Epstein-Barr virus latent membrane protein 1 (LMP1) is an Epstein-Barr virus (EBV) protein that regulates its own expression and the expression of human genes. LMP1 has a molecular weight of approximately 63 kDa, and its expression induces many of the changes associated with EBV infections and activation of primary B cells. LMP1 is the best-documented oncoprotein of the EBV latent gene products, as it is expressed in most EBV-related human cancers. The structure of LMP1 consists of a short cytoplasmic N-terminus tail, six trans-membrane domains, and a long cytoplasmic C-terminus, which contains three activating domains: CTARt, CTAR2, and CTAR3. Each CTAR domain contains an amino acid sequence that serves as a recognition site for cellular adaptors to bind and trigger a series of signal transduction pathways that can lead to a change in gene expression. LMP-1 is a functional homologue of tumor necrosis factor and mediates signaling through the nuclear factor-κB pathway, mimicking CD40 receptor ...
Chang KC*(co-corresponding author), Chen PC, Chang Y, Wu YH, Chen YP, Lai CH, Medeiros LJ, Su IJ, Wang HW*. Epstein-Barr virus latent membrane protein-1 upregulates cytokines and correlates with older age and poorer prognosis in Hodgkin lymphoma. Histopathology. 2017 Feb 8;70(3):442-455 ...
Epstein-Barr virus (EBV) latent membrane protein 2 (LMP2) are two viral proteins of the Epstein-Barr virus. LMP2A/LMP2B are transmembrane proteins that act to block tyrosine kinase signaling. LMP2A is a transmembrane protein that inhibits normal B-cell signal transduction by mimicking an activated B-cell receptor (BCR). The N-terminus domain of LMP2A is tyrosine phosphorylated and associates with Src family protein tyrosine kinases (PTKs) as well as spleen tyrosine kinase (Syk). PTKs and Syk are associated with BCR signal transduction. Latent Membrane Protein 2 (LMP2) is a rightward transcribing gene. LMP2s transcript originates across the fused terminal repeats in sequences at opposite ends of the genome. 16‍-‍24 hours after infection, the genome circularizes and the open reading frame is created. 1.7 kb and 2.0 kb messages are created by alternative promoter usage and differ only in the sequences of the first exon. These messages are expressed in Epstein-Barr Virus transformed ...
Nasopharyngeal carcinoma (NPC) is an epithelial malignancy, which commonly occurs in Southern China, Taiwan, North Africa and Southeast Asia. Nasopharyngeal carcinoma is strongly associated with Epstein-Barr virus infection. The p53 tumour suppressor protein is rarely mutated in NPC suggesting that the inactivation of p53 pathway in NPC could be due to the presence of EBV proteins. The aim of this work was to determine the effects of EBV proteins namely LMP1 and LMP2A on the expression levels of p53 protein. In this work we found that LMP1, but not LMP2A, decreased p53 protein levels. Overexpression of LMP1 resulted in increased ubiquitination of p53 suggesting that the decreased p53 protein levels by LMP1 was due to increased degradation of the protein. The reduction of p53 protein levels was independent of the PI3K-Akt pathway. LMP1, but not LMP2A, reduced p53 protein levels through the increase in the polyubiquitination of p53 protein and was independent of the PI3K-Akt pathway.
The experiments reported here investigate the role of NIK, IKKα, IKKβ, and IKKγ in LMP1-induced p100 processing, the relative contributions of the LMP1 TRAF and death domain-binding sites to p100 processing and p52/RelB nuclear translocation, and the dependence of LMP1-induced gene expression on IKKα, IKKβ, and IKKγ. We now find that LMP1 induces p100 processing in a NIK/IKKα-dependent, IKKβ/IKKγ-independent manner similar to CD40, LTβR, TIRs, and BAFF-R (15-18, 20, 21, 24-26). Because EBV transformed LCLs have sustained p52 levels as well as RelA containing NF-κB complexes, LMP1-induced NF-κB activation likely has substantial canonical and noncanonical components. Because NF-κB is required for LCL survival (56), NIK and IKKα may have a role in LCL survival, and inhibitors of their activity may precipitate cell death or arrest cell growth.. Another important aspect of these data are the identification of the dominant role of the LMP1 TRAF1/2 and TRAF3/5-binding site in p100 ...
