179 results about "Nuclear protein" patented technology

Disclosed are methods of producing eukaryotic disulfide bond-containing polypeptides in bacterial hosts, and compositions resulting therefrom. Co-expression of a eukaryotic foldase and a disulfide bond-containing polypeptide in a bacterial host cell is demonstrated. In particular embodiments, the methods have been used to produce mammalian pancreatic trypsin inhibitor and tissue plasminogen activator (tPA) in soluble, biologically-active forms, which are isolatable from the bacterial periplasm. Also disclosed are expression systems, recombinant vectors, and transformed host cells.

Disclosed and claimed are methods of non-invasive genetic immunization in an animal and/or methods of inducing a systemic immune or therapeutic response in an animal, products therefrom and uses for the methods and products therefrom. The methods can include contacting skin of the animal with a vector in an amount effective to induce the systemic immune or therapeutic response in the animal. The vector can include and express an exogenous nucleic acid molecule encoding an epitope or gene product of interest. The systemic immune response can be to or from the epitope or gene product. The nucleic acid molecule can encode an epitope of interest and/or an antigen of interest and/or a nucleic acid molecule that stimulates and/or modulates an immunological response and/or stimulates and/or modulates expression, e.g., transcription and/or translation, such as transcription and/or translation of an endogenous and/or exogenous nucleic acid molecule; e.g., one or more of influenza hemagglutinin, influenza nuclear protein, tetanus toxin C-fragment, anthrax protective antigen, HIV gp 120, human carcinoembryonic antigen, and/or a therapeutic, an immunomodulatory gene, such as co-stimulatory gene and/or a cytokine gene. The immune response can be induced by the vector expressing the nucleic acid molecule in the animal's cells. The immune response can be against a pathogen or a neoplasm. A prophylactic vaccine or a therapeutic vaccine or an immunological composition can include the vector.

Disclosed and claimed are methods of non-invasive genetic immunization in an animal and/or methods of inducing a systemic immune or therapeutic response in an animal, products therefrom and uses for the methods and products therefrom. The methods can include contacting skin of the animal with a vector in an amount effective to induce the systemic immune or therapeutic response in the animal. The vector can include and express an exogenous nucleic acid molecule encoding an epitope or gene product of interest. The systemic immune response can be to or from the epitope or gene product. The nucleic acid molecule can encode an epitope of interest and/or an antigen of interest and/or a nucleic acid molecule that stimulates and/or modulates an immunological response and/or stimulates and/or modulates expression, e.g., transcription and/or translation, such as transcription and/or translation of an endogenous and/or exogenous nucleic acid molecule; e.g., one or more of influenza hemagglutinin, influenza nuclear protein, influenza M2, tetanus toxin C-fragment, anthrax protective antigen, anthrax lethal factor, rabies glycoprotein, HBV surface antigen, HIV gp 120, HIV gp 160, human carcinoembryonic antigen, malaria CSP, malaria SSP, malaria MSP, malaria pfg, and mycobacterium tuberculosis HSP; and/or a therapeutic, an immunomodulatory gene, such as co-stimulatory gene and/or a cytokine gene. The immune response can be induced by the vector expressing the nucleic acid molecule in the animal's cells. The animal's cells can be epidermal cells. The immune response can be against a pathogen or a neoplasm. A prophylactic vaccine or a therapeutic vaccine or an immunological composition can include the vector. The animal can be a vertebrate, e.g., a mammal, such as human, a cow, a horse, a dog, a cat, a goat, a sheep or a pig; or fowl such as turkey, chicken or duck. The vector can be one or more of a viral vector, including viral coat, e.g., with some or all viral genes deleted therefrom, bacterial, protozoan, transposon, retrotransposon, and DNA vector, e.g., a recombinant vector; for instance, an adenovirus, such as an adenovirus defective in its E1 and/or E3 and/or E4 region(s). The method can encompass applying a delivery device including the vector to the skin of the animal, as well as such a method further including disposing the vector in and/or on the delivery device. The vector can have all viral genes deleted therefrom. The vector can induce a therapeutic and/or an anti-tumor effect in the animal, e.g., by expressing an oncogene, a tumor-suppressor gene, or a tumor-associated gene. Immunological products generated by the expression, e.g., antibodies, cells from the methods, and the expression products, are likewise useful in in vitro and ex vivo applications, and such immunological and expression products and cells and applications are disclosed and claimed. Methods for expressing a gene product in vivo and products therefor and therefrom including mucosal and/or intranasal administration of an adenovirus, advantageously an E1 and/or E3 and/or E4 defective or deleted adenovirus, such as a human adenovirus or canine adenovirus, are also disclosed and claimed.

A human synthetic peptide-based influenza vaccine for intranasal administration comprises a mixture of flagella containing at least four epitopes of influenza virus reactive with human cells, each expressed individually in Salmonella flagellin, said influenza virus epitopes being selected from the group consisting of: (i) one B-cell hemagglutinin (HA) epitope; (ii) one T-helper hemagglutinin (HA) or nucleo-protein (NP) epitope that can bind to many HLA molecules; and (iii) at least two cytotoxic lymphocyte (CTL) nucleoprotein (NP) or matrix protein (M) epitopes that are restricted to the most prevalent HLA molecules in different human populations.

