Ask about this productRelated genes to: TMEM176A antibody
- Gene:
- TMEM176A NIH gene
- Name:
- transmembrane protein 176A
- Previous symbol:
- -
- Synonyms:
- HCA112, MS4B1
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-04
- Date modifiied:
- 2015-06-04
Related products to: TMEM176A antibody
Related articles to: TMEM176A antibody
- SERPING1, which encodes the C1 inhibitor (C1-INH) of the complement system, and plays a key regulator in regulating inflammatory responses and immune homeostasis. SERPING1 is downregulated in various disease, this downregulation occurs through the body's negative feedback resulting from the overactivation of the complement system in diseases such as infections and acute inflammatory responses. Additionally, SERPING1 is vital for tumor immunomodulation. Diffuse large B-cell lymphoma (DLBCL) is a common and aggressive type of non-Hodgkin lymphoma. More treatment options are becoming available for this disease. However, some patients still experience recurrence or even disease progression during treatment. Consequently, elucidating the molecular underpinnings of DLBCL's malignant behavior and identifying novel prognostic markers and therapeutic targets are paramount for improving patient outcomes. - Source: PubMed
Publication date: 2026/06/03
Wang JinhuiLi ZhihuiZhan XinrongZhang YanpingWang ZhongliangXing PengtaoLiu MengmengGuo MengyiXu KailiWang Haoyan - - Source: PubMed
Publication date: 2025/11/15
Zhang YatingWang QiHe DongqiangWei YucaiLiu YatingTang FutianLi Yumin - We aimed to identify key molecular drivers of gastric cancer progression and poor prognosis by integrating multi-omics analyses with experimental validation. Single-cell RNA-seq data were clustered to delineate major cell types. InferCNV identified tumor epithelial cells, and reclustering revealed a malignant subset with poor prognosis. The overlap between subset markers and The Cancer Genome Atlas Stomach Adenocarcinoma (TCGA-STAD) upregulated differentially expressed genes (DEGs) was modeled with univariate, LASSO-, and multivariate Cox to derive a prognostic signature. Patients were stratified according to signature scores, and group differences in survival and immunologic features were compared. Spatial transcriptomics defined the localization patterns of key signature genes. In vitro functional assays (CCK-8, colony formation, EdU incorporation, flow cytometry, Transwell migration and invasion, and wound healing) confirmed the pivotal role of SRI. Reclustering of tumor epithelial cells yielded seven subsets (C0-C6), with C5 displaying marked malignant features and correlating with poor prognosis in multiple cohorts. Intersecting 208 genes yielded a five-gene signature (ASCL2, REPIN1, CXCL3, TMEM176A, SRI). The signature stratified patients into high- and low-risk groups. The high-risk cohort exhibited significantly poorer survival, distinct immune-infiltration patterns, elevated immune-evasion scores, and a reduced predicted response to immunotherapy. Single-cell and spatial transcriptomics localized TMEM176A to fibroblasts and SRI to the tumor epithelium. Finally, in vitro knockdown of SRI inhibited tumor cell proliferation, migration and invasion. Our multi-omics approach identified a malignant epithelial subset, C5, and a five-gene signature that stratifies gastric cancer prognosis and immune response. Functional assays showed that SRI knockdown impairs tumor cell growth, migration and invasion. - Source: PubMed
Publication date: 2025/10/29
Gong ZhijieWang WeiweiHe YinghaoZhou JunYang QiangbangFeng AiwenHuang ZudongPan JianLi YingzeYuan XiaoluMa Minghui - Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, yet the molecular mechanisms underlying its progression are not fully understood. TMEM176A, a transmembrane protein implicated in immune regulation and tumor biology, has an undefined role in GC. This study aims to elucidate the functional significance and mechanistic involvement of TMEM176A in GC. - Source: PubMed
Publication date: 2025/11/08
Zhang YatingWang QiHe DongqiangWei YucaiLiu YatingTang FutianLi Yumin - Perturbed secretion of insulin and other pancreatic islet hormones is the main cause of type 2 diabetes (T2D). The islets harbor five cell types that are potentially altered differently by T2D. Whole-islet transcriptomics and single-cell RNA-sequencing (scRNAseq) studies have revealed differentially expressed genes without reaching consensus. Here, we demonstrate that further insights into T2D disease mechanisms can be obtained by network-based analysis of scRNAseq data from individual cell types. We developed differential gene coordination network analysis (dGCNA) and analyzed islet SmartSeq2 scRNAseq data from 16 T2D and 16 non-T2D individuals. dGCNA reveals T2D-induced cell type-specific networks of dysregulated genes with remarkable ontological specificity, thus allowing for a comprehensive and unbiased functional classification of genes involved in T2D. In beta cells eleven networks of genes are detected, revealing that mitochondrial electron transport chain, glycolysis, cytoskeleton organization, cell proliferation, unfolded protein response and three networks of beta cell transcription factors are perturbed, whereas exocytosis, lysosomal regulation and insulin translation programs are instead enhanced in T2D. Furthermore, we validated the ability of dGCNA to reveal disease mechanisms and predict the functional context of genes by showing that TMEM176A/B regulates beta cell microfilament organization and that CEPBG is an important regulator of the unfolded protein response. In addition, when comparing beta- and alpha cells, we found substantial differences, reproduced across independent datasets, confirming cell type-specific alterations in T2D. We conclude that analysis of networks of differentially coordinated genes provides detailed insight into cell type-specific gene function and T2D pathophysiology. - Source: PubMed
Publication date: 2025/10/27
Martínez-López J ALindqvist ALopez-Pascual AHarder AChen PNgara MShcherbina LSiffo SCowan EBaira S MKryvokhyzha DKaragiannopoulos AChriett SSkene N GPrasad R BLancien MJohnson P FEliasson PEliasson LLouvet CSpégel PMuñoz-Manchado A BSandberg RHjerling-Leffler JWierup N