOD3, MET, EFNB2, TPX2, AGPS, OSBPL9, KDM5A, NRAS, SCP-1, GAGE, RAB5A, ANO6, CHMP2B, and PAK2). All candidates were initially selected based on aberrant tumor expression and further prioritized using stratification strategies incorporating antigen-presenting cell infiltration, immune-related cell death pathways such as ferroptosis and pyroptosis, and functional relevance to tumor progression. ADAM9 and PAK2 showed high expression in pancreatic cancer and strong associations with tumor proliferation, invasion, and immune regulation. SCP-1 and GAGE, as cancer-testis antigens, exhibited high tumor specificity and immunogenic potential. In addition, KDM5A and ANO6 may enhance antitumor efficacy through modulation of ferroptosis or pyroptosis. Nevertheless, several candidates remain constrained by normal tissue expression or limited mechanistic evidence. This review provides a stratified framework for antigen prioritization and highlights key challenges in pancreatic cancer mRNA vaccine development, offering guidance for future multi-antigen vaccine design and translational immunotherapy. - Source: PubMed
Publication date: 2026/04/28
Xue YuzheYu JiaqiZhou HongkunChen WeiChen QiHu LingyuLuo RunzhouChen YingjingWang XiaoguangHe Xuesong - 1. Wooden breast (WB) is a common muscle abnormality in the (PM) muscle of broilers that results in significant economic losses for the poultry industry, although its incidence varies in different broiler lines. However, there are few reports on the genes and pathways involved in WB using RNA-seq or microarray data across multiple lines.2. The current study obtained three datasets (GSE127806, GSE144000 and GSE79276) from different broiler lines in the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was then performed using GSE127806 and GSE144000 datasets and identified consensus modules significantly correlated with WB ( ≤ 0.05). Preservation analysis showed that one consensus module was strongly preserved ( < 2), and two others were moderately preserved (2 < < 10) in the GSE79276 dataset.3. Functional enrichment analysis revealed seven key genes (, , , , , and ) related to WB were significantly enriched in the extracellular matrix (ECM)-receptor interaction pathway and in the apoptosis pathway in one consensus module. The genes , and were significantly enriched in the tricarboxylic acid cycle (TCA) cycle pathway. From the protein-protein interaction analysis, hub genes linked to WB were identified. Seven of these genes are known to participate in muscle contraction (, , , , , and ) and three others in the TCA cycle (, and ).4. This study identified key genes and pathways associated with WB, deepening the understanding of the mechanism by which fibrosis (mediated by genes such as ) influences WB. It further revealed the important role of the TCA cycle and apoptosis in the pathogenesis of WB. - Source: PubMed
Publication date: 2026/01/07
Yuan HXu KXu QLiu SWang S - Apolipoprotein E (APOE) epsilon4 (ε4) is a major genetic risk factor for late-onset Alzheimer's disease (AD), with women exhibiting heightened vulnerability to APOE ε4-associated cognitive impairment. Despite recognition of this sexual dimorphism, the underlying biological mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2025/12/02
Huang ShuaiWu JiaweiHe Ling - The widespread clinical application of paclitaxel (PTX) in cancer treatment has been significantly limited by the emergence of drug resistance and the presence of drug-tolerant persister cells. To systematically identify key regulators of this resistance, we conducted a genome-wide CRISPR/Cas9 knockout screen, which revealed that cell division cycle 6 (CDC6) is a critical determinant of cell adhesion-mediated PTX resistance. Furthermore, our results illustrate that CDC6, an essential DNA replication licensing factor, functions through a pathway distinct from previously well-characterized resistance mechanisms. Genetic depletion of CDC6 considerably sensitizes cells, markedly increasing PTX-induced cell death. In addition to its established role in chromosome stability, CDC6 physically interacts with tropomodulin-3 (Tmod3) in the cytoplasmic compartment. This interaction enhances CDC6 protein stability and drives drug resistance phenotypes through the regulation of actin cytoskeleton remodeling and facilitating focal adhesion assembly. In addition, combination treatment with PTX and actin filament inhibitors synergistically enhanced the antitumor efficacy both in vitro and in vivo. Overall, our studies elucidate the mechanisms through which CDC6 functions as a key regulator of PTX resistance and provide a potential therapeutic strategy to increase PTX efficacy through the modulation of the cytoskeletal-adhesion axis. - Source: PubMed
Publication date: 2025/12/04
Liu YueWang HuiruiZhan JieSun JiaboSun YanFu XiaojieLv DongxueLi XiuyunDong TingLou Hongxiang - Duck enteritis virus (DEV) is responsible for duck viral enteritis, a contagious and lethal disease in waterfowls. The host proteins targeted by DEV are unknown. In this study, we developed a recombinant DEV rVP26-Flag and identified 17 host proteins that interact with VP26 in infected chicken embryo fibroblast cells using co-immunoprecipitation in conjunction with liquid chromatography-tandem mass spectrometry (Co-IP-MS/MS). The 17 potential targets of VP26 proteins include Xirp1, TMOD3, DCN, ATP5PD, AP3M1, MYO5A, MYH10, MYH9 (non-muscle myosin IIA heavy chain), and GSN. Most of these proteins are microfilament or cytoskeletal proteins with functions such as cytoskeletal protein binding, actin filament interaction, microfilament motor activity, and myosin II interaction. Using the Search Tool for the Retrieval of Interacting Genes analysis, we predicted a functional network of microfilament cytoskeletal proteins interacting with VP26. Interaction between DEV VP26 and the carboxyl-terminus domain of MYH9 (1651-1960 aa) was verified via co-localization and Co-IP assays. We also demonstrated that the inhibition of actin polymerization with cytochalasin D and latrunculin A reduced the DEV titer. Furthermore, siRNA-mediated knockdown of MYH9, which has intrinsic ATPase activity, also resulted in a reduced viral titer. A targeted inhibitor of myosin II ATPase, (-)-Blebbistatin, significantly suppressed DEV infection both in vitro and in vivo. These results suggest that the actin-myosin II network plays a crucial role in DEV proliferation, with MYH9 being an important host factor influencing DEV infection. - Source: PubMed
Publication date: 2025/09/18
Chen LiuZhu Yin-ChuYun TaoYe Wei-ChengNi ZhengHua Jiong-GangZhang Cun