4_Aminophenyl ether 95%
- Known as:
- 4_Aminophenyl ether 95%
- Catalog number:
- A27145
- Product Quantity:
- 100 G
- Category:
- -
- Supplier:
- pfalslandbauer.
- Gene target:
- 4_Aminophenyl ether 95%
Related genes to: 4_Aminophenyl ether 95%
- 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: 4_Aminophenyl ether 95%
(+)-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-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(2S,3R,4E)-2-Amino-4-decene-1,3-diol Ethyl Ether C12H25NO2 CAS:(2S,3R,4E)-2-Amino-4-decene-1,3-diol Ethyl Ether CAS: Formula: C12H25NO2(2S,3R,4E)-2-Amino-4-hepten-1,3-diol Ethyl Ether C9H19NO2 CAS:(2S,3R,4E)-2-Amino-4-hepten-1,3-diol Ethyl Ether CAS: Formula: C9H19NO2(2Z)-3-Methyl-4-(benzyloxy)-2-buten-1-ol tert-Butyldimethylsilyl Ether CAS: Formula: C18H30O2Si(3-Aminophenyl)acetic Acid C8H9NO2 CAS: 14338-36-4(3-Aminophenyl)acetic Acid CAS: 14338-36-4 Formula: C8H9NO2(3-Aminophenyl)boronic acid hydrochloride (3-Aminophenyl)boronic acid hydrochloride For research use only.(3β)-Cholest-5-ene-3,24-diol 24-Methylbenzenesulfonate 3-O-Tetrahydropyranyl Ether CAS: 70141-04-7 Formula: C36H54O5S(3β,5α)-5,8-[N,N-(4-Phenylurazole)]-3-O-acetyl-25-phenylsulfonyl-cholest-6-ene-3,22,25-triol 25-Tetrahydropyranyl Ether CAS: 137143-30-7 Formula: C49 Related articles to: 4_Aminophenyl ether 95%
- Bone marrow stromal antigen 2 (BST-2, or tetherin) is an interferon-inducible host restriction factor that inhibits the release of enveloped viruses by tethering nascent virions to cellular membranes. While its antiviral function is well established in retroviral systems, its role in SARS-CoV-2 egress remains unclear. Here, we used a virus-like particle (VLP) system composed of SARS-CoV-2 structural proteins M, E, and N to investigate the impact of BST-2 on viral particle release. BST-2 significantly inhibited VLP release in HEK293T and Calu-3 lung epithelial cells. Confocal microscopy revealed that BST-2 colocalizes with viral structural proteins at the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), the main site of coronavirus assembly. We next evaluated the roles of the SARS-CoV-2 accessory proteins ORF3a and ORF7a in overcoming this restriction. ORF3a localized to endolysosomal compartments and promoted VLP release through a BST-2-independent mechanism, without altering BST-2 expression or localization. In contrast, ORF7a colocalized with both BST-2 and ERGIC markers and restored VLP release by promoting BST-2 degradation. Notably, ORF7a also relieved BST-2-mediated restriction of HIV-1 VLP release, suggesting a conserved antagonistic function. These findings demonstrate BST-2 as an intracellular inhibitor of SARS-CoV-2 particle release and establish ORF7a as viral accessory antagonist that neutralizes this host defense. - Source: PubMed
Publication date: 2026/06/02
Smith AdamDong Xinhong - Although advancements in antiretroviral therapy (ART) have been able to control HIV infection in people with HIV (HIV+) to achieve suppressed viral loads and recovered CD4 T cell counts, the virus persists in latent reservoirs. Characterizing the molecular, biological, and immunological features of HIV-1 genes from these HIV+ virologically controlled individuals is essential for the development of eradication strategies. The HIV-1 accessory gene, vpu, plays important roles in the release of progeny virions and modulation of innate immune signaling, contributing to viral pathogenesis and persistence in the host. In this study, we analyzed the vpu sequences from 21 predominantly older HIV+ individuals with long-term ART-mediated viral suppression (mostly undetectable viral load) and mostly restored CD4 T cell counts. - Source: PubMed
Publication date: 2026/05/22
