Resorufin benzyl ether
- Known as:
- Resorufin benzyl ether
- Catalog number:
- 15020
- Product Quantity:
- 10 mg
- Category:
- -
- Supplier:
- FanBo Biochemicals
- Gene target:
- Resorufin benzyl ether
Related genes to: Resorufin benzyl ether
- Gene:
- BST2 NIH gene
- Name:
- bone marrow stromal cell antigen 2
- Previous symbol:
- -
- Synonyms:
- CD317, tetherin
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-17
- Date modifiied:
- 2016-07-29
Related products to: Resorufin benzyl ether
(+)-N-Acetyl 3,4,4a,5,6,10b-Hexahydro-2H-naphtho[1,2-b][1,4]oxazine-9-ol Triisopropylsilyl Ether CAS: 1034706-81-4 Formula: C23H37NO3Si(-)-1’-Methyl-N-Benzyl Normetazocine C22H27NO CAS:(-)-1’-Methyl-N-Benzyl Normetazocine CAS: Formula: C22H27NO(-)-N-(1-R-Ethoxycarbonxyl-3-phenylpropyl)-D-alanine, Benzyl Ester C22H27NO4 CAS: 93836-47-6(-)-N-(1-R-Ethoxycarbonxyl-3-phenylpropyl)-D-alanine, Benzyl Ester CAS: 93836-47-6 Formula: C22H27NO4(-)-N-(1-R-Ethoxycarbonxyl-3-phenylpropyl)-L-alanine Benzyl Ester C22H27NO4 CAS: 93841-86-2(-)-N-(1-R-Ethoxycarbonxyl-3-phenylpropyl)-L-alanine Benzyl Ester CAS: 93841-86-2 Formula: C22H27NO4(1-Methylcyclohexanyl)methyl-4-aminophenyl Ether C14H21NO CAS: 887406-96-4(1-Methylcyclohexanyl)methyl-4-aminophenyl Ether CAS: 887406-96-4 Formula: C14H21NO(1-Methylcyclohexanyl)methyl-4-nitrophenyl Ether C14H19NO3 CAS: 85002-76-2(1-Methylcyclohexanyl)methyl-4-nitrophenyl Ether CAS: 85002-76-2 Formula: C14H19NO3(1R) Perindopril-d4 Benzyl Ester C26H34D4N2O5 CAS:(1R) Perindopril-d4 Benzyl Ester CAS: Formula: C26H34D4N2O5(1R,3S,5R)-2-Azabicyclo[3.3.0]octane-3-carboxylic Acid, Benzyl Ester C15H19NO2 CAS: 130609-48-2(1R,3S,5R)-2-Azabicyclo[3.3.0]octane-3-carboxylic Acid, Benzyl Ester CAS: 130609-48-2 Formula: C15H19NO2 Related articles to: Resorufin benzyl ether
- Tetherin is an interferon-inducible transmembrane protein that inhibits the detachment of enveloped viruses from infected cells. HIV-1 Vpu counteracts this restriction by removing tetherin from sites of virus release. Accordingly, Vpu mutations that disrupt tetherin antagonism increase Env accumulation on the surface of HIV-infected cells. We found that Vpu mutations that impair tetherin antagonism also increase the susceptibility of HIV-infected cells to antibody-dependent cellular phagocytosis (ADCP). Increased sensitivity to ADCP was lost in tetherin-knockout cells and conditionally restored by doxycycline-inducible tetherin. Thus, Vpu protects HIV-infected cells from ADCP by preventing virion accumulation on the cell surface, similar to its protection against antibody-dependent cellular cytotoxicity (ADCC). By serving as a link between innate and adaptive immunity, the antiviral activity of tetherin may be amplified in vivo by Fc-mediated antibody effector functions and therefore much greater than initially appreciated based solely on its ability to inhibit virus release in cell culture assays. - Source: PubMed
Publication date: 2026/09/30
Snow Brian JKeles Nida KAli AhmedBehrens Ryan TJanaka Sanath KumarEvans David T - The long noncoding RNA H19 has been widely attested as a promoter of breast cancer by favoring proliferation, migration, invasion, and tumor growth. In this study, we attempted to decipher molecular mechanisms underlying oncogenic activities of H19. Transcriptomic analyses revealed that H19 overexpression correlates with increased BST2 expression at both transcriptional and protein levels in breast cancer cell lines. Functional assays demonstrated that BST2 overexpression mimics H19 oncogenic effects by enhancing tumor cell aggressiveness in vitro and tumor growth in vivo. Interestingly, we also observed a reciprocal regulation, where BST2 expression modulates H19 levels, suggesting a cross-regulatory mechanism. Further mechanistic studies identified miR-760 as a key post-transcriptional regulator orchestrating this interplay. Using luciferase reporter assays and miRNA modulation strategies, we found that miR-760 directly targets both H19 and BST2, thereby regulating their expression in a coordinated manner. Our findings uncover a novel H19/miR-760/BST2 regulatory axis that enhances breast cancer progression and suggest that this axis could be studied to identify potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/09/30
