12 results about "Dominant negative" patented technology

Disclosed are compositions comprising dominant negative chimeric tumor necrosis factor receptor 1 (TNFR1) fusion proteins and methods for use in cell therapies.

The method as disclosed herein utilizes a high throughput screening assay (GigaAssay) to produce a comprehensive mutation effect on gene activity (MEGA)-mutation activity profile (Map). The methods as disclosed herein can be used to assess the mutational effect for any gene, under any condition (e.g., drug treatment) with any assay in mammalian cells in culture. Thus, the methods provided herein can be utilized to discover and screen dominant negative variants, and provide a reliable solution to the problem of identifying unique pharmacologically active variants of proteins. Furthermore, the method provided herein can be integrated to cell-based assays to investigate disease pathology and test potential drugs.

To provide, in part, methods and compositions for selectively editing a genome to create a dominant negative allele or a dominant positive allele.SOLUTION: The present disclosure provides methods and compositions for generating dominant alleles using targeted editing technologies. Also provided are modified chromosomes, cells, tissues, and plants comprising a modified dominant allele.SELECTED DRAWING: Figure 1

The present invention relates to a population of small extracellular vesicles (sEVs) for use in the treatment of obesity in a subject in need thereof, wherein the sEVs comprise at least one polynucleotide encoding a D168A dominant negative AMP-activated protein kinase alpha 1 (AMPKa1-DN) mutant protein operably linked and under the control of a steroidogenic factor 1 (SF1) promoter, wherein the sEVs are engineered to transiently express in their outer membrane at least one fusion protein comprising the neurotrophic rabies virus (RVG) peptide fused to lysosome-associated membrane protein 2b. Said population is highly safe and effective, as the sEVs, when administered systematically, are capable of exerting their effect in the SF1 expressing neurons located in the ventromedial nucleus of the hypothalamus.

A composition including modified ASFV outer-membrane protein antigen mutants (termed dominant negative toxoid antigens) that exhibit non-binding affinity to RBCs while inducing an antibody-mediated response capable of neutralizing unmodified proteins found on infectious outer-membrane-laden ASFV virions. A method for the treatment and / or prevention of ASFV by administering a dominant negative toxoid antigenic composition to animals, thereby averting RBC aggregation caused by the antigen and concurrently treating and / or preventing ASFV. An ASFV vaccine composition including dominant negative toxoid antigens. A composition including dominant negative toxoid antigens in conjunction together and in conjunction with antigens derived from capsid-based proteins, which collectively target both lysogenic and lytic viral replication cycles, thereby achieving optimal immune stimulatory protection. Methods and compositions allowing for differentiation of infected from vaccinated animals (DIVA).

This invention discloses the soybean dominant negative-effect allele Gmspp-D and its application. Two dominant negative-effect alleles Gmspp-D (Gmspp-D-CDS-1 and Gmspp-D-CDS-2) regulating soybean pubescence density were cloned and overexpression vectors were constructed. Stable overexpression lines were obtained by transforming these vectors into the soybean cultivar Williams82 (W82). Compared to the control material W82, overexpression of both dominant negative-effect alleles significantly reduced soybean pubescence density, thus validating the function of the target genes. This invention provides the application of the soybean dominant negative-effect allele Gmspp-D in regulating plant pubescence density and demonstrates the feasibility and efficiency of constructing dominant negative-effect mutants for rapid gene function studies, showing promising application prospects in the field of breeding technology.

There is provided a therapeutic nucleic acid capable of binding to a target indel allele associated with a pathogenic allele, wherein the pathogenic allele causes a dominant negative genetic disorder or gain-of function genetic disorder, and wherein the disorder is not Huntington's disease. There is further provided a conjugate, delivery particle, and pharmaceutical composition thereof and their uses. There is further provided a therapeutic nucleic acid which is capable of binding to a target indel allele of an intronic indel selected from: rs59464879, rs751205475 and rs78373442 associated with a pathogenic HTT allele which causes Huntington's disease, and uses thereof.

The present disclosure is directed to an engineered protein (e.g., a chimeric protein) comprising one or more of an extracellular domain, a transmembrane domain and / or an intracellular domain, which are capable of binding a negative signal and functioning as a sink, dominant negative, or signal inverter for the negative signal. The disclosure is further directed to methods of generating a modified cell expressing one or more of the engineered proteins (e.g., chimeric proteins), and methods of using the modified cells in treating a disease or a condition in a subject in need thereof.

A composition including modified ASFV outer-membrane protein antigen mutants (termed dominant negative toxoid antigens) that exhibit non-binding affinity to RBCs while inducing an antibody-mediated response capable of neutralizing unmodified proteins found on infectious outer-membrane-laden ASFV virions. A method for the treatment and / or prevention of ASFV by administering a dominant negative toxoid antigenic composition to animals, thereby averting RBC aggregation caused by the antigen and concurrently treating and / or preventing ASFV. An ASFV vaccine composition including dominant negative toxoid antigens. A composition including dominant negative toxoid antigens in conjunction together and in conjunction with antigens derived from capsid-based proteins, which collectively target both lysogenic and lytic viral replication cycles, thereby achieving optimal immune stimulatory protection. Methods and compositions allowing for differentiation of infected from vaccinated animals (DIVA).

Compositions and methods for reducing one or more symptoms associated with fibrosis are disclosed. The compositions include one or more agents that inhibit SUN2 expression or activity, directly, or indirectly. The composition includes one or more functional nucleic acids that inhibit the production or stability of SUN2, CTDNEP1, and / or NEP1R1. In some forms, the compositions include a dominant negative protein or peptide to disrupt SUN2 function, including dominant negative truncations of Sun or Nesprin proteins In some forms the composition is a gene editing composition targeting SUN2, CTDNEP1, and / or NEP1R1. The compositions can include nucleic acids and / or small molecule activators that increase expression of CK2. The compositions can be administered to a subject in need thereof to treat one or more conditions in which fibrosis is implicated.

Provided herein are nucleic acids containing dominant negative STING alleles and compositions containing the same. Further provided are methods of using the nucleic acids containing dominant negative STING alleles for treating STING-associated vasculopathy with onset in infancy (SAVI). Also provided are methods of delivering the nucleic acids containing dominant negative STING alleles to treat STING-mediated conditions or diseases in human subjects in need thereof.