13 results about "Prion Proteins" patented technology

Provided herein is a nucleic acid encoding a prion protein, wherein the prion protein (a) comprises an amino acid sequence comprising a protective sequence variant such as a G127V mutation and (b) lacks a fully functional 3' glycosylphosphatidylinositol (GPI)-anchor attachment sequence. Also provided are viral vectors and pharmaceutical compositions comprising the nucleic acids. Further provided are methods and uses of treating prion diseases or other neurodegenerative diseases that confer toxicity through cell surface- anchored prion proteins in a subject, comprising administering to the subject an effective amount of a pharmaceutical composition or viral vector described herein.

The invention belongs to the technical field of gene detection, and particularly relates to a dual MIRA-LFD primer probe group, a kit and a method for identifying 23bp insertion / deletion polymorphic sites of a bovine prion protein gene promoter region. The primer probe group comprises an upstream primer as shown in SEQ ID NO: 2, a downstream primer as shown in SEQ ID NO: 5, an insertion type probe as shown in SEQ ID NO: 6 and a deletion type probe as shown in SEQ ID NO: 7. By utilizing the primer probe group disclosed by the invention, the 23bp insertion / deletion polymorphism of the bovine PRNP promoter region can be specifically detected, and a scientific basis is provided for bovine genotype identification and mad bovine disease susceptibility risk assessment.

The invention provides a primer group, a kit and a method for identifying 23bp insertion / deletion polymorphic sites of a bovine prion protein gene promoter region, and belongs to the technical field of gene detection. The primer group disclosed by the invention comprises an upstream outer primer 23-PF1, an upstream inner primer 23-IFA4, a downstream inner primer 23-AR2 and a downstream outer primer 23-PR3. A specific primer group is designed aiming at 23bp insertion / deletion polymorphic sites, an ARMS-PCR typing system is established by optimizing annealing temperature and primer concentration gradient, and 23bp insertion / deletion homozygotes and hybrid genotypes of the 23bp insertion / deletion homozygotes in a bovine prion protein gene promoter region can be specifically detected. The technical problem that the current identification of the 23bp insertion / deletion polymorphic site of the prion protein gene promoter region of the cattle product is tedious is solved, the disease resistance of the cattle to the mad cattle disease can be judged, and a scientific basis is provided for genotype identification of the cattle product and mad cattle disease susceptibility evaluation.

The invention discloses an RNA co-immunoprecipitation kit for specific binding of prion protein in muscle cells and an RNA extraction method, and relates to the technical field of bioengineering. According to the present invention, the specific co-precipitation kit preparation and the specific extraction steps comprise cell lysis, cell lysis solution-antibody-magnetic bead incubation, protein digestion and RNA extraction, such that the high purity and the sufficient amount of the enriched RNA are successfully ensured so as to completely meet the strict requirements of the subsequent RNA-seq sequencing. The method overcomes the inherent defects of the existing RIP technology in the research of non-classical RNA binding proteins, realizes the optimization of the whole process from high-specificity enrichment to high-quality sequencing sample preparation through the integrated innovation of methodology and the kit, has the outstanding advantages of strong specificity, high sensitivity, good repeatability, simple operation and the like, and has a wide application prospect in the research of non-classical RNA binding proteins. And remarkable technical progress is achieved, and a positive application effect is generated.

The disclosure provides polymeric compounds that inhibit binding of an amyloid-β-oligomer to cellular prion protein, methods for identifying such compounds, and their therapeutic use. In particular, the present disclosure provides a collection of anionic polymers and methods of using these compounds to treat amyloid-related disorders, e.g., Alzheimer's disease.

Provided are RNAi agents, pharmaceutical compositions, and methods for reducing the amount or activity of PRNP RNA in a cell or a subject, and in certain instances reducing the amount of prion protein in a cell or a subject. Such RNAi agents, pharmaceutical compositions, and methods are useful to ameliorate at least one symptom or hallmark of a neurodegenerative disease. Such neurodegenerative diseases include prion diseases, such as Creutzfeldt-Jakob disease (CJD) (e.g., variant Creutzfeldt-Jakob Disease (vCJD), classic Creutzfeldt-Jakob Disease (cCJD), familial Creutzfeldt-Jakob Disease (fCJD), or sporadic Creutzfeldt-Jakob Disease (sCJD)), Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, or kuru; synucleinopathies such as Alzheimer's disease, Parkinson's disease, or dementia with Lewy bodies; or tauopathies such as frontal temporal dementia associated with a Tau mutation, Pick's disease, progressive supranuclear palsy, corticobasal neurodegeneration, or chronic traumatic encephalopathy (CTE).

