ULBP1 Pre-design Chimera RNAi
- Known as:
- ULBP1 Pre-design Chimera RNAi
- Catalog number:
- H00080329-R02
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ULBP1 Pre-design Chimera RNAi
Related genes to: ULBP1 Pre-design Chimera RNAi
- Gene:
- ULBP1 NIH gene
- Name:
- UL16 binding protein 1
- Previous symbol:
- -
- Synonyms:
- RAET1I
- Chromosome:
- 6q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: ULBP1 Pre-design Chimera RNAi
Related articles to: ULBP1 Pre-design Chimera RNAi
- Intestinal barrier (IB) dysfunction contributes to metabolic endotoxemia and associated diseases. Specifically, intestinal inflammation upregulates natural killer cell receptor 2D ligands (NKG2DLs) in intestinal epithelial cells (IECs), which triggers excessive immune responses and exacerbates IB injury. The prebiotic xylooligosaccharides (XOS) hold promise for ameliorating such injury by regulating NKG2DLs, yet the underlying mechanisms remain elusive. This study aimed to investigate the efficacy of XOS in improving IB injury and explore its role and molecular mechanisms in mitigating IB damage via NKG2DLs modulation. IB injury models were established in differentiated Caco-2 and MODE-K cells by treatment with 20 ng/mL tumor necrosis factor-α (TNF-α), followed by XOS intervention at concentrations of 50, 100, 150, and 200 μg/mL. Tight junction (TJ) proteins (ZO-1, Occludin) were detected using Western blotting (WB) and immunofluorescence, while barrier permeability was evaluated via transepithelial electrical resistance (TEER), phenol red permeability assay, and transmission electron microscopy (TEM). Additionally, the RhoA/ROCK/MLCK signaling pathway, apoptosis-related factors (Caspase-3, Bcl-2), and the expression of human NKG2DLs (MICA, MICB, ULBP-1) and murine NKG2DLs (Rae-1ε, H60, MULT-1) were analyzed by quantitative real-time PCR (qRT-PCR) or WB, and apoptotic cells were labeled using the TUNEL assay. To further investigate the involvement of NKG2DLs in the protective effect of XOS, RNA interference (RNAi) was performed to knock down NKG2DLs in Caco-2 and MODE-K cells. This conserved mechanism relies on Argonaute (Ago) family proteins that associate with small RNAs to mediate sequence-specific degradation of complementary target RNAs. Subsequently, both cell lines were treated with TNF-α and XOS, and the expression levels of NKG2DLs, ZO-1, and Occludin were determined by qRT-PCR or WB. Compared with TNF-α treatment alone, XOS at the concentrations used in this study significantly attenuated the downregulation and mislocalization of ZO-1 and Occludin in both Caco-2 and MODE-K cells (p < 0.05), increased TEER in Caco-2 cell (p < 0.05), reduced phenol red permeability (p < 0.05), and improved the ultrastructure of TJs and the integrity of microvilli. XOS at the tested concentrations also inhibited the activation of the RhoA/ROCK/MLCK signaling pathway (p < 0.05), suppressed Caspase-3 (p < 0.05) and the number of TUNEL-positive apoptotic cells, and alleviated TNF-α-induced overexpression of both human and murine NKG2DLs (p < 0.05). Notably, RNAi-mediated knockdown of Rae-1ε or H60 in MODE-K cells abrogated the XOS-induced restoration of ZO-1 and Occludin expression under TNF-α challenge. Collectively, under the experimental conditions of this study, XOS mitigate IB injury by inhibiting apoptosis, RhoA/ROCK/MLCK signaling and NKG2DLs in IECs. - Source: PubMed
Publication date: 2026/04/26
Yang JunyiGuo LeiRen ShijingLai QiuyuYang ShunyuWu YanhuaYing ShihaoMeng YitingLi Qing - UL-16 binding protein 1 (ULBP1), a ligand for the NK cell-stimulatory receptor NKG2D, is expressed as a cell-surface protein on malignant cells. While accumulating evidence links ULBP1 to cancer progression, its pan-cancer immunological and clinical significance remains underexplored. Through systematic bioinformatics analyses of 33 malignancies, we uncovered that widespread ULBP1 dysregulation across cancers was associated with advanced tumor staging and patient survival. ROC curve analysis further identified ULBP1 as a robust diagnostic biomarker. Subsequent exploration demonstrated ULBP1's epigenetic regulation through DNA/RNA methylation and its influence on tumor microenvironment remodeling. Functional validation in head and neck squamous cell carcinoma (HNSCC) confirmed that ULBP1 overexpression promoted cellular migration, invasion, proliferation in vitro and in vivo, while inhibiting apoptosis, suggesting NK cell-independent oncogenic mechanisms. We discovered that ULBP1 protein was upregulated in HNSCC tissue, induced epithelial-mesenchymal transition (EMT), as well as activation of the KRAS signaling pathway. Intriguingly, elevated ULBP1 was correlated with improved clinical outcomes following PD-1/PD-L1 blockade therapy, indicating its potential as a predictive biomarker for checkpoint inhibitor response. This study comprehensively delineates ULBP1's functional mechanisms across multiple cancers and experimentally validates its oncogenic role in HNSCC. - Source: PubMed
