80 results about "P53 proteins" patented technology

Systemic lupus erythematosus (SLE) can be prevented or treated by down-regulating the autoimmune response to the C-terminal-DNA-binding domain of the p53 protein (p53) by an active principle selected from the group consisting of: (i) a peptide of, or comprising, the C-terminal DNA-binding domain of the p53 protein; (ii) a monoclonal antibody (mAb) specific for said domain of p53 (Ab1), and fragments thereof; (iii) an mAb specific for Ab1 (hereinafter Ab2), and fragments thereof; (iv) a peptide based on a complementarity determining region (CDR) of the heavy or light chain of said Ab1 or Ab2; (v) a DNA molecule coding for (i) and (iv) of for the variable region of said Ab1 and Ab2 of (ii) and (iii); and (vi) T cells specific for (i) to (iv), fragments thereof, T cell receptor (TCR) thereof and peptides comprising the variable region of said TCR. SLE can also be diagnosed by assaying for antibodies (Ab1) against the C-terminal DNA-binding domain of p53 or antibodies (Ab2) specific to the Ab1 antibodies.

The invention relates to a fusion protein polymer. The fusion protein polymer consists of a component A and a component B, wherein the component A is a single domain antibody, while the component B is peptide sequences which perform multimerization on fusion protein and are derived from TNF alpha protein, ACRP30 protein, P53 protein, COMP protein, C4BP protein and mutants of the TNF alpha protein, the ACRP30 protein, the P53 protein, the COMP protein and the C4BP protein. The fusion protein polymer has the advantages of successful expression in Escherichia coli, high expression quantity, relatively simple preparation and low cost. Poly-antibodies of the fusion protein polymer have high dissolubility and biological activity and greatly improve the affinity of antibody protein. The fusion protein polymer can be prepared into various biotech products such as diagnostic reagents used for diagnosing melanoma and the like, and used for target treatment of the melanoma and the like by carrying a therapeutic medicament. When the poly-antibodies based on the fusion protein polymer are clinically applied, the problem of strong immunogenicity can be solved.

The invention relates to an esophageal squamous cell carcinoma autoantibody molecular marker model and an application thereof. The molecular model mainly comprises an ALDOA autoantibody, an ENO1 autoantibody, a p53 autoantibody, and an NY-ESO-1 autoantibody, and can be used for preparing a kit for distinguishing esophageal squamous carcinoma patients and healthy medical examiners. The kit for detecting esophageal squamous cell carcinoma patients mainly comprises recombinant ALDOAD protein, recombinant ENO1 protein, recombinant p53 protein, and recombinant NY-ESO-1 protein. According to the esophageal squamous cell carcinoma autoantibody molecular marker model and the application thereof, the ENO1 autoantibody is found to be elevated in serum level in the esophageal squamous carcinoma patients for the first time, and is jointly detected with the ALDOA autoantibody, the p53 autoantibody, and the NY-ESO-1 autoantibody for distinguishing the esophageal squamous cell carcinoma patients andthe healthy medical examiners, and has a better distinguishing effect than a single index detection; and in addition, the detection method adopted by the invention is an enzyme-linked immunosorbent assay indirect method, is simple and convenient to implement, has good sensitivity and specificity, and is a method which is mature and reliable and can be widely used in base layer hospitals.

The invention discloses a high-sensitivity protein detection method, wherein one of the following modes is selected optionally: mode 1, performing a tube wall solid phase PLA (proximity ligation assay) by a direct coating method, namely, directly adsorbing the protein or the antibody to a real-time fluorescence quantification PCR (Polymerase Chain Reaction) tube wall to perform PLA detection; and mode 2, performing a tube wall solid phase PLA by a cross-linking agent fixing method, namely, cross-linking the protein or the antibody to the real-time fluorescence quantification PCR tube wall by glutaraldehyde to perform PLA detection. Specifically, the method comprises the following steps of: using a monoclonal antibody pab240, and sequentially establishing PLA detection of P53 protein (P53 protein mutant) and cTnI (cardiac troponin I). According to the method disclosed by the invention, the antibody is fixed on a PCR tube so as to perform protein PLA detection, magnetic beads are not needed in the detection process, defects caused by application of the magnetic beads are overcome, and the detection sensitivity to the protein is also improved greatly.

An assay method for determining the effect of Product R on virus infection of Hela cells. The method comprising the following step: (1) dividing Hela cells into several groups, (2) treating one group with Product R prior to infecting the cells with a virus and treating another group with Product R after the cells being infected with the virus, and (3) determining the effects of Product R on virus infection by comparing the changes in the cell cycle, DNA fragmentation and p53 protein in cells undergone the different treatments in step (2).

A method for determining if a subject with cancer or precancerous lesions or a benign tumor, will respond to treatment with an inhibitor selected from the group comprising an inhibitor of one or more enzymes in the mevalonate pathway, an inhibitor of geranylgeranyl transferase, an inhibitor of farnesyl transferase or an inhibitor of squalene synthase, by (i) obtaining a sample of the cancer cells, precancerous cells or benign tumor cells from the subject, (ii) assaying the cells in the sample for the presence of a mutated p53 gene or a mutant form of p53 protein or a biologically active fragment thereof, and (iii) if the cells have the mutated p53 gene or mutant form of the p53 protein, then determining that the subject will respond to treatment with the inhibitor or combinations thereof. Some embodiments are directed to treatment with the inhibitors.