Epstein-Barr virus (EBV) is closely associated with nasopharyngeal carcinoma (NPC), a common cancer in Hong Kong. The EBV-encoded LMP1 protein is believed to play an important role in cell transformation. We have previously identified a prevalent LMP1 variant (2117-LMP1) that is expressed in 86% of primary NPC in Hong Kong. In this study, the biologic phenotypes induced by 2117-LMP1 were compared with those of the prototypic B95.8-LMP1 in an immortalized nasopharyngeal epithelial cell line, NP69. The 2117-LMP1 could induce cell proliferation and resistance to apoptosis induced by growth factor deprivation. Expression of 2117-LMP1 also suppressed expression of p16, p21 and Bax but induced expression of CDK2 and A20. Compared with B95.8-LMP1, 2117-LMP1 could induce a higher migration ability in NP69 cells but was less efficient in inducing morphologic changes, anchorage-independent growth and cell invasion. Relatively weaker ability of 2117-LMP1 than B95.8-LMP1 in upregulation of vimentin, VEGF ...
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3D18: Crystal structure of HLA-B*2709 complexed with a variant of the latent membrane protein 2 peptide (LMP2(L)) of epstein-barr virus
|strong|Anti-EBV (CS1) is a latent membrane protein 1 antibody, which detects a specific epitope upon LMP fusion protein in B-cell
HLA-A*02:01 EBV LMP2 I6M Tetramer-TVCGGMMFL-PE(Human Class I) from MBL.MHC tetramers can be used for direct detection of antigen specific T cells.
HLA-A*02:01 EBV LMP2 C1S Tetramer-SLGGLLTMV-APC(Human Class I) from MBL.MHC tetramers can be used for direct detection of antigen specific T cells.
Purchase Recombinant Epstein-Barr virus Latent membrane protein 1(LMP1),partial. It is produced in Yeast. High purity. Good price.
Antisera to the type-specific internal influenza virus matrix (M) protein of a type A influenza virus were produced in goats. In the presence of complement, anti-M serum was cytotoxic for target cells which were infected with a variety of serologically distinct type A influenza viruses, but did not react with type B influenza virus-infected cells. Absorption experiments indicated that anti-M serum detected a common antigen(s) on the surface of type A-infected cells. This serological cross-reactivity parallels the cross-reactivity observed for the cytotoxic T-cell response to type A viruses. ...
Extensive leukocyte infiltration is a feature of several cancers, including the EBV associated malignancies NPC, Hodgkins Disease (HD) and gastric cancer. We have used a model of epithelial carcinogeneisis, transgenic mice expressing the primary oncogene of EBV, LMP1, to explore the inflammatory processes prior to neoplasia. The ears of the L2LMP1CAO mice (the tissue where LMP1 is expressed at the highest level) and to a lesser extent other regions of body skin develop a preneoplastic pathology of hyperplasia with increased vascularisation, progressing to acanthosis, hyperkeratosis, parakeratosis and erosive or ulcerative dermatitis, which can lead to the development of keratoacanthoma, papilloma and ultimately carcinoma. Examination of the preneoplastic stages has revealed that the tissue is inflamed, with infiltrates of T-cells, mast cells and neutrophils, that occasional plasma cells are observed and IgG is deposited in the dermis and that several cytokines and chemokines involved in ...
