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30 results about "Dominant-Negative Mutant" patented technology
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A dominant-negative mutation usually means that the resulting protein is has lost a certain part of its function (negative), but it can out-compete the endogenous protein in some way (dominant).
Disclosed are mutantCDK inhibitor (CKI) polypeptides having dominant negativeantagonist activity against wild-type CKI proteins, as well as related compositions, including nucleic acids and vectors encoding the mutant CKI polypeptides and transformed host cells and transgenic plants comprising such nucleic acids and vectors. Also disclosed are related methods for using the mutant proteins to modulate cell division in cells, particularly plant cells.
The invention provides mutant forms of pore-forming toxins. These mutant toxins may be used in vaccines for the prevention of bacterial infection. Additionally, dominant negative mutants may be administered as therapeutics for the treatment of bacterial infection.
The invention relates to plants and plant cells which have a transient or permanent virus resistance as a result of modulation of the gene expression and / or binding behavior of vegetable DnaJ-like proteins. The invention also relates to methods for the production of transgenic plants with increased virus resistance, wherein the expression of vegetable DnaJ-like proteins which interact with viral components is substantially prevented by silencing the DnaJ-like proteins. The invention further relates to methods for the production of transgenic plants with increased virus resistance, wherein the interaction of viral components with vegetable DnaJ-like proteins is substantially prevented by expression of dominant-negative mutants of the DnaJ-like proteins, by antibodies against DnaJ-like proteins or by specific inhibitors.
The present invention provides a genetically modified plant that biosynthesizes an increased amount of capsinoids, a method of producing the genetically modified plant, and a production method of capsinoids from the genetically modified plant. More particularly, the present invention provides a genetically modified plant capable of producing capsinoids, which shows a decreased expression or activity of an enzyme that catalyzes an amino group conversion reaction from vanillin to vanillylamine as compared to wild strains, and the like. As a method of suppressing expression or activity of an enzyme, an introduction of DNA encoding an antisense RNA, iRNA, ribozyme or dominant-negative mutant for the target gene, a destruction of the gene by a knockout method, mutagen treatment or transposon insertion, an introduction of a gene encoding an antibody against the enzyme and the like can be mentioned.
Disclosed are mutantCDK inhibitor (CKI) polypeptides having dominant negativeantagonist activity against wild-type CKI proteins, as well as related compositions, including nucleic acids and vectors encoding the mutant CKI polypeptides and transformed host cells and transgenic plants comprising such nucleic acids and vectors. Also disclosed are related methods for using the mutant proteins to modulate cell division in cells, particularly plant cells.
The invention provides a reporter gene carrier which comprises an AP2alpha specific cis acting element. The carrier is characterized in that the AP2alpha specific cis acting element consists of four GCCCGCGG nucleotide sequences connected in series, wherein the four GCCCGCGG nucleotide sequences are connected in series through a nucleotide sequence TT. The reporter gene carrier designed by the invention is easy to prepare, simple to operate and good in repeatability, and can effective transfect different mammalian cells. The carrier is more accurate and reliable than EMSA (Electrophoretic Mobility Shift Assay) when is used to detect activity change of a dominant negativemutant-mediated transcription factor. The carrier is suitable for in vitro study of biological activity of the AP2alpha transcription factor in various mammalian cells.
Anti-cytokine therapy has revolutionized immunological disease treatment, but is not always effective and subject to treatment resistance as the cytokinecascade is highly redundant and multiple cytokines are involved in inflammation. Targeting a critical common regulator of inflammatory effectors is desirable. Lipopolysaccharide (LPS)-responsive beige-like anchor (LRBA) is a master regulator of multiple genes important for inflammation. Subcellular localization shows that LRBA translocated to the nucleus upon LPS stimulation and colocalized with multiple proteins associated with the endosome membrane system, indicating a critical role in membrane / vesicle trafficking essential for deposition, secretion and signal transduction of immune effectors. Deregulation, deficiency, down-regulation and overexpression of LRBA causes defective trafficking and signaling of immune effector molecules, resulting in immunodeficiency and autoimmunity diseases associated with a broader spectrum of severe symptoms when compared to other CVID genes. Modulating LRBA through antibodies, dominant negative mutants, or small interference RNA can be used to treat inflammatory diseases.
The present invention provides a genetically modified plant that biosynthesizes an increased amount of capsinoids, a method of producing the genetically modified plant, and a production method of capsinoids from the genetically modified plant. More particularly, the present invention provides a genetically modified plant capable of producing capsinoids, which shows a decreased expression or activity of an enzyme that catalyzes an amino group conversion reaction from vanillin to vanillylamine as compared to wild strains, and the like. As a method of suppressing expression or activity of an enzyme, an introduction of DNA encoding an antisense RNA, iRNA, ribozyme or dominant-negative mutant for the target gene, a destruction of the gene by a knockout method, mutagen treatment or transposon insertion, an introduction of a gene encoding an antibody against the enzyme and the like can be mentioned.
The invention provides a nontoxic anthrax live vaccine.The active ingredient of the nontoxic anthrax live vaccine includes a nontoxic anthrax strain for expressing anthrax protective antigenmutantprotein (rPA).The nontoxic anthrax strain is obtained by performing locus mutation on pXO1 plasmid of an original Sterne vaccine strain, and locus mutation covers R178A and K197A double-locus mutants of a protective antigen.The live vaccine is prepared from the strain including the PA dominant negative mutants of the protective antigen, and has the advantages that the live vaccine loses the capability of being combined with lethal factors and edema factors, toxins cannot be generated, and it is proved that the immunogen of the live vaccine is not changed at all; meanwhile, biologically-inactivated rPA can be in competitive combination with cell receptors, and the purpose of neutralizing anthrax toxins can be achieved.The mutant strain completely loses the sporeforming function, the vaccine standard requirements for not harming operators and not causing environment pollution are met, subcutaneous injection and oral administration can be selected as administration routes, and the defect that a Sterne vaccine strain is not suitable for certain livestock due to large residual toxicity is overcome.
Anti-cytokine therapy has revolutionized immunological disease treatment, but is not always effective and subject to treatment resistance as the cytokinecascade is highly redundant and multiple cytokines are involved in inflammation. Targeting a critical common regulator of inflammatory effectors is desirable. Lipopolysaccharide (LPS)-responsive beige-like anchor (LRBA) is a master regulator of multiple genes important for inflammation. Subcellular localization shows that LRBA translocated to the nucleus upon LPS stimulation and colocalized with multiple proteins associated with the endosome membrane system, indicating a critical role in membrane / vesicle trafficking essential for deposition, secretion and signal transduction of immune effectors. Deregulation, deficiency, down-regulation and overexpression of LRBA causes defective trafficking and signaling of immune effector molecules, resulting in immunodeficiency and autoimmunity diseases associated with a broader spectrum of severe symptoms when compared to other CVID genes. Modulating LRBA through antibodies, dominant negative mutants, or small interference RNA can be used to treat inflammatory diseases.