53 results about "Nuclear factor kappa b" patented technology

The diterpenic labdane 3-[2-[decahydro-6-hydroxy-5-(hydroxymethyl)-5,ha-dimethyl-2-methylene-1-naphthalenyl]ethylidene]-dihydro-4-hydroxy-2(3h)-furanone, chemically diagrammed as

inhibits the synthesis of pro-inflammatory cytokines, activates the PPAR-gamma receptor and diminishes nuclear factor kappa B. The compound is useful to treat auto-immune diseases, for organ and tissue transplantation, and to treat immunodeficiency (e.g., AIDS).

The present invention relates to the field of infection and inflammation and, more specifically, to the field of pathogen-induced nuclear factor kappa B activation. More specifically, a novel splice variant of MyD88, (MyD88_S), which has been identified encoding a protein that inhibits LPS-induced NF-κB activation. MyD88_S is a target to inhibit the phenomenon of endotoxin-tolerance that occurs in sepsis.

The invention discloses antibodies that bind high specificity to human RANKL (Receptor Activator for Nuclear Factor kappa B Ligand), wherein, the antibodies are used for the treatment of bone erosion caused by astogeny, hormonotherapy, postmenopausal osteoporosis, bone metastasis, and inflammation. The invention also discloses DNA sequences and supposed amino acid sequences of the antibodies.

The invention provides an RANKL-TNF (Receptor Activator of Nuclear Factor Kappa-B Ligand-Tumour Necrosis Factor) sample region fusion protein, and in particular relates to a fusion protein of an RANKL-TNF sample region protein and a Th2 cell epiposition segment with broad host range property. An experiment shows that an antibody produced by an RANKL-TNF sample region fusion protein immune mouse has the effect of combining RANKL with TNF-alpha, can be used for treating diseases such as rheumatoid arthritis and the like and can play effects of antagonistic bone destruction and inflammation inhibition. The RANKL-TNF sample region fusion protein disclosed by the invention can be used as a therapeutic vaccine and provides a new therapeutic approach and thinking for the diseases such as rheumatoid arthritis and the like. According to the invention, the RANKL-TNF sample region fusion protein is expressed in vitro, and therefore the method has the advantages of high expression yield, strong controllability and relatively low production cost;, and the product has good immunogenicity and is easy to realize mass production.

The invention relates to a preparation method for nacre protein N16 and the application of the nacre protein N16 in preparation of drugs for prevention or treatment of orthopedic diseases such as osteoporosis and fracture. The nacre protein N16 is expressed in bacteria by using the method of genetic recombination, and a separation and purification scheme of the nacre protein N16 is established. The experiments of cells and animals prove that the nacre protein N16 can inhibit receptor activator of nuclear factor kappa B ligand (RANKL) from inducing the proliferation and the differentiation of osteoclast precursors RAW 264.7 cells, promotes the differentiation and the maturation of precursor osteoblast MC3T3-E1 cells, enhances the mineralization function of osteoblasts, treat the osteoporosis caused by ovariectomizing, and can be used in the preparation of drugs used for the prevention or the treatment of orthopedic diseases such as the osteoporosis and the fracture.

The invention relates to application of dendrobium officinale polysaccharides in preparation of harm-reducing cigarettes. Harm reduction means reducing risks of lung inflammation caused by smoking. The harm-reducing cigarettes are prepared by dissolving the dendrobium officinale polysaccharides by utilizing water, evenly spraying the dendrobium officinale polysaccharides on cut tobaccos, naturally airing the cut tobaccos, and then rolling the cigarettes according to regular cigarette rolling technology. The application of dendrobium officinale polysaccharides in preparation of harm-reducing cigarettes can reduce the occurrence rate of lung inflammation caused by smoking and reduce expression of kinase beta (IKKbeta) of a lung tissue nuclear factor Kappa B(NF-kB) inhibitor caused by smoking.

