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
- Familial hypercholesterolemia (FH) is a common hereditary dyslipidemia characterized by high levels of low-density lipoprotein (LDL) cholesterol and a risk of premature atherosclerosis. Previous studies showed that cardiovascular risks persist in FH even after hypolipidemic therapy is started and are linked to a proinflammatory status of circulating monocytes. In the current study we aimed to identify FH-specific gene expression patterns of monocyte-derived M1-like macrophages in response to lipid accumulation. RNAseq was performed for four patient and four control paired samples of M1-like macrophages before and after incubation with oxidized LDL (oxLDL). A validation step was performed in 10 patients and 10 controls using real-time PCR and ELISA. RNAseq data analysis revealed 22 DEGs between FH patients and the control group before and 47 DEGs after incubation with oxLDL. Pathway enrichment analysis suggested dysregulation of inflammatory pathways especially IL-1 and chemokine signaling in response to lipid accumulation in FH M1-like macrophages. Validation experiments demonstrated increased interleukin-1β secretion by lipid-laden M1-like macrophages in FH patients and reduced and gene expression compared to controls. Our results suggest FH M1-like macrophages may be predisposed to an accelerated immune response via interleukin-1β due to reduced TMEM176A/B activity. - Source: PubMed
Publication date: 2026/07/29
Izyumchenko ArtemUsenko TatianaDracheva KseniiaLegostaeva KristinaUrazgildeeva SoreiiaTanayants KseniiaGrunina MariaLarionova EkaterinaSuchko PavelGlotov OlegKulikov AlexandrPchelina SofyaMiroshnikova Valentina - This study aims to determine the role of acid‑sensitive nonspecific cation channels transmembrane protein 176A (TMEM176A) and TMEM176B in autoimmune diseases, with a focus on primary Sjögren's Syndrome (pSS). - Source: PubMed
Yuan YuanLuo HanxiYang BohaoYu XiaoyuXiong ZiqiGao YimingLiu ChenWang Pingzhang - 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