Dipropyl ether Purity 0,99
- Known as:
- Dipropyl ether Purity 0,99
- Catalog number:
- [111-43-3]
- Product Quantity:
- 5 g
- Category:
- -
- Supplier:
- VUP
- Gene target:
- Dipropyl ether Purity 99
Ask about this productRelated genes to: Dipropyl ether Purity 0,99
- 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
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(+)-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(2-Methoxyethyl)-methylamine Purity 0,98(2-Methoxyethyl)-methylamine Purity 0,98(2-Methoxyethyl)-methylamine Purity 0,98(2-Methoxyethyl)-methylamine Purity 0,98(2-Methoxyethyl)-methylamine Purity 0,98(2-Methoxyethyl)-methylamine Purity 0,98(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 Related articles to: Dipropyl ether Purity 0,99
- Dengue virus (DENV) is a growing global public health threat. The lack of symptomatic immune competent animal models for Dengue has hindered the screening and development of effective therapeutics that can be used to control dengue virus replication and thereby control the progression to severe dengue disease. To address this, we established an infection model in neonatal C57BL/6 mice and showed that a systemic Dengue challenge leads to ataxia, seizures, paralysis, and death within 15 days. The virus was found predominantly in the eye and brain where DENV infects neurons but not astrocytes and causes extensive infiltration of macrophages and microglia activation. The response to infection included upregulation of multiple genes linked to interferons ( and ), inflammation (), complement (), cytolysis () consistent with antiviral responses and inflammation together with neuroprotective regulatory signals (. The increased proinflammatory signature was associated downregulation neurodevelopmental genes and . We tested the utility of this mouse model by assessing the protection conferred by direct antivirals JNJ-A07 and ST-148 and host-directed antiviral immunomodulatory CpG oligodeoxynucleotide (ODN), alone or in combination against lethal dengue viral infection. The data showed that immunomodulatory CpG ODN and antiviral JNJ-A07 improved survival of neonatal mice, and protection from lethal neurotropic infection was optimal when treatments were combined. This study suggests that combination of an effective dengue antiviral along with a host directed therapeutic may be a useful strategy to protect against Dengue virus infections. - Source: PubMed
Publication date: 2025/03/10
Mendoza MirianIreland Derek D CLee Ha-NaKelly-Baker LoganChowdhury MonicaVerthelyi DanielaManangeeswaran Mohanraj - Primary membranous nephropathy (pMN) often progresses to end-stage renal disease (ESRD) in the absence of immunosuppressive therapy. The immunological mechanisms driving pMN progression remain insufficiently understood. - Source: PubMed
Tie XuanChen ZhiangYao ShuleiWu BinxinYan BingjuanZhai HuifangQiao XiSu XiaoleWang Lihua - Bone marrow stromal cell antigen 2 (BST-2) is a restriction factor for human immunodeficiency virus type I (HIV-1) and plays an important role in regulating the release of viral particles. However, the antiviral efficacy of BST-2 is antagonized by the HIV-1-encoded accessory protein Vpu, which facilitates the degradation of BST-2 by recruiting E3 ubiquitin ligase β-TrCP. The involvement of deubiquitinases (DUBs) in counteracting BST-2 ubiquitination and influencing its stability during HIV-1 infection remains inadequately explored. In this study, we conducted a small interfering RNA (siRNA) screening of human DUBs and determined that OTUD1 interacts with BST-2, leading to a reduction in its K48- and K63-linked ubiquitination. This reduction increases BST-2 protein stability, and subsequently inhibits HIV-1 release. Our findings reveal a novel regulatory mechanism by which DUBs influence the stability of the HIV-1 restriction factor BST-2 to dampen viral release, providing a potential therapeutic target for HIV-1 antiviral intervention. - Source: PubMed
Publication date: 2025/02/14
Zhang Man-DiChen FanHe Wen-QiangLu YingLiu Feng-LiangZhang Hong-GuangYang Liu-MengDong Chun-ShengXiong Si-DongZheng Yong-Tang - Severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1) and -2 (SARS-CoV-2) are beta-coronaviruses (β-CoVs) that have caused significant morbidity and mortality worldwide. Therefore, a better understanding of host responses to β-CoVs would provide insights into the pathogenesis of these viruses to identify potential targets for medical countermeasures. In this study, our objective is to use a systems biology approach to explore the magnitude and scope of innate immune responses triggered by SARS-CoV-1 and -2 infection over time in pathologically relevant human lung epithelial cells (Calu-3/2B4 cells). Total RNA extracted at 12, 24, and 48 hours after β-CoVs or mock infection of Calu-3/2B4 cells were subjected to RNA sequencing and functional enrichment analysis to select genes whose expressions were significantly modulated post-infection. The results demonstrate that SARS-CoV-1 and -2 stimulate similar yet distinct innate antiviral signaling pathways in pathologically relevant human lung epithelial cells. Furthermore, we found that many genes related to the viral life cycle, interferons, and interferon-stimulated genes (ISGs) were upregulated at multiple time points. Based on their profound modulation upon infection by SARS-CoV-1, SARS-CoV-2, and Omicron BA.1, four ISGs, i.e., bone marrow stromal cell antigen 2 (BST2), Z-DNA Binding Protein 1 (ZBP1), C-X-C Motif Chemokine Ligand 11 (CXCL11), and Interferon Induced Transmembrane Protein 1 (IFITM1), were identified as potential drug targets against β-CoVs. Our findings suggest that these genes affect both pathogens directly and indirectly through the innate immune response, making them potential targets for host-directed antivirals. Altogether, our results demonstrate that SARS-CoV-1 and SARS-CoV-2 infection induce differential effects on host innate immune responses. - Source: PubMed
Publication date: 2025/01/28
Tat Vivian YDrelich Aleksandra KHuang PinghanKhanipov KamilHsu Jason CWiden Steven GTseng Chien-Te KentGolovko George - Bone marrow stromal antigen 2 (BST2) is a host-restriction factor that plays multiple roles in the antiviral defense of innate immune responses, including the inhibition of viral particle release from virus-infected cells. BST2 may also be involved in the endothelial adhesion and migration of monocytes, but its importance in the immune system is still unclear. Immune cell adhesion and migration are closely related to the initiation of immune responses. In this study, we found that the expressions of the lymph node homing marker chemokine receptor 7 (CCR7) and an adhesion molecule intercellular adhesion molecule 1 (ICAM-1) in conventional dendritic cells (cDCs) were associated with BST2 expression. Interestingly, cDCs showed lower chemotactic ability, including velocity and accumulative distance toward chemokine ligand 19 (CCL19) gradient in vitro, compared to wild-type cDCs. cDCs also showed reduced migration and reduced retention capacity in draining lymph nodes in vivo. As a result, cDCs as antigen-presenting cells induced lower antigen-specific B cell and T cell responses compared to cDCs. Notably, mice administered the influenza vaccine via cDCs exhibited substantially inefficient virus clearance compared to mice administered the cDCs vaccine. Therefore, we propose that BST2, which plays a critical role in the effective migration and retention of cDCs, is involved in the development of optimal immunological effects in draining lymph nodes. - Source: PubMed
Publication date: 2024/12/27
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