Abstract of the Disclosure Methods of identifying agents which alter the NAD-dependent acetylation status and mono-ADP-ribosylation of nuclear proteins are disclosed. The methods further include identifying agents which alter the life span or aging of a cell or an organism by determining the level of NAD-dependent acetylation and/or ADP ribosylation of a nuclear protein. The invention also relates to a mammalian Sir2 protein which acetylates or deacetylates nuclear proteins in a NAD-dependent manner and has mono-ADP-ribosyltransferase activity. Host cells producing the Sir2 protein and antibodies to the Sir2 protein are also provided.

The present invention relates to immunogenic but non-depositing-forming polypeptides or peptides homologous to amyloid β, prion, amylin or α-synuclein which can be used alone or conjugated to an immunostimulatory molecule in an immunizing composition for inducing an immune response to amyloid β peptides and amyloid deposits, to prion protein and prion deposits, to amylin and amylin deposits, to α-synuclein and deposits containing α-synuclein, or to polyglutamine repeats and deposits of proteins containing polyglutamine repeats. Described are also antibodies directed against such peptides, their generation, and their use in methods of passive immunization to such peptides and deposits.

A modified P. aeruginosa type III secretion system has been developed that efficiently delivers selected proteins into a host cell. In one example, a functional nuclear Cre Recombinase is injected into embryonic stem (ES) cells and can be used to induce pluripotent stem (iPS) cells. This method of in vitro lineage directed differentiation prevents insertional mutagenesis and provides a route to selected stem cell renewal and cell-based therapies.

The present invention provides modified erythrocytes which comprise viral receptor proteins capable of mediating entry of respective viruses into the modified erythrocytes. The present invention also provides methods of using the modified erythrocytes for the treatment or prevention of viral infections. In one embodiment, the modified erythrocytes of the present invention comprise CD4 and at least one HIV coreceptor, such as CXCR4 or CCR5. The modified erythrocytes, when administered to an HIV patient, bind to the plasma virus and induce the injection of the HIV ribonucleoprotein complex into the cells. The entrapped viral content is either degraded or deactivated within the erythrocytes, or destroyed by erythrophagocytosis.

This invention provides novel methods of detecting or treating aberrant cell cycle regulation associated with expression of a nuclear protein encoded by a gene that is linked to map position 8q22.3 of the human genome, and to novel reagents that are useful therefor. More particularly, the invention provides novel nucleic acid and proteinaceous probes, for detecting a gene that is linked to map position 8q22.3 of the human genome or the expression products thereof, wherein expression or elevated expression of said gene is associated with the appearance or occurrence of tumors associated with cancer, DNA damage and progesterone-receptor-mediated effects on cells. The invention also provides reagents and methods for detecting or modulating the expression products of the gene, such as, for example, in the diagnosis or treatment of cancer, cellular proliferation, DNA damage or progesterone receptor-mediated effects on cells.

The invention discloses a preparation and purification method of an antibody for inhibiting a chronic rejection of a transplanted organ. The preparation and purification method comprises the following steps of: step 1, collecting a periphery blood mononuclear cell through a lymphocyte separating medium and carrying out induction culture with 20ng/ml MICA; step 2, extracting a mononuclear cell protein through a nuclear protein and cytoplasm protein extraction kit; step 3, carrying out series connection on a high performance liquid chromatography (HPLC) purification anti-MICA antibody; and step 4, identifying the anti-MICA antibody and using rMICA and WesternBlot to carry out a reverse authentication. The anti-MICA antibody prepared through the method can inhibit a genetic expression of an endogenous MICA by sealing an endogenous MICA protein, an endogenous MICA and an siRNA, and therefore, an expression effect of an MICA of a transplanted organ is blocked, namely, expressions of an MICA gene and an MICA protein in a donator organ after an organ transplantation operation are effectively reduced.

The invention relates to the field of biomedicine, and in particular relates to novel human cell penetrating peptide hPP10 and a use of using the human cell penetrating peptide as an intracellular drug delivery carrier. The hPP10 deviates from a section of polypeptide sequence of lysine-specific demethylase 4A of human cell nuclear proteins, has a function of penetrating a cell membrane and can carry the proteins and nucleic acid (deoxyribonucleic acid DNA plasmid) to enter a plurality of cells in a transmembrane mode; and therefore, the cell penetrating peptide hPP10 is a transmembrane delivery carrier of bioactive molecules such as protein and nucleic acid which has good development prospect.

The invention relates to a method for quantitatively detecting alpha-synuclein auto-antibodies in human sera, and prepares recombinant human alpha-synuclein as antigens and rabbit anti-human alpha-synuclein polyclonal antibodies as antibodies into a kit, wherein, the quantities of alpha-synuclein auto-antibodies in the sera of patients with Parkinson's disease (PD) and in the sera of normal healthy persons are detected by utilizing the antigen-antibody reaction principle and are compared; and the presence and quantity of alpha-synuclein auto-antibodies in human sera are judged by the kit on the basis of color reaction.

