摘要:
Sialyl Lewis X mimetics based on mannose glycosides are synthesized and shown to mimic the configuration and essential functional groups of sialyl Lewis X in space. The mannose based mimetics exhibit comparable biological activity as sialyl Lewis X in the E- selectin binding assay and can be employed for blocking neutrophil inflamatory conditions.
摘要:
Oligosaccharide compounds that are substrates and inhibitors of glycosyltransferase and glycosidase enzymes and compositions containing such compounds are disclosed. A method of glycosylation is also disclosed. An E. coli transformed with phagemid CMPSIL-1, which phagemid comprises a gene for a modified CMP-sialic acid synthetase enzyme, which transformed E. coli has the ATCC accession No. 68531 is also provided.
摘要:
Oligosaccharide compounds that are substrates and inhibitors of glycosyltransferase and glycosidase enzymes and compositions containing such compounds are disclosed. A method of glycosylation is also disclosed. An E. coli transformed with phagemid CMPSIL-1, which phagemid comprises a gene for a modified CMP-sialic acid synthetase enzyme, which transformed E. coli has the ATCC accession No. 68531 is also provided.
摘要:
Glycan arrays that can detect and distinguish between various sub-types and strains of influenza virus are provided. Methods for using the glycan arrays with assays using nanoparticle amplification technique are disclosed. Sandwich assays using gold nanoparticles conjugated to phage particles comprising influenza virus-specific antibodies for detecting multiple serotypes using a single reaction are provided. Plurality of glycans directed to specific target HA of influenza virus comprises the array. Detector molecules comprising noble metals conjugated to (a) phage display particles expressing antibodies against hemagglutinin and (b) neuraminidase binding agents are disclosed.
摘要:
Cellular receptors are identified that induce plasma leakage and other negative effects when infected with flaviviruses, such as dengue virus or Japanese encephamyelitis virus. Using fusion proteins disclosed herein, the receptors to which a pathogen, such as flavivirus, binds via glycan binding are determined. Once the receptors are determined, the effect of binding to a particular receptor may be determined, wherein targeting of the receptors causing a particular symptom may be targeted by agents that interrupt binding of the pathogen to the receptor. Accordingly, in the case of dengue virus and Japanese encephamyelitis virus, TNF-α is released when the pathogen binds to the DLVR1/CLEC5A receptor. Interrupting the DLVR1/CLEC5A receptor with monoclonal antibodies reduced TNF-α secretion without affecting secretion of cytokines responsible for viral clearance thereby increasing survival rates in infected mice from nil to around 50%.
摘要:
Methods for identifying agents capable of disrupting a salt bridge in an influenza A virus nucleoprotein corresponding to the E339 . . . R416 salt bridge in SEQ ID NO:1, and thus the trimerization of the NP protein; and uses of such agents, e.g., small molecules and peptides, for inhibiting influenza virus replication and treating infection caused by influenza virus.
摘要:
Methods for metabolic oligosaccharide engineering that incorporates derivatized alkyne-bearing sugar analogs as “tags” into cellular glycoconjugates are disclosed. Alkynyl derivatized Fuc and alkynyl derivatized ManNAc sugars are incorporated into cellular glycoconjugates. Chemical probes comprising an azide group and a visual or fluorogenic probe and used to label alkyne-derivatized sugar-tagged glycoconjugates are disclosed. Chemical probes bind covalently to the alkynyl group by Cu(I)-catalyzed [3+2] azide-alkyne cycloaddition and are visualized at the cell surface, intracellularly, or in a cellular extract. The labeled glycoconjugate is capable of detection by flow cytometry, SDS-PAGE, Western blot, ELISA, confocal microscopy, and mass spectrometry.
摘要:
Novel 5-membered iminocyclitol derivatives were found to be a potent and selective inhibitors of the glycoprotein processing α- and β-glucosidase which were further found to be active antiviral agents against Japanese encephalitis virus, dengue virus serotype 2 (DEN-2), human SARS coronavirus and human β-hexosaminidase, a new target for development of osteoarthritis therapeutics.
摘要:
The present disclosure relates to the discovery of methods of isolating subfractions of an F3 Reishi extract, and of administration of these novel isolates to eukaryotic cells in order to induce certain immumodulatory, hematopoeitic and tumor-inhibiting phenotypic changes in those eukaryotic cells, mediated through particular toll-like receptor (TLR) and other transmembrane receptors. F3 subfractions F301 and F331 have demonstrated that F331 is capable of activating at least TLR-2 while F301 is capable of activating at least TLR-2, TLR-4, and TLR-5.
摘要:
The disclosure provides fusion proteins comprising a carbohydrate recognition domain of an innate immunity receptor and a heterologous polypeptide. The fusion proteins of the disclosure may be used, for example, to fingerprint polysaccharide compositions and to purify polysaccharide compositions. Polysaccharide compositions include those isolated from Ganoderma lucidum (Reishi). The methods and reagents of the disclosure may also be used to identify innate immunity receptors and cell types that bind to polysaccharide compositions (including polysaccharide compositions associated with pathogens), whereupon modulators of the identified receptors can then be obtained. The fusion proteins also may be used to inhibit the interaction between a polysaccharide composition and an innate immunity receptor on a cell surface. The methods and reagents of the disclosure are used in one example to determine that the DLVR1 innate immunity receptor on macrophages interacts with Dengue virus (DV), and that DLVR1 is responsible for DV-mediated secretion of proinflammatory cytokines from macrophages. The disclosure also provides DVLR1 antibodies that prevent the secretion of proinflammatory cytokines by DV-infected macrophages.