Gene therapy - an advanced technique developed to insert or inject therapeutic genes into human cells - has shown some success in treating the disease. In a previous study, Xiao and co-investigators at State Key Laboratory of Biotherapy, and the Department of Thoracic Oncology Cancer Center, West China Hospital, Sichuan University, had used a gene therapy approach to induce cancer cell death. Their study found that Vesicular Stomatitis Virus Matrix Protein (VSVMP), when inserted into a cancer cell, compromises the cellular skeletal framework, which is made up of structural proteins. Cell death ensued as a consequence. In the current study, the research team further armed with VSVMP gene delivery vessel with Interleukin-12 (IL-12) - a protein known to recruit and switch on the cancer-killing functions of immune cells. The novel drug particles are based on Heparin-polyethyleneimine (HPEI) nanoparticles. To overcome the high toxicity and non-biocompatible nature of PEI, the team used a method to ...
Gene therapy - an advanced technique developed to insert or inject therapeutic genes into human cells - has shown some success in treating the disease. In a previous study, Xiao and co-investigators at State Key Laboratory of Biotherapy, and the Department of Thoracic Oncology Cancer Center, West China Hospital, Sichuan University, had used a gene therapy approach to induce cancer cell death. Their study found that Vesicular Stomatitis Virus Matrix Protein (VSVMP), when inserted into a cancer cell, compromises the cellular skeletal framework, which is made up of structural proteins. Cell death ensued as a consequence. In the current study, the research team further armed with VSVMP gene delivery vessel with Interleukin-12 (IL-12) - a protein known to recruit and switch on the cancer-killing functions of immune cells. The novel drug particles are based on Heparin-polyethyleneimine (HPEI) nanoparticles. To overcome the high toxicity and non-biocompatible nature of PEI, the team used a method to ...
The cytopathogenicity of vesicular stomatitis virus (VSV) has been attributed mainly to the host shut-off activity of the viral matrix (M) protein, which inhibits both nuclear transcription and nucleocytoplasmic RNA transport, thereby effectively suppressing the synthesis of type I interferon (IFN). The M protein from persistently VSV-infected cells was shown to harbour characteristic amino acid substitutions (M51R, V221F and S226R) implicated in IFN induction. This study demonstrates that infection of human fibroblasts with recombinant VSV containing the M51R substitution resulted in IFN induction, whereas neither the V221F nor the S226R substitution effected an IFN-inducing phenotype. Only when V221F was combined with S226R were the host shut-off activity of the M protein abolished and IFN induced, independently of M51R. The M33A substitution, previously implicated in VSV cytotoxicity, did not affect host shut-off activity. M-mutant VSV containing all four amino acid substitutions retained cytotoxic
Nasopharyngeal carcinoma (NPC) is a common cancer in Southern China and is closely associated with infection of Epstein-Barr virus (EBV). The EBV encoded latent membrane protein 1 (LMP1) is frequently detected in NPC and may play a role in its pathogenesis. Previous studies have shown that LMP1 transformed rodent fibroblasts and altered growth properties in B cells and epithelial cells. However, the pathological role of LMP1 in NPC cells is still poorly understood. In order to investigate the downstream target genes of LMP1 in NPC cells, suppression subtractive hybridization was used to clone and identify the genes differentially expressed in a LMP1 expressing NPC cell line, CNE-2. Two subtractive cDNA libraries were constructed: one enriched for the genes upregulated by LMP1 and one was for the genes downregulated by LMP1. A total of 192 clones were screened by reverse Northern blotting. Fourteen of them were confirmed to be overexpressed while eight of them were suppressed. The upregulation of ...
The EBV-encoded latent membrane protein 1 (LMP1) suppresses appoptosis in B lymphocytes through up-regulation of Bcl-2. However, the maximum induction of Bcl-2 by LMP1 takes about 48-72 h. We show in this report that up-regulation of the Bcl-2 homologue Mcl-1 by LMP1 preceded the induction of Bcl-2 and that the up-regulation was transient; therefore, Mcl-1 levels decreased when Bcl-2 levels started to increase. This finding supports the hypothesis that Mcl-1 functions as a rapidly inducible, short-term effector of cell viability. LMP1 also blocked the decline in the Mcl-1 levels in response to apoptotic stimulation triggered by elevated cyclic AMP. This effect of LMP1 was associated with a delayed cell death in the EBV-negative Burkitt lymphoma cell line BL41. The maintenance of Mcl-1 expression by LMP1 is likely to be a crucial immediate-early response that enables cells to survive until Bcl-2 can be up-regulated.. ...
