Ask about this productRelated genes to: TMEM176B Blocking Peptide
- Gene:
- TMEM176B NIH gene
- Name:
- transmembrane protein 176B
- Previous symbol:
- -
- Synonyms:
- LR8, MS4B2
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-04
- Date modifiied:
- 2015-06-04
Related products to: TMEM176B Blocking Peptide
Related articles to: TMEM176B Blocking Peptide
- Excessive extracellular matrix accumulation, primarily as a result of hepatic stellate cell activation, is a hallmark of hepatic fibrosis, a progressive outcome of chronic liver injuries. Recent research studies suggest that stem cells, hepatocytes, and extracellular vesicles may provide therapeutic advantages due to their anti-inflammatory, antioxidative, and regenerative activities. This study aimed to comparatively evaluate the therapeutic efficacy of these agents in a rat model of carbon tetrachloride (CCl)-induced hepatic fibrosis. - Source: PubMed
Publication date: 2026/06/09
Rahimi SaharKhoshnazar Seyedeh MahdiehDerakhshani AliShahrokhi Nader - Transmembrane proteins have emerged as pivotal regulators of the tumor immune microenvironment. They coordinate immune regulation through the modulation of antigen presentation, cytokine signaling, ion homeostasis, and immune checkpoint activity. A growing body of evidence highlights their dual functional roles: certain TMEM family members promote antitumor immunity by enhancing immune activation, while others contribute to immune evasion in a context-dependent manner influenced by cellular and tissue environments. Notably, TMEM173 (STING) and TMEM176B exemplify the immune-activating and context-dependent regulatory functions of this family, underscoring its therapeutic potential. Despite these advances, the majority of TMEM proteins remain incompletely characterized, with limited insights into their molecular architectures, interaction networks, and context-specific regulatory mechanisms. Furthermore, challenges related to selective targeting and the safe translation of findings into clinical applications continue to impede therapeutic development. This review summarizes recent progress in understanding TMEM-mediated mechanisms within the tumor immune microenvironment, underscores their potential as therapeutic targets and prognostic biomarkers, and discusses key challenges and future directions for integrating TMEM biology into precision immunotherapy. - Source: PubMed
Publication date: 2026/03/20
Fan ShangqianZu TianyiHu XiaojiaZhong JiatengZhu Huifang - Aniridia, driven by PAX6 mutations, causes aniridia-associated keratopathy (AAK), a progressive condition linked to limbal stem cell deficiency. A major hurdle to developing targeted therapies for AAK is the incomplete understanding of the molecular abnormalities in affected corneas. To address this, we leveraged Pax6± (Pax6 het) mice, a model of AAK, and applied single-cell RNA sequencing (scRNA-seq) to profile the transcriptomic changes at a single-cell resolution. - Source: PubMed
Foroozandeh ParisaKaplan NihalQi XiaolinYang WendingChen XiaopingLee Sun KyongRen ZiyouLavker Robert MKume TsutomuPeng Han - Cancer-associated thrombosis (CAT), encompassing both venous thromboembolism and arterial thrombosis, contributes to up to 14% of cancer-related mortality and remains difficult to treat due to the bleeding risks of conventional anticoagulants. Protein disulfide isomerase (PDI) and its family member ERp57 (PDIA3) are thiol isomerases that regulate both arterial and venous thrombosis and are also upregulated in tumors, where they promote growth, metastasis, and immune evasion. Here, we evaluated the therapeutic potential of two thiol isomerase inhibitors-isoquercetin (ISOQ), a selective PDI inhibitor, and zafirlukast (ZAF), a broad-spectrum inhibitor of thiol isomerases such as PDI and ERp57-individually and in combination, in a xenograft model of ovarian cancer. ISOQ inhibited both platelet aggregation and Factor Xa generation induced by tumor cells and significantly suppressed tumor growth, thromboinflammatory markers, and expression of tissue factor, VEGF, TMEM176B, and PD-L1. ISOQ also potentiated standard cisplatin/gemcitabine chemotherapy. Notably, the combination of low-dose ISOQ plus ZAF achieved ≥ 80% inhibition of key tumor-associated markers at one-third the monotherapy dose and outperformed either agent alone. These findings support ISOQ and ZAF as promising agents for the treatment of cancer and CAT and establish thiol isomerase inhibition as a strategy to simultaneously target thrombosis, tumor progression, and immune escape. - Source: PubMed
Keovilay Justine AHoskins Jason WKinet Jean-PierreLines Thomas CKennedy Daniel R - Hepatic ischemia-reperfusion (I/R) injury, a major complication in liver transplantation and extensive resection, involves complex mechanisms with limited therapeutic options. The M1 polarization of macrophages has been confirmed as one of the contributing factors to hepatic I/R injury. Paeoniflorin (PF), a bioactive compound from traditional Chinese medicine, exhibits hepatoprotective and immunomodulatory properties, its precise mechanism in regulating macrophage polarization during hepatic I/R remains unclear. - Source: PubMed
Publication date: 2025/10/14
Tang XiaoTan YawenGao FengqiangWang ZhouchengYe XinyuQiu XunLou ZijianYang XinyuChen JunXu HaoChen JianXu XiaoWang Kai