The invention relates to a medicament for treating neurodegenerative diseases and particularly relates to an application of chitosan oligosaccharide in preparation of medicaments for preventing and/or treating neurodegenerative diseases, i.e., the chitosan oligosaccharide can be further applied to the medicaments for preventing and/or treating the neurodegenerative diseases. According to the medicament and the application thereof, with lipopolysaccharide (LPS) as an inducing factor and mouse microglia as a research object, a result shows that the chitosan oligosaccharide can remarkably restrict the expression of the activated microglia iNOS (Inducible Nitric Oxide Synthase) in mRNA (Messenger Ribonucleic Acid) and protein level, can restrict the generation of activated microglia NO (Nitric Oxide), can effectively restrict the generation of activated microglia ROS (Reactive Oxygen Species), can effectively restrict the activation of an MAPK (Mitogen Activated Protein Kinase) signal channel caused by LPS, and can effectively restrict the activation of transcription factor NF-kB (Nuclear Factor-Kappa B) and AP-1 (Activator Protein-1).

The present invention relates to nuclear factor-kappa B p65 subunit antagonisbic peptide and its application, and is especially one group of nuclear factor-kappa B (NF-p65 kappa B) p65 subunit antagonisbic peptide for treating. More particularly, the present invention is one group of small molecular peptides capable of combining specifically with nuclear factor-kappa B p65 subunit. The present invention also relates to the preparation and application of these nuclear factor-kappa B p65 subunit antagonisbic peptides.

Interaction of Rel proteins and steroid receptors is known to result in repression of target genes. Here we describe the discovery of a new mechanism in which Rel proteins and steroid receptors act synergistically to activate a regulatory element. This mechanism is shown to influence the expression of the brain-specific 5HT1A receptor wherein the estrogen receptor acts synergistically with the Nuclear Factor kappa B to enhance the activity of the promoter for the 5HT1A receptor gene. In addition, synergistic effects of Rel proteins with the mineralocorticoid receptor were observed, showing that synergism with Rel proteins may be expected for other steroid receptors as well. The synergism between Rel proteins and estrogen receptor or mineralocorticoid receptor provides a tool for the development of compounds that interact with the estrogen or mineralocorticoid receptor in such a way that only the synergistic effect is modulated whereas other effects are left intact. Such compounds would be invaluable for the development of medicaments for the treatment of diseases of the central nervous or cardiovascular system and other disorders in which Rel proteins play a role.

The invention discloses a mouse RANKL (Receptor Activator of Nuclear Factor Kappa B Ligand) mutant as well as establishment, expression and application of an expression carrier of the mutant, provides the mouse RANKL mutant, an establishment method of the expression carrier of the mouse RANKL mutant, and a preparation method for transfecting the expression carrier of the mouse RANKL mutant into a cell, and further provides a cell and an expression system for expressing the expression carrier of the mouse RANKL mutant. The problem in the prior art that the mouse RANKL cannot be conveniently and efficiently studied is solved.

Previously we have identified a conserved domain (SAP, for SAF-A/B, Acinus, and PIAS) in the foot-and-mouth disease virus (FMDV) leader (L) protein coding region that is required for proper sub-cellular localization and function. Mutation of isoleucine 55 and leucine 58 to alanine (I55A, L58A) within the SAP domain resulted in a viable virus that displayed a mild attenuated phenotype in cell culture, along with altered sub-cellular distribution of L and failure to induce degradation of the transcription factor nuclear factor kappa-B. Here we report that inoculation of swine and cattle with this mutant virus results in the absence of clinical disease, the induction of a significant FMDV-specific neutralizing antibody response, and protection against subsequent homologous virus challenge. Remarkably, swine vaccinated with SAP mutant virus are protected against wild type virus challenge as early as two days post-vaccination suggesting that a strong innate as well as adaptive immunity is elicited. This variant could serve as the basis for construction of a live-attenuated FMD vaccine candidate.

The present invention relates to a use of ZFP91 based on the functions of ZFP91 (Zinc Finger Protein 91) and the interaction of ZFP91 with NF-κB (Nuclear factor kappa B) signal transduction pathway proteins, more precisely a method to inhibit the activation of NF-κB alternative pathway by regulating ZFP91 activation, to inhibit tumor growth by inhibiting the transcription factor HIF-1 (hypoxia inducible factor-1) activation, to inhibit cancer malignancy by inhibiting angiogenesis, or reversely a method to increase the activation of NF-κB alternative pathway or to increase angiogenesis by increasing activation of HIF-1. The method of regulating ZFP91 activation of the present invention can increase or reduce HIF-1α stability by increasing or reducing the activation of NF-κB alternative pathway, so that it can be effectively used for the development of an anticancer agent, a therapeutic agent for arthritis, a therapeutic agent for ulcerative colitis, an anti-inflammatory agent and an angiogenesis inducer.