Previously, we found in gastric cancers a significant association between EBV and p16 loss, as determined by IHC.40 This association was confirmed in our current set of tumours (p = 0.0001). Furthermore, the presence of EBV was highly associated with methylation of the CDKN2A promoter (p = 0.0003). In all cases but three, tumours were both negative by immunostaining and methylation positive. In one case, IHC could not be performed, but the tumour showed methylation. In another case, a tumour with methylation was p16 positive by IHC. Such an event could occur if methylation was present in only one allele of the gene. In the third case, no methylation was present, although p16 protein was not detected by IHC. Such results could be explained by gene inactivation by mutation or homozygous deletion.. Suppression of p16 expression associated with EBV infection or EBV proteins has been observed in other systems. In mouse embryo fibroblasts, EBV latent membrane protein 1 (LMP1) acts to prevent ...
HostPlay tailored standard VPS Server plans to the needs web application developers, businesses, and web hosting resellers. Ebola virus (EBOV) particles exit host cells by budding from the plasma membrane, a process j2ee web hosting service involves interaction between virus-encoded and cellular proteins 12 The viral matrix protein VP40 j2ee web hosting service a major component of EBOV virions and is necessary j2re the formation of the filamentous particles 34 Oligomerization of VP40 at the plasma membrane is required for assembly of particles and for virus budding 5-7 There is increasing evidence that many different viruses, including the filoviruses and retroviruses, use servkce proteins normally involved in the vacuolar protein sorting (vps) pathway for the final steps of budding 89 This requires movement of the vps proteins create httpserverutility instance multivesicular bodies to hostig plasma membrane, an event mediated or performed by viral proteins. Accordingly, channeling device 78 in ...
An investigation of properties of the influenza A virus M2 protein indicated that it is synthesized by 2 h postinfection together with other viral polypeptides and is transported to the infected-cell surface with a half-time of approximately 30 to 40 min. The available evidence suggests that M2 is not N-glycosylated even though it contains a potential glycosylation site, and the intracellular pattern of protein distribution includes localization to the Golgi apparatus. Proteolysis of intracellular microsome vesicles followed by immunoprecipitation with antiserum to a synthetic oligopeptide indicated that the M2 protein contains an extensive region of COOH-terminal amino acids exposed on the cytoplasmic side of the infected-cell membrane. A cDNA clone of the M2 mRNA was obtained and expressed in an SV40 recombinant vector. The M2 protein expressed by the vector became associated with the Golgi complex and was found on the surface of vector-infected cells. M2 is antigenically conserved among all ...
To study the phenotypic changes induced by gene products of EBV in B cells, we have made use of a conditional EBV-immortalized B-cell line in which the function of the viral gene product EBNA2 is controllable by estrogen. As expected, many of the activation markers and adhesion and costimulatory molecules were upregulated by EBV. Only a few of the surface markers studied (i.e., CD38, IgM, and HLA-A, -B, and -C) were found to be regulated in an opposite fashion, i.e., they were downregulated by viral gene products and upregulated when estrogen was withdrawn. Among the surface markers studied, CD83 attracted our particular attention because it was the only surface molecule that totally disappeared from the cell surface after estrogen withdrawal and rapidly reappeared after the addition of estrogen. The rapid time course of disappearance and reappearance of CD83 on the cell surface prompted us to study the mechanism of regulation of CD83 expression by viral gene products in more detail. The rapid ...