Mishra NehaKummet NathanKlotz StephenAhmad Nafees - The HIV-1 envelope glycoprotein (Env) represents the only viral antigen at the surface of infected cells, making it an ideal target for antibody-based therapies. Most antibodies elicited in people with HIV (PWH) do not recognize Env in its native "closed" conformation but readily bind to Env when it samples the CD4-bound "open" conformation. Downregulation of CD4 at the surface of infected cells by the viral accessory proteins Nef and Vpu prevents the premature opening of Env and has been shown to protect infected cells from antibody-dependent cellular cytotoxicity (ADCC) mediated by PWH plasma. Here, we report that deletion of Nef and Vpu from primary infectious molecular clones renders infected cells vulnerable to antibody-dependent cellular phagocytosis (ADCP) mediated by PWH plasma. This is in part linked to the premature engagement of Env with CD4. In agreement with an "open" Env being vulnerable to ADCP, small CD4 mimetic compounds (CD4mc) sensitize -infected cells and -expanded CD4 T cells to ADCP mediated by autologous monocytes in presence of PWH plasma. This effect was further improved by increasing cell surface Env through IFN-induced BST-2 upregulation. - Source: PubMed
Publication date: 2026/05/15
Bélanger ÉtienneTauzin AlexandraTajebe FitsumbrhanChandravanshi MonikaYang DerekChen Hung-ChingChiu Ta-JungBourassa CatherineMedjahed HalimaTolbert William DDurand MadeleineRichard JonathanHuryn Donna MStäger SimonaPazgier MarzenaFinzi Andrés - The skin harbors a complex immune microenvironment that integrates innate and adaptive components and plays a critical role in vector-borne pathogen transmission. To investigate immune responses during tick-mediated transmission of Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV), we analyzed skin from BALB/c mice bitten by artificially infected Amblyomma testudinarium nymphs. Skin samples were collected at time points corresponding to peak viral RNA levels (days 6-7 post-attachment) and analyzed by transcriptomics, followed by real-time PCR and immunohistochemical (IHC) analyses. Transcriptomic analysis revealed increased expression of immune-related genes, particularly those associated with type I interferon signaling. Interferon-stimulated genes (e.g., Rsad2, Ifit family members) and monocyte-associated markers (e.g., Ly6c2) were elevated in RNA sequencing data, while real-time PCR analysis showed similar trends but did not reach statistical significance. IHC revealed colocalization of viral antigens with macrophages in the infected skin, as characterized by Iba1 expression. Further analysis demonstrated a higher density of Ly6c2-positive inflammatory monocytes, consistent with transcriptomic observations. In addition, BST2 (Tetherin) expression was increased, consistent with activation of a localized Type I IFN-mediated antiviral response. However, the strong inflammatory response induced by tick feeding may obscure infection-specific transcriptional changes at these later time points. Overall, our findings demonstrate that tick-mediated SFTSV infection was associated with interferon-related gene expression and recruitment of monocyte-lineage cells at the skin interface, while highlighting the complex interplay between viral infection and tick-induced host responses. - Source: PubMed
Publication date: 2026/05/18
Lau Alice C CMori HiroshiSakai YusukeShimoda HiroshiNagata NoriyoMatsumura TakayukiShimojima MasayukiToyoda AtsushiHayasaka DaisukeSuzuki TadakiEbihara HidekiTakano Ai - Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality worldwide. The tumor microenvironment (TME) plays a pivotal role in LUAD progression, but the specific molecular mechanisms driving malignancy and immune evasion remain incompletely understood. Bone marrow stromal cell antigen 2 (BST2) has been implicated in other cancers, yet its functional role and therapeutic potential in LUAD require further elucidation. - Source: PubMed
Zhu KeyunLin MingrongLin ChengbinHu TaoCao ZhikaiHuang ShuoShen YanZeng JingHe JinxianShen WeiyuYing Jianjian