There are disclosed therapies and preventions of prion protein complex infections. The transcription of the amyloid precursor protein gene and PrP gene and the RNA transcript are the rate-limiting steps and are most susceptible for blockage and control of the process of amyloid protein formation and PrPsc formation. Thus, therapies and prevention regimes for prion protein complex infections interrupt this process at the level of DNA transcription to RNA, RNA transport to the mitochondrion for protein synthesis and deposition in the cerebral cortex neurons.

The present invention relates to biparatopic antigen-binding molecules, such as biparatopic antibodies or functional fragments thereof, and mixtures comprising at least two monospecific antibodies or functional fragments thereof, that can be employed for the prevention, alleviation, treatment and / or diagnosis of diseases, disorders and abnormalities associated with CNS proteins such as alpha-synuclein (α-synuclein, A-synuclein, aSynuclein, A-syn, α-syn, aSyn, a-syn), Tau, TDP-43, ASC, NLRP3, C5a, C1q, C3, huntingtin or prion protein. The present invention further relates to the use of the molecules of the invention for determining a pre-disposition to a disorder, disease or abnormality, monitoring residual disorder, disease or abnormality associated with CNS proteins such as alpha-synuclein (α-synuclein, A-synuclein, aSynuclein, A-syn, α-syn, aSyn, a-syn), Tau, TDP-43, ASC, NLRP3, C5a, C1q, C3, huntingtin or prion protein, or predicting the responsiveness of a patient who is suffering from such a disorder, disease or abnormality to the treatment with a certain medicament.

The application discloses a tumor marker for colorectal cancer diagnosis and a nucleic acid aptamer-based detection method, relates to a nucleic acid aptamer sequence for specifically recognizing epithelial cell adhesion molecule (EpCAM) and prion protein (PRNP), EpCAM and PRNP proteins as colorectal cancer diagnosis markers and a method for detecting expression levels in exosomes. The nucleic acid aptamer sequence is obtained by screening a cell-SELEX (systematic evolution of ligands by exponential enrichment) technology with colorectal cancer cells as targets, can be chemically synthesized in vitro, is stable in structure, easy to modify and replace, low in cost and high in reproducibility; and the target protein is highly enriched in exosomes derived from colorectal cancer tumor cells and can be used as a colorectal cancer diagnosis marker. The nucleic acid aptamer obtained by the application can be applied to imaging of human colorectal cancer related malignant tumor cells and derived exosomes, preparation of coupled drugs, clinical diagnosis and development of related kits.

There are disclosed therapies and preventions of prion protein complex infections. The transcription of the amyloid precursor protein gene and PrP gene and the RNA transcript are the rate-limiting steps and are most susceptible for blockage and control of the process of amyloid protein formation and PrPsc formation. Thus, therapies and prevention regimes for prion protein complex infections interrupt this process at the level of DNA transcription to RNA, RNA transport to the mitochondrion for protein synthesis and deposition in the cerebral cortex neurons.

The present invention is directed to a novel therapeutic strategy for treating a disease mediated by copper, by inhibiting the function of cellular prion protein (PrP).

Methods of treating and preventing prion protein complex infection are disclosed. Transcription of an amyloid protein precursor protein gene and a PrP gene and RNA transcription are speed limiting steps, and the process of amyloid protein formation and PrPsc formation is most easily blocked and controlled. Thus, the regimen for the treatment and prevention of prion protein complex infection interrupts this process at the level of DNA transcription to RNA, RNA transport to mitochondria for protein synthesis and deposition at cerebral cortical neurons.

The invention provides a primer probe group, a kit and a method for identifying 12bp insertion / deletion polymorphic sites of an intron region of a bovine prion protein gene, and belongs to the technical field of gene detection. The primer probe group comprises 12 to mF1 as shown in SEQ ID NO: 2, 12 to mR2 as shown in SEQ ID NO: 4, 12 to IP1 as shown in SEQ ID NO: 6 and 12 to DP1 as shown in SEQ ID NO: 7, and a nucleotide sequence of an intron region 12bp is as shown in SEQ ID NO: 1. The primer probe group can specifically detect the 12bp insertion / deletion polymorphism of the bovine PRNP intron region, and provides a scientific basis for bovine genotype identification and mad bovine disease susceptibility risk assessment.