1EA3: Combined Results from Solution Studies on Intact Influenza Virus M1 Protein and from a New Crystal Form of its N-Terminal Domain Show that M1 is an Elongated Monomeric
Many EBV-associated cancers express virally-encoded transmembrane proteins. Two such proteins Latent Membrane Protein1 (LMP1) and Latent Membrane Protein 2 (LMP2) that play roles in oncogenesis. Both are multi-spanning transmembrane proteins, with a small extracellular region that is exposed on the surface of the infected cell. Our hypothesis is that the exposed extracellular regions of LMP1 and LMP2 could be targeted by cytotoxic T cells expressing chimeric antigen receptors (CARs). However, the development of CAR based therapies to target LMP-expressing malignancies are currently hampered by a lack of antibodies that recognize the extracellular domains of these proteins. Using a humanized mouse model, we are working to isolate human antibodies that specifically recognize the extracellular domains of membrane-anchored LMP1 and LMP2, and to convert these antibodies into chimeric antigen receptors that can be used to direct potent T-cell-mediated killing to EBV+ cancer cells.. ...
...   The M2 protein is a proton-selective ion channel protein, integral in the viral envelope of the influenza A virus. The channel itself is a
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Not clearly understood. Prevent the release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. In certain cases, prevent virus assembly during virus replication ...
TY - JOUR. T1 - The ebola virus matrix protein VP40 selectively induces vesiculation from phosphatidylserine-enriched membranes. AU - Soni, Smita P.. AU - Stahelin, Robert V.. PY - 2014/11/28. Y1 - 2014/11/28. N2 - Ebola virus is from the Filoviridae family of viruses and is one of the most virulent pathogens known with ∼60% clinical fatality. The Ebola virus negative sense RNA genome encodes seven proteins including viral matrix protein 40 (VP40), which is the most abundant protein found in the virions. Within infected cells VP40 localizes at the inner leaflet of the plasma membrane (PM), binds lipids, and regulates formation of new virus particles. Expression of VP40 in mammalian cells is sufficient to form virus-like particles that are nearly indistinguishable from the authentic virions. However, how VP40 interacts with the PM and forms virus-like particles is for the most part unknown. To investigate VP40 lipid specificity in a model of viral egress we employed giant unilamellar vesicles ...
pathogen (EBV) latent membrane proteins 2A (LMP2A) is certainly widely portrayed in EBV-infected cells inside the contaminated individual host and EBV-associated malignancies suggesting that LMP2A is essential for EBV latency persistence and EBV-associated tumorigenesis. B lymphocytes contaminated in vitro with EBV become immortalized building lymphoblastoid cell lines DMH-1 (LCLs). This technique constitutes an in vitro model for the contribution of EBV to B lymphoid disease. EBV gene appearance in LCLs is fixed to six nuclear antigens (EBNA1 -2 -3 -3 -3 and -LP) three essential membrane protein (latent membrane proteins 1 DMH-1 [LMP-1] -2 and -2B) two nonpolyadenylated RNAs. ...
Li, P. [李佩瑜]. (1999). The roles of latent membrane protein 1 of Epstein-Barr virus in cell growth, proliferation and survival in a rat fibroblast cell line. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_ ...
Epstein-Barr virus (EBV) infection is closely associated with nasopharyngeal carcinoma (NPC) and can be detected in early premalignant lesions of nasopharyngeal epithelium. The latent membrane protein 1 (LMP1) is an oncoprotein encoded by the EBV and is believed to play a role in transforming premalignant nasopharyngeal epithelial cells into cancer cells. RASSF1A is a tumor-suppressor gene commonly inactivated in many types of human cancer including NPC. In this study, we report a novel function of LMP1, in down-regulating RASSF1A expression in human epithelial cells. Downregulation of RASSF1A expression by LMP1 is dependent on the activation of intracellular signaling of NF-kappaB involving the C-terminal activating regions (CTARs) of LMP1. LMP1 expression also suppresses the transcriptional activity of the RASSF1A core promoter. RASSF1A stabilizes microtubules and regulates mitotic events. Aberrant mitotic spindles and chromosome aberrations are reported phenotypes in RASSF1A inactivated cells. In
Myeloid-derived suppressor cells (MDSCs) are expanded in tumor microenvironments, including that of Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC). The link between MDSC expansion and EBV infection in NPC is unclear. Here, we show that EBV latent membrane protein 1 (LMP1) promotes MDSC expansion in the tumor microenvironment by promoting extra-mitochondrial glycolysis in malignant cells, which is a scenario for immune escape initially suggested by the frequent, concomitant detection of abundant LMP1, glucose transporter 1 (GLUT1) and CD33+ MDSCs in tumor sections. The full process has been reconstituted in vitro. LMP1 promotes the expression of multiple glycolytic genes, including GLUT1. This metabolic reprogramming results in increased expression of the Nod-like receptor family protein 3 (NLRP3) inflammasome, COX-2 and P-p65 and, consequently, increased production of IL-1β, IL-6 and GM-CSF. Finally, these changes in the environment of malignant cells result in enhanced ...