Klouyovo KekelyPeperstraete EvodieMabille LéaLouvieaux JoséphineMarmuse JimLecerf ClémentLagadec ChannLe Bourhis XuefenAdriaenssens Éric - To develop an innovative prognostic model for colon adenocarcinoma (COAD), we integated anoikis- and cell matrix adhesion (CMA related mechanisms using TCGA and GEO datasets. Six genes (BST2, NAT1, OFCC1, HOTAIR, TRIP6, ADAMTS13) were identified, risk model stratified patients into high- and low risk groups with distinct survival (p=0.025), validated in GSE17536. A nomogram showed good predictive accuracy. Functional enrichment highlighted tumor-, anoikis-, and CMA-related pathways, immune infiltration correlated with prognostic signature and risk score. High-risk patients were more sensitive to afatinib, osimertinib, and navitoclax; low-risk patients to paclitaxel, docetaxel, and gemcitabine. These genes may serve as prognostic biomarkers and guide tailored COAD therapy. - Source: PubMed
Publication date: 2026/09/23
Zheng TingLi XingxingZhou LiJin Jianjiang - Intrinsic resistance to anti-PD-1 immunotherapy remains a major obstacle in treating metastatic gastric cancer (GC), particularly in tumors harboring concurrent YAP hyperactivation and TP53 loss. Here, using a genetically engineered mouse model with conditional YAP hyperactivation and Tp53 deletion in gastric Atp4b cells (AYP), we show this "double-hit" alone suffices to recapitulate human refractory GC, including histopathological heterogeneity, multi-organ metastasis, and intrinsic PD-1 resistance. We identified BST2 as a direct YAP-TEAD transcriptional target. In human GC, BST2-high tumor correlates with poor anti-PD-1 response. Mechanistically, tumor cell-derived BST2 engages the inhibitory receptor PIRA2 on neutrophils and liver Kupffer cells, instructing an immunosuppressive, pro-metastatic phenotype that inhibits T cells antitumor response and confers PD-1 resistance. Therapeutically, dual BST2/PD-1 blockade in the AYP model suppresses primary tumor growth and eradicates established liver metastases. Thus, YAP activation, cooperating with TP53 loss, fuels metastatic GC and immunotherapy resistance via BST2 induction. - Source: PubMed
Publication date: 2026/09/21
Zhang WeihongWang ShilongWang MengYu RuixianYue JingwuShao LinZhang HuiZhu MengwenTian LuyangCheng ShutingQin WeiminTang YangHan YiWang WenjiaAn LiweiMeng YanJiao ShiZhou Zhaocai - Artesunate is a worldwide prevalent antimalarial medicine, which has also been demonstrated for anti-tumor, anti-virus and anti-autoimmune diseases. Yet the underlying molecular and cellular mechanisms remain largely unexplored. Here, we examined immunological features of 5 immune tissues (spleen, bone marrow, thymus, lymph nodes and peritoneal cavity) of mice with artesunate administration through label-free proteomics and high-dimensional single-cell mass cytometry (CyTOF). Label-free proteomics uncovered dramatic alterations for the interferon-I (IFN-I) induced proteins, especially BST2 and IFIT1 downregulation in spleen and bone marrow. CyTOF analysis further indicated that the percentage of MDSCs was significantly elevated in spleen and bone marrow. The follow-up LPS-induced inflammatory model confirmed that pretreatment with artesunate attenuated the inflammatory damage, and the expression of BST2 was decreased in the spleen of mice with artesunate administration. Together, our findings presented an immune landscape of multiple tissues of mice with artesunate administration. These datasets provide comprehensive biological resources to develop therapeutic strategies for inflammatory diseases. - Source: PubMed
Publication date: 2026/04/12
Hong RongjianWang AitingLi YiyangDing Xianting