TRAIL-R2, Human Recombinant Protein (FITC labeled)
- Known as:
- TRAIL-R2, Human Recombinant Protein (fluorecein labeled)
- Catalog number:
- tr-006
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- TRAIL-R2 Human Recombinant Protein (FITC labeled)
Related genes to: TRAIL-R2, Human Recombinant Protein (FITC labeled)
- Gene:
- TNFRSF10B NIH gene
- Name:
- TNF receptor superfamily member 10b
- Previous symbol:
- -
- Synonyms:
- DR5, KILLER, TRICK2A, TRAIL-R2, TRICKB, CD262, TRAILR2
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2018-01-25
Related products to: TRAIL-R2, Human Recombinant Protein (FITC labeled)
Related articles to: TRAIL-R2, Human Recombinant Protein (FITC labeled)
- Upper tract urothelial carcinoma (UTUC) is characterized by a high incidence of muscle invasion and distinct molecular heterogeneity, with tumor microenvironment (TME) heterogeneity playing a pivotal role in its malignant progression. However, the spatial distribution patterns of functional cell populations in UTUC and their regulatory mechanisms driving high-grade (HG) and muscle-invasive (MI) progression remain largely unelucidated. Herein, we integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptome sequencing (ST-seq) to systematically characterize the cellular landscape, spatial molecular network, and intercellular communication profile of UTUC tissues. Six tumor cell subpopulations were identified in UTUC, among which SLC14A1⁺ tumor cells were correlated with favorable clinical prognosis, whereas S100A8/9⁺ tumor cells were associated with poor clinical outcomes. Mechanistically, SLC14A1⁺ tumor cells decelerated UTUC progression via modulating cell apoptosis mediated by the FASLG-TNFRSF10B ligand-receptor pair. In contrast, S100A8/9⁺ tumor cells promoted the malignant progression of UTUC by regulating extracellular matrix remodeling and epithelial-mesenchymal transition (EMT) via the CCL19-CCR7, CCN2-EGFR, ADAM28-ITGA4 and CD14-ITGB2 ligand-receptor pairs. Collectively, our study uncovers the cellular and spatial heterogeneity of the UTUC TME, identifies SLC14A1⁺ tumor cells as a tumor-suppressive subpopulation and S100A8/9⁺ tumor cells as a key driver of UTUC malignant progression, and further delineates the core spatial signaling pathways underlying HG and MI progression of UTUC. These findings provide novel prognostic biomarkers and potential therapeutic targets for UTUC, and advance our mechanistic understanding of spatial TME regulation in urothelial carcinoma. - Source: PubMed
Publication date: 2026/09/03
Liu JiangWei YangyangLiu YiSun ShiweiDilixiati DiliyaerZhou ZhouLu XiangyunLu PingZhao YangZhang YuShi - Epithelial ovarian cancer (EOC) is typically diagnosed at an advanced stage and is associated with high mortality due to metastasis and chemoresistance. Cancer stem cells (CSCs) are central to EOC progression, recurrence, and treatment resistance, with their functional behavior shaped by the tumor immune microenvironment. While M1 and M2 macrophages have been well-characterized, the role of interferon-stimulated gene-enriched subpopulations, particularly interferon-induced protein with tetratricopeptide repeats 1 tumor-associated macrophages (IFIT1 TAMs), in regulating CSC properties in EOC remains largely unexplored. - Source: PubMed
Liu RuiFang YilinZheng RuxiLin LiyaHuang DaZhai LingyunHe QionghuaZhang ZhigangZhou JianweiZhang Xiaoming - Capsid assembly modulators (CAMs) are promising antiviral agents for chronic hepatitis B virus (HBV) infection. This study investigates the anti-HBV activity and immunomodulatory effects of Class I CAMs (CAM-A) in vitro and in vivo. In HepAD38 cells, CAM-A treatment significantly upregulated the expression of interferon-stimulated genes (IP-10, MX1, OAS1). In AAV-HBV mice, CAM-A (GLS4) induced rapid reductions in HBV DNA and delayed HBsAg decline accompanied by transient ALT elevation, upregulated interferons and Tnfsf10/Tnfrsf10b gene expression, while terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunohistochemistry (IHC) experiments indicated caspase-3-independent cell death in HBV-infected hepatocytes. Importantly, the antiviral and HBsAg-lowering effects of CAM-A did not require adaptive immunity. Furthermore, combination of CAM-A with a TLR7 agonist in AAV-HBV mice, or with Peg-IFN-α in primary human hepatocytes (PHH) resulted in synergistic antiviral effects, underscoring the therapeutic potential of these agents to promote sustained HBsAg decline and support functional cure strategies in chronic HBV infection. - Source: PubMed
Publication date: 2026/08/31
Wang PuLiu XinchangXie YongZhang YingjunGu BaohuaLi JingChen Yunfu - Inflammatory bowel disease (IBD) is a systemic disorder that affects not only the gastrointestinal tract but also extraintestinal organs and is associated with a significantly increased risk of osteoporosis. This study aims to investigate the association between plasma proteomic profiles and the subsequent risk of osteoporosis in patients with IBD. - Source: PubMed
Publication date: 2026/08/04
Yue MinYe XiaohuaJin ZhenheYe KexinXu ChengweiZhou TianyuShen Zhe - TRAIL is a TNF family ligand that trimerizes TRAIL-R1 (DR4) or TRAIL-R2 (DR5) to induce apoptosis, necroptosis, and/or NF-κB activation in receptor-bearing cells. We previously identified TRAILshort as a splice variant of TRAIL that lacks cysteine 230, cannot trimerize, and acts as a dominant-negative ligand that blocks TRAIL-mediated apoptosis. TRAILshort is expressed on cell surfaces and within extracellular vesicles, enabling it to confer TRAIL resistance to both producing and bystander cells. In this study, we showed that elevated TRAILshort levels were associated with chronic viral infections, cancer, and autoimmune diseases, suggesting a link to impaired immune regulation. Using unbiased phosphoproteomics and mechanistic studies, we demonstrated that TRAILshort binding to DR5 recruited and activated the phosphatase Src homology region 2 domain-containing phosphatase 1 (SHP-1), leading to zeta-chain-associated protein kinase 70 (ZAP-70) dephosphorylation, disruption of ZAP-70-CD3ζ interactions, and impaired T cell receptor signaling, thereby reducing T cell activation, proliferation, and cytokine production in response to antigen or CD3/CD28 ligation. Genetic or pharmacologic SHP-1 inhibition reverses these effects. In humanized mouse models, TRAILshort promoted the persistence of transformed mouse embryonic fibroblasts (MEFs) and L428 and antagonized CD19-directed CAR T cell activity, revealing TRAILshort as an immunomodulator of T cell function with therapeutic implications, including blocking TRAILshort to restore T cell immunity or delivering TRAILshort to enforce tolerance. - Source: PubMed
Publication date: 2026/08/03
Jalali ShahrzadNatesampillai SekarNie ZilinZhang YingCan IsmailChandrasekar Aswath PHameister Brianna MCorreia CristinaZhao Tuantuan VMun Dong-GiGarcia-Rivera EnriqueMatson RobertKrogman AshtonMaynes Mark ABatchelor RobinMonie Dileep DLi HuBehfar AttaKenderian Saad SPandey AkhileshAnsell Stephen MTaner TimucinWeyand CorneliaBilladeau Daniel DBadley Andrew D