Since the onset of antiviral therapy, viral resistance has compromised the clinical value of small-molecule drugs targeting pathogen components. As intracellular parasites, viruses complete their life cycle by hijacking a multitude of host-factors. Aiming at the latter rather than the pathogen directly, host-directed antiviral therapy has emerged as a concept to counteract evolution of viral resistance and develop broad-spectrum drug classes. This approach is propelled by bioinformatics analysis of genome-wide screens that greatly enhance insights into the complex network of host-pathogen interactions and generate a shortlist of potential gene targets from a multitude of candidates, thus setting the stage for a new era of rational identification of drug targets for host-directed antiviral therapies. With particular emphasis on human immunodeficiency virus and influenza virus, two major human pathogens, we review screens employed to elucidate host-pathogen interactions and discuss the state of database
There are no specific protocols for Recombinant Cytomegalovirus pp28 protein (ab43038). Please download our general protocols booklet
Gyulai, Zsófia and Endrész, Valéria and Burián, Katalin and Pincus, Steve and Toldy, József and Cox, William I. and Meric, Claude and Plotkin, Stanley and Gönczöl, Éva and Berencsi, Klára (2000) Cytotoxic T lymphocyte (CTL) responses to human cytomegalovirus pp65, IE1-exon4, gB, pp150, and pp28 in healthy individuals: Reevaluation of prevalence of IE1-specific CTLs. Journal of Infectious Diseases, 181. pp. 1537-1546. ISSN 0022-1899 (print), 1537-6613 (online) ...
Candidate and Environment: My career goal is to become a leading independent scientist in the field of herpesvirology. During the mentored phase of the Pathway...
Article Stap-2 negatively regulates both canonical and noncanonical nf-b activation induced by epstein-barr virus-derived latent membrane protein 1. The signal-transducing adaptor protein 2 (STAP-2) is a recently identified adaptor protein that conta...
TB stays a major reason for impairment and fatality worldwide as an approximated 8.6 million folks fell ill with TB as well as 1.3 million individuals pass
Reto Guler from the Division of Immunology & International Centre for Genetic Engineering and Biotechnolog at the IDM, UCT will present the MCB seminar with a talk entitled, Host-directed drug therapy for tuberculosis. ...
Complete information for MAS1 gene (Protein Coding), MAS1 Proto-Oncogene, G Protein-Coupled Receptor, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Sequence Variations of Latent Membrane Protein 2A in Epstein-Barr Virus-Associated Gastric Carcinomas from Guangzhou, Southern China. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
TY - JOUR. T1 - Specific binding of adamantane drugs and direction of their polar amines in the pore of the influenza M2 transmembrane domain in lipid bilayers and dodecylphosphocholine micelles determined by NMR spectroscopy. AU - Cady, Sarah D.. AU - Wang, Jun. AU - Wu, Yibing. AU - Degrado, William F.. AU - Hong, Mei. PY - 2011/3/30. Y1 - 2011/3/30. N2 - The transmembrane domain of the influenza M2 protein (M2TM) forms a tetrameric proton channel important for the virus lifecycle. The proton-channel activity is inhibited by amine-containing adamantyl drugs amantadine and rimantadine, which have been shown to bind specifically to the pore of M2TM near Ser31. However, whether the polar amine points to the N- or C-terminus of the channel has not yet been determined. Elucidating the polar group direction will shed light on the mechanism by which drug binding inhibits this proton channel and will facilitate rational design of new inhibitors. In this study, we determine the polar amine direction ...