More than 90% of mutations found in the p53 protein produce a conformational change in p53 which results in the exposure of an epitope, which is otherwise hidden in the hydrophobic core of the molecule. A single chain antibody (scFv) which specifically recognizes this common mutant epitope in mutant p53 but not in wild type p53 is disclosed. Also described are a DNA molecule encoding the scFv, pharmaceutical compositions comprising the antibody and methods of treatment using the pharmaceutical compositions.

In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.

The invention discloses a fluorescence detection agent for a p53 protein. The fluorescence detection agent comprises a magnetic nano-particle, double-stranded DNA, and a functional layer coating the surface of the magnetic nano-particle and connected with the double-stranded DNA; the double-stranded DNA is obtained through hybridizing DNA-1 single strand and DNA-2 single strand; the DNA-1 is a carboxyl oligonucleotide probe, and the sequence is COOH-(CH2)6-TTT TTT TCC GGG CAT GCC CGG CAT TGC-3'; and the DNA-2 is the partial complementary sequence of the DNA-1, and the sequence is 5'-GGG CAT GCC C-3'. The invention also discloses a preparation method of the fluorescence detection agent, and an application of the fluorescence detection agent in the detection of the wild p53 protein. The agent has the advantages of low preparation cost, realization of sensitive, rapid and accurate capture of the p53 protein, realization of ultra-sensitive, highly- selective and highly-accurate detection of the p53 protein, low detection limit, and realization of quantitative analysis and detection of the p53 protein in normal cells and cancer cell lysate, and can be used in clinical diagnosis and early detection of cancers.

The invention discloses a small interfering RNA (siRNA) for inhibiting canine p53 gene expression. The sequence of the siRNA is shown as SEQ ID No: 1 or SEQ ID No: 2 in a sequence table. The invention also discloses a DNA for coding the siRNA and a recombinant vector containing the siRNA or the DNA. Preferably, the recombinant vector is a slow virus vector for infecting a canine cell to obtain a canine cell model of p53 gene silence. The canine p53 gene siRNA sequence can effectively degrade mRNA of p53 genes so as to inhibit the expression of the p53 genes. By using the siRNA sequence for interfering with the expression of the canine p53 genes, on the one hand, a treatment medicament for diseases related with the p53 genes such as cell apoptosis related diseases can be prepared; and on the other hand, the established p53 knock down cell model has great significance for researching the effect of p53 protein on innate immunity of cells and possible specific mechanisms.

The invention belongs to the related fields of biomedical products and clinical detection and the like, and mainly relates to a new method for separating and purifying wild-type p53 protein. The separation and purification method of the wild-type p53 protein comprises cloning of a p53 gene, construction of recombinant expression plasmid, protein induced expression and purification, prokaryotic system-based inducible expression, ultrasonic cracking of thalli, and separation and purification of the p53 protein in the obtained cracked supernate by using nickel column affinity chromatography. High-concentration active target protein is separated and purified by the prokaryotic system-based inducible expression and the nickel column affinity chromatography in the ultrasonic cracked thalli supernate. Denaturation and renaturation of inclusion bodies are not performed, and the protein is directly purified from the ultrasonic cracked supernate, so that the activity of the target protein is furthest kept; and compared with the conventional method, the method has the advantage that: the yield of the target protein is greatly improved by optimizing the inducible expression and using a purification scheme.

The invention belongs to the technical field of tumor cells, and particularly relates to application of knocking out p53 genes in inhibiting proliferation and metastasis of glioma cells. According to technical scheme, the p53 genes in malignant glioma cells in a human body change by knocking out the p53 genes, thus p53 protein expression is reduced even completely deleted, and the purpose of inhibiting proliferation and metastasis of the glioma cells is achieved.

The invention discloses a protein nano-drug for cancer targeted therapy and a preparation method thereof. The protein nano-drug is an exosome of humanized p53 protein transferred with covalent cross-linked triphenylphosphine (TPP). A protein nano-drug delivery system TPP/p53@Exos developed by the invention can recognize specific cancer cells in a targeted manner, efficiently inhibits the growth ofthe cancer cells by activating endogenous apoptosis pathways of the cells, has no toxic or side effect, and provides a new means for cancer treatment. The preparation method of the nano-drug deliverysystem has a high protein loading rate (about 75%), and can also be used for protection and targeted delivery of other protein drugs.

The invention discloses a kit for detecting drug sensitivity of rectal cancer cells based on gene mutation analysis, which comprises the following substances: (1) a rectal cancer cell drug reagent, (2) a magnetic nanoparticle indicating liquid A with a green fluorescent protein labeling a wild P53 protein antibody for surface modification, (3) a magnetic nanoparticle indicating liquid B with a redfluorescent protein labeling an anti-mutation P53 protein antibody for surface modification and (4) a substrate medium and a dilution buffer. The sensitivity of a patient to the drug is measured through simultaneous calculation of the expression levels of the wild P53 gene protein and the mutant P53 gene protein, the individualization is more prominent, the detection result is more accurate, a sensitive drug is screened for the treatment of the disease, and an optimal chemotherapy regimen is selected.