Publication date: 2026/05/09
Peng YuZhou YeXu CongCui LanzhenZhang LijunDi BinLi Xiaoming - Pancreatic ductal adenocarcinoma (PDAC) often escapes T cell–mediated immunity through impaired major histocompatibility complex class I (MHC-I) antigen presentation, contributing to its limited responsiveness to T cell–based immunotherapies. Because natural killer (NK) cells are capable of eliminating MHC-I–low tumor cells, redirecting NK cytotoxicity represents a promising strategy for these immune-cold tumors such as PDAC. Among activating NK receptors, NKG2D has been widely exploited in NK cell–engaging platforms through the incorporation of NKG2D ligands (MICA/B and ULBP family members). However, the impact of NKG2D ligand (NKG2DL) identity and binding affinity on NK cell engager potency has not been quantitatively defined. - Source: PubMed
Publication date: 2026/03/10
Lee Seul-GiLee MyungjeeLee Hye-MinSon Ga-HyunYoon Sang-RokChae Byeong-HoKim Dae-SeongLee Kyung-MiKim Yong-Sung - High-risk neuroblastoma (NB) often relapses and becomes refractory to treatment, making it a significant contributor to childhood cancer mortality despite its relative rarity. Addressing the challenges posed by NB's resistance to conventional apoptosis-inducing therapies (e.g., chemotherapy and radiation) has become a pressing concern in pediatric oncology research. In recent years, the growing comprehension of alternative cell death modalities distinct from apoptosis has revealed a promising avenue in the endeavor to combat treatment-resistant cancers. One such mechanism, ferroptosis, has attracted increasing attention for its potential role in combating therapy-resistant cancer cells. High-risk NB typically exhibits an immune-excluded phenotype, characterized by minimal immune cell infiltration. Despite this characteristic, the mechanisms underlying immune exclusion and impaired immune activation in NB remain unclear. Here, we demonstrate that the induction of ferroptosis using Erastin, a cystine-glutamate antiporter inhibitor, reduces NB cell proliferation and foci formation. Furthermore, our transcriptomics analysis revealed that treatment with Erastin in NB cells led to increased expression of ULBP1, a ligand to the activating natural killer (NK) cell receptor, NKG2D. Upon ferroptosis induction, the transcription factor ATF4 was found to drive ULBP1 expression in NB cells. Consistent with this, pre-treatment with Erastin sensitized NB cells to NK cell cytotoxicity in co-culture experiments. These results suggest the NK cell's cytotoxic function can be enhanced with Erastin-mediated ferroptosis, which may be beneficial for NB patients. - Source: PubMed
Publication date: 2026/02/10
Anthonydhason VimalaIslamagic ErnaLeijon NikkiGaarder JennieMartinsson TommyFransson SusanneThorén Fredrik BUmapathy Ganesh - Metastatic melanoma is an aggressive malignancy with limited long-term treatment success due to therapeutic resistance and immune evasion. The transient receptor potential melastatin 8 (TRPM8) ion channel is overexpressed in melanoma but its role as therapeutic target remains unexplored. We investigated the anti-tumor effects of novel TRPM8 modulators in metastatic melanoma cells using viability assays, apoptosis markers, mitochondrial function analyses, reactive oxygen species (ROS) measurements and gene silencing. Their functional impact was further assessed in 3D melanoma organoids, clonogenic survival assays, and natural killer (NK) cell co-culture systems. TRPM8 is significantly overexpressed in metastatic melanoma, as compared with the normal counterparts. Its pharmacological inhibition with novel modulators selectively induces calcium-independent mitochondrial apoptosis characterized by ROS accumulation, mitochondrial membrane depolarization, cytochrome c release, and caspase-3 activation. This process involves activation of the ATM/p53 pathway and upregulation of pro-apoptotic proteins. Additionally, TRPM8 modulators increase expression of the NK cell-activating ligand ULBP1, enhancing melanoma susceptibility to NK-mediated cytotoxicity. Our study identifies TRPM8 as a promising biomarker in melanoma. Its targeting triggers mitochondrial cell death and simultaneously boosts NK cell recognition via ULBP1/NKG2D engagement. TRPM8 targeting in combination with immunotherapy might be, hence, further explored in clinical setting of advanced melanoma. - Source: PubMed
Publication date: 2026/02/14
Sorrentino CarmelaLauretta CarmineD'Angiolo RosaMusella SimonaGiovannelli PiaBertamino AlessiaOstacolo CarmineGomez Monterrey IsabelMigliaccio AntimoCastoria GabriellaDi Donato Marzia