Ask about this productRelated genes to: LGALS9 Blocking Peptide
- Gene:
- LGALS9 NIH gene
- Name:
- galectin 9
- Previous symbol:
- -
- Synonyms:
- LGALS9A
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-25
- Date modifiied:
- 2016-05-13
Related products to: LGALS9 Blocking Peptide
Related articles to: LGALS9 Blocking Peptide
- Tumor-associated macrophages (TAMs) are key regulators of immune homeostasis within the tumor microenvironment (TME) and play critical roles in malignant progression. However, the molecular mechanisms linking macrophage metabolic remodeling to immune regulation remain incompletely understood. Glycine cleavage system H protein (GCSH), a core regulator of copper-dependent cell death, has been implicated in metabolic regulation in triple-negative breast cancer (TNBC), suggesting a potential role in macrophage-mediated TME remodeling. - Source: PubMed
Publication date: 2026/05/06
Ge JiahaoChen TingMa YuanyuanWei Shuzhen - Prostate-specific membrane antigen (PSMA)-based vaccination represents a promising immunotherapeutic strategy for prostate cancer; however, its efficacy remains constrained by tumor-induced immune evasion and insufficient activation of antigen-presenting cells. Galectin-9 (LGALS9), an immunoregulatory lectin that contributes to immune suppression, is therefore an attractive target for overcoming tumor-induced immune tolerance. - Source: PubMed
Publication date: 2026/05/08
Lu BowenLiu NingZhao WantingChen HaominShao YingxiangLu HaosenLiu ShanshanYang JieZheng YanyanDing JiageChai DafeiMao Lijun - Chromoblastomycosis (CBM) is a chronic, neglected tropical fungal infection. Its immunopathogenesis, particularly the mechanism underlying its chronicity, remains poorly understood. - Source: PubMed
Publication date: 2026/04/17
Lei KexinTian JieZhang LuGong ZhuoqingLiu WenjieWan ZheWang YangLi RuoyuDong BilinWang Xiaowen - Immune thrombocytopenia (ITP) is an autoimmune disease. Megakaryocyte dysfunction caused by autoimmune response can lead to thrombocytopenia, and the underlying mechanism is still unclear. Single-cell sequencing analysis revealed the heterogeneity of CD34 + HSPCs in bone marrow between ITP patients and healthy groups. Pre-B cell population 1 (pre-B1) showed a significantly lower percentage contribution in ITP groups, and the underlying mechanism involves cell cycle-, cell apoptosis- and cell death-related pathways. The number of eosinophil-basophil mast cell progenitors (EBMPs) is significantly increased in ITP patients and the DEGs of the EBMPs in ITP patients were significantly enriched in immune-related pathways. Further, immunofluorescent staining and Western blot assay highlight C-X-C Motif Chemokine Ligand 8 (CXCL8) and Interferon Regulatory Factor 1 (IRF1) expression were significantly increased in the EBMPs of ITP patients. Furthermore, cell-cell communication analysis identified an impaired LGALS9-CD44 axis between EBMP cells and MkP1 cells in ITP patients, suggesting that targeting the LGALS9-CD44 interaction might hold promise as a therapeutic approach for ITP. Our observations indicate that ITP patients exhibit an elevated proportion of EBMP cells alongside a reduced proportion of pre-B1 cells. CXCL8 and IRF1 are potentially associated with EBMP cell dysfunction and the ITP disease process. Furthermore, the diminished LGALS9-CD44 axis between EBMP and MkP1 cells may contribute to ITP progression, suggesting a direction for future therapeutic investigation. - Source: PubMed
Publication date: 2026/04/15
Xie MeiDeng HaimeiLiu FangjieXiao WeiXu XiaojunXie RongliSun Tiantian - Dermatomyositis (DM) is an immune-mediated myopathy marked by chronic inflammation and heterogeneous clinical trajectories. The molecular determinants driving disease onset and progression remain poorly defined. This study aimed to construct a high-accuracy diagnostic risk model, identify causally relevant genes, and uncover cell-type-specific immune circuits contributing to DM pathogenesis, with emphasis on BTN3A2. - Source: PubMed
Publication date: 2026/04/30
Yang JingYin Long-KuanTang Jin