The invention belongs to the technical field of biological pharmacy and particularly relates to LAG-3 affinity peptide N13, a preparing method and application thereof to the anti-tumor aspect. The affinity peptide comprises twelve amino acids, the molecular weight is 1634.8 Da, and the sequence is DDFRVWWPNFPR specifically. An Fmoc solid-phase polypeptide synthesis method is adopted for preparing the peptide, and the peptide can be applied to drugs for treating tumor. According to the affinity peptide N13, eukaryon protein rhLAG3-Fc serves as target molecules, hIgG1-Fc serves as tag protein, and the phage display peptide library high-throughput technology is used for screening the affinity peptide N13 of an LAG-3 extracellular domain. For the peptide, further in-vitro signal channel blocking tests and mouse tumor-bearing tests show that the peptide has good application prospects in the aspects of treating tumor and prolonging the survival period of a living body, and new possibility is provided for immune therapy for tumor of the living body.

The invention provides methods for detecting abnormal prostate conditions, such as benign prostatic hyperplasia (BPH), prostatic intraepithelial neoplasia (PIN), and adenocarcinoma, in an animal by comparing the amount of the Breast Tumor Kinase (BRK) tyrosine kinase in the nuclei of prostate luminal epithelial cells in a test sample with an amount of nuclear BRK protein in epithelial cells of normal prostate glands.

The invention relates to a method for detecting the content of phosphorylated alpha-synuclein combined with hemoglobin in erythrocytes of blood. The method comprises the following steps: taking an anti-human hemoglobin monoclonal antibody as a capturing antibody; taking an anti-phosphorylation human alpha-synuclein monoclonal antibody as a detection antibody; and detecting the content of the phosphorylated alpha-synuclein combined with the hemoglobin of Parkinson patients and normal healthy persons by utilizing an antigen-antibody reaction principle, and comparing.

Parkinson's disease (PD) is a neurodegenerative disorder which is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major component of which are filaments consisting of .alpha.-synuclein. The present invention provides .alpha.-synuclein mutations which accelerate .alpha.-synuclein aggregation and can thus be utilized for transgenic animal production and generation of the first progressive PD model. Also provided is an in vitro aggregation assay which can be utilized to identify .alpha.-synuclein nucleation inhibitors for the treatment of PD.

The invention provides a protein composite identifying method based on a graph model; a protein interactive network of a given species is regarded as a network drawing =(V, E), wherein V is combining point of protein, and E is set of protein-protein interaction side; the self-connecting side and the repeat side in a network are removed from the set of all sides; the method includes steps of firstly acquiring a nuclear protein vertex set of the protein composite, and then expanding a first-order neighbor of the edge combining point thereof, and forming a graph model; judging its connectivity according to characteristics of the graph model, and finding out all dense subgraphs, namely, protein composite. The method provided by the invention can regard the graph model as the nucleus of the protein composite; through investigating and expanding the first-order neighbor combining point of the graph model, the protein composite is identified; an algorithm provided by the invention is applied to the known yeast protein network; the experimental result indicates that the algorithm can identify multiple protein composites with biological significance, and the algorithm is not sensitive to the input parameter.

The invention discloses a recognition method of protein complexes. The method comprises following steps: constructing a weighted protein-protein interaction network, wherein weight value represents similarity between gene representing modes corresponding to proteins with codes interacting each other; recognizing nucleuses of protein complexes based on the weighted protein-protein interaction network; recognizing accessory proteins for the nucleuses of protein complexes based on the number of nuclear proteins interacting with non-nuclear proteins and weight; and combining recognized nucleuses and recognized accessory proteins to recognize the protein complexes. The method does not take internal structures of protein complexes into consideration and utilizes the feature of code interaction with high protein gene expression. Therefore, the method is capable of recognizing protein complexes with overlapping structures and the recognized protein complexes reflect actual internal structures of protein complexes.

The invention relates to methods for separating and identifying DNA (deoxyribonucleic acid) binding protein, in particular to methods for separating and identifying DNA binding protein through a DNA co-immunoprecipitation technology. The separating method comprises the steps of extracting nucleoprotein of a cell, mixing a target DNA molecule and nucleoprotein, adding a molecular entity capable of being bound with the target DNA molecule, separating to obtain a nucleoprotein ingredient bound with the target DNA molecule, further separating the obtained nucleoprotein ingredient, and obtaining the DNA binding protein. The identifying method further comprises the step of identifying the DNA binding protein obtained by separating. The methods have the characteristics of good stability and repeatability, and significantly improve the experiment efficiency of identifying the unknown DNA binding protein. The methods provide beneficial help for subjects such as molecular behavioristics, molecular oncology, cytobiology and biochemistry deeply researching into cytogene transcriptional control and genetic transcription.