There is described a therapeutic agent capable of directly or indirectly having an effect on the proteins N-methyl-D-aspartate (NMDA), Cyclooxygenase-2 (COX-2), Tumour Necrosis factor alpha (TNF-a), Nuclear factor-kappa B (NFKB), Cyclin-dependent kinases, e.g. CDK2/A and CDK5/p25, Histone acetyltransferase (HAT) and Farnesyltransferase, simultaneously, sequentially or separately. There is especially described dexanabinol, or a derivative thereof, as the therapeutic agent.

The invention provides a constructing object for expressing receptor activator of nuclear factor kappa B ligand (RANKL)-HBaAg recombinant protein and a preparation method thereof. The constructing object comprises 1 to 15 expression boxes, wherein each expression box comprises an initiating signal element alternative oxidase (AOX) (a), RANKL-HBsAg recombinant protein coding sequences (b) and a termination signal element AOX (TT). The invention also provides yeast cells, virus-like particles and a purpose of the particles, wherein the yeast cells comprise the constructing object, the virus-like particles are generated by the yeast cells and comprise the RANKL-HBsAg recombinant protein. The yeast cells constructed in the invention can be used for generating a large amount of RANKL-HBsAg recombinant protein, so the RANKL-HBsAg recombinant protein is used for treating or preventing diseases or symptoms such as osteoporosis and the like relative to RANK/RANKL/ osteoprotegerin (OPG) systems.

The invention relates to an anti-inflammatory peptide with membrane penetration effect, in particular to a mutant peptide which is used for treatment and takes a nuclear factor-kappa B (NF-kappa B) rho65 subunit antagonistic peptide as a matrix. The mutant peptide has membrane penetration effect. More particularly, the invention relates to a small molecular peptide Lys(D-Pro)ValCit which not only can antagonize the activity of a nuclear factor-kappa B rho65 subunit, but also can act on other unknown targets. The invention also relates to the preparation and application of the anti-inflammatory peptide.

The invention discloses a new application of isopentene-based flavonoids compound IAA (isoangustone A) in a drug. The new application disclosed by the invention is as follows: pharmaceutically acceptable salt, ester, solvolyte, stereoisomers, tautomers, prodrugs and a mixture of the salt, the ester, the solvolyte, the stereoisomers, the tautomers and prodrugs are applied in the following aspects: 1) preparing an anti-inflammatory bowel disease drug; 2) preparing a drug for preventing and/or treating colorectal cancer; 3) preparing an eucaryon colorectal cancer cell apoptosis inducer; and 4) preparing an NF-kB (nuclear factor-kappa B) signal inhibitor. The compound IAA can obviously induce the colon cancer cell apoptosis, and inhibit the activity of colon cancer cell and inflammation signals, and also can obviously alleviate the colon inflammation induced by dextran sulfate.

The invention discloses a mouse model capable of the monitoring activity of IFN-beta (interferon-beta) or NF-kappa B (nuclear factor-kappa B) in a liver via living imaging and a construction method for the same. According to the construction method disclosed by the invention, the mouse model integrating the firefly luciferase (Fluc) reporter gene which is regulated and expressed by IFN-beta promoter or NF-kappa B gene into the liver of a mouse is obtained by constructing a recombinant vector carrying bacteriophage integrase recognition site attB gene, the IFN-beta promoter or the NF-kappa B gene and the firefly luciferase (Fluc) reporter gene, and leading the recombinant vector into the body of the mouse by a hydrodynamic method. The mouse model disclosed by the invention can be used for evaluating the regulation effects of different factors on the activity of the IFN-beta promoter or the NF-kappa B in the body, can also be used as an evaluation model for interferon or inflammatory factor regulation medicines, molecules and viruses in innate immunity, and can be widely applied to the biomedical animal experiments of various categories.