Preface -- EBV latency -- Chap. 1. EBNA1 � Lori Frappier, University of Toronto, Canada -- Chap. 2. EBNA2 and its coactivator EBNA-LP � Bettina Kempkes, Helmholtz Center Munich, Germany, and Paul D. Ling, Baylor College of Medicine, Houston, USA -- Chap. 3. The EBNA3 family: two oncoproteins and a tumour suppressor that are central to the biology of EBV in B cells� Martin J. Allday, Quentin Bazot and Robert E. White, Imperial College London, UK. Chap. 4. The latent membrane protein 1 (LMP1) � Arnd Kieser and Kai R. Sterz, Helmholtz Center Munich, Germany. Chap. 5. Latent membrane protein 2 (LMP2) � Osman Cen and Richard Longnecker, Northwestern University, Chicago, USA. Chap. 6. EBV non-coding RNAs � Rebecca L. Skalsky and Bryan R. Cullen, Duke University, Durham, USA -- E. Lytic EBV infection -- 7. Viral entry � Liudmila S. Chesnokova, Ru Jiang1 and Lindsey M. Hutt-Fletcher, Louisiana State University, Shreveport, USA -- Chap. 8. Epstein Barr virus lytic cycle reactivation � ...
Cytomegalovirus Pp28, 1 mg. |span class=Body|CMV belongs to the Betaherpesvirinae subfamily of Herpesviridae which includes herpes simplex virustypes 1 and 2, varicella-zoster virus, and Epstein-Barrvirus.
T-bet:Eomes balance, effector function, and proliferation of cytomegalovirus-specific CD8+ T cells during primary infection differentiates the capacity for durable immune control.
Dendritic cells (DCs) are potent antigen-presenting cells that initiate protective T-cell immunity in mice. To study the immunogenicity of DCs in humans, we injected 9 healthy subjects subcutaneously with a control injection of autologous monocyte-derived, mature DCs, followed 4-6 weeks later by DCs pulsed with keyhole limpet hemocyanin (KLH), HLA-A*0201-positive restricted influenza matrix peptide (MP), and tetanus toxoid (TT). Four more subjects received these antigens without DCs. Injection of unpulsed DCs, or antigens alone, failed to immunize. Priming of CD4(+) T cells to KLH was observed in all 9 subjects injected with KLH-pulsed DCs, and boosting of TT-specific T-cell immunity was seen in 5 of 6 subjects injected with TT-pulsed DCs. Injection of antigen-pulsed DCs led to a severalfold increase in freshly isolated MP-specific, IFN-gamma-secreting CD8(+) T cells in all 6 HLA-A*0201-positive subjects, as early as 7 days after injection. When T cells were boosted in culture, there was an increase in
The recognition of an increased risk of certain malignancies in immunocompromised individuals has led to a growing understanding of the role of the immune system in the surveillance for and...
People react differently when they are diagnosed with a disease of chronic Epstein-Barr virus. Some depressed people, while others remain positive and hopeful. In fact, some people find that EBV disease using grow emotionally, making them stronger and more tolerant, more understanding.. Here are some methods that can help you better cope with the disease of chronic Epstein-Barr virus.. First, it is important that the expression of emotions. Be honest and admit your health, instead of pretending not to exist. People who communicate their feelings tend to need less treatment, and offers fewer symptoms and keep more independence and physical performance.. The next thing to do is to control. And more people to actively manage chronic Epstein-Barr virus themselves, the better they do. Set goals, such as what you eat, and how they stay fit, and how it will be easier to manage your stress, what supplements to take and what is much better than the passive acceptance of what the treatment is given for ...
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