15 results about "Abnormal protein" patented technology

The invention relates to methods and compositions for preventing or treating a neuropathology in a subject associated with or induced or caused by a P. gingivalis infection, preventing the deposition of or reducing the level of P. gingivalis gingipain in neuronal tissue, delaying the onset of a P. gingivalis-induced or associated neuropathology, for preventing or slowing the rate of abnormal protein deposition in the neuronal tissue, and / or reducing neuroinflammation, the methods comprising administering an RNA polynucleotide encoding a protein comprising or consisting of: - one or more amino acid sequences of an active site of an Arg- or Lys-gingipain of P. gingivalis, or a sequence that is at least 80% identical thereto; and / or - the amino acid sequence of one or more adhesin binding motifs (ABMs) of an adhesin domain of an Arg- or Lys-gingipain of P. gingivalis, or a sequence that is at least 80% identical thereto, wherein the polynucleotide is capable of being translated in a mammalian cell.

The present application relates to TAT-PO1 and its application in treating amyotrophic lateral sclerosis (ALS). The polypeptide connects TAT sequence (SEQ ID NO. 1) and PO1 sequence (SEQ ID NO. 2) through amino hexanoic acid (AHX), and its amino acid sequence is YGRKKRRQRRR{AHX}RHIFLIRHSQYHVDGSLEKDRTLTPLGREQAE. TAT-PO1 can competitively block the interaction between PGAM5 and OMA1, thereby interfering with the pathological mechanism of ALS. The polypeptide TAT-PO1 of the present application can be prepared into a drug, and directly targets the central nervous system through intrathecal injection or intravenous administration, thereby providing a new strategy for the treatment of ALS. In addition, the design idea can also be applied to other neurodegenerative diseases caused by abnormal protein interaction, thereby providing a technical paradigm for the development of related drugs.

Diagnostic and therapeutic methods for neurodegenerative diseases. Are provided involving assaying abnormal proteins (hyperphosphorylated tau, α-synuclein, TDP-43) associated with neuronal turnover inhibition or promotion in patient samples. Abnormal protein expression and apoptotic activity are detected, aiding disease progression assessment. Therapeutically, a method is provided for treating neurodegenerative diseases, administering compounds promoting neuronal turnover or modulating proteins involved in the process. The invention extends to identifying suitable drugs, employing neuronal turnover induction, miRNA modulation, and protein activity inhibition or enhancement. The claims also encompass various species, tissues, and cultured cells. Furthermore, the invention is applicable to diverse neurodegenerative diseases with abnormal protein accumulation, presenting novel diagnostic and treatment approaches.

The present invention relates to series of peptidomimetic compounds as an inhibitor targeting protein N-terminal methyltransferase pharmacological pathway. Pharmaceutical compositions of those compounds and methods of using them in the treatment of diseases caused by abnormal protein methyltransferase pathway, including cancer, inflammation, neurodegenerative and cardiovascular diseases, are within the scope of this disclosure.

The present invention relates to series of peptidomimetic compounds as an inhibitor targeting protein N-terminal methyltransferase pharmacological pathway. Pharmaceutical compositions of those compounds and methods of using them in the treatment of diseases caused by abnormal protein methyltransferase pathway, including cancer, inflammation, neurodegenerative and cardiovascular diseases, are within the scope of this disclosure.

Provided herein are methods for treating conditions and diseases characterized by SCN1A, SCN8A, or SCN5A protein deficiency by targeting variable splicing events in the SCN1A gene and modulating expression levels of functional proteins and / or inhibiting aberrant protein expression in Delavir Syndrome patients.

The invention relates to TAT-PO1 and application of TAT-PO1 in treatment of neurodegenerative disease amyotrophic lateral sclerosis. The polypeptide is connected with a TAT sequence (SEQ ID NO.1) and a PO1 sequence (SEQ ID NO.2) through aminocaproic acid (AHX), and the amino acid sequence of the polypeptide is as follows: YGRKKRRQRRR {AHX} RHIFLIRHSQYHVDGSLEKDRTLTPLGREQAE. The TAT-PO1 can competitively block the interaction between the PGAM5 and the OMA1, so that the pathological mechanism of the ALS is intervened. The polypeptide TAT-PO1 disclosed by the invention can be prepared into a medicine, and directly targets a central nervous system through intrathecal injection or intravenous administration, so that a new strategy is provided for ALS treatment. In addition, the design thought can also be applied to other neurodegenerative diseases caused by abnormal protein interaction, and a technical normal form is provided for development of related drugs.

The present invention provides compositions and methods of inhibiting tyrosine phosphorylation. In one aspect, a composition includes comprising a low-dosage tyrosine kinase inhibitor, where the low-dosage tyrosine kinase inhibitor decreases tyrosine phosphorylation. In another aspect, a method is described for treating cardiovascular disease or condition associated with a RASopathy having aberrant protein tyrosine phosphorylation. Methods for treating congenital heart disease associated with Noonan or Noonan syndrome with multiple lentigines and decreasing aberrant levels of Protein Zero-Related (PZR) tyrosyl phosphorylation are also described.

Provided are compounds, methods, and pharmaceutical compositions for reducing the amount or activity of PRNP RNA in a cell or animal, and in certain instances reducing the amount of PrP protein in a cell or animal. Such compounds, methods, and pharmaceutical compositions are useful to ameliorate at least one symptom or hallmark of a neurodegenerative disease. Such symptoms and hallmarks spongiform changes in the brain, development of abnormal protein aggregates, neuronal loss, markers of neuronal loss, rapidly progressing dementia, and death. Such neurodegenerative diseases include prion diseases, Creutzfeldt-Jakob disease (CJD), variant Creutzfeldt-Jakob Disease (vCJD), familial Creutzfeldt-Jakob Disease (fCJD), Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, kuru, Alzheimer's disease, or Parkinson's disease.

The invention provides a preserved egg appearance grade classification system and method based on machine vision, machine vision identifies appearance characteristics of preserved egg shells, determines structure abnormal areas and color abnormal areas of the preserved egg shells, and comprehensively identifies condition problems possibly caused in a preserved egg pickling process; according to the structure abnormal region, estimating the penetration state characteristics of the pickling ingredients in the preserved egg so as to calibrate the solidification abnormal region in the preserved egg; according to the color abnormal area, a metal salt accumulation area in the preserved egg is calibrated, and abnormal protein solidification and excessive metal element enrichment which possibly occur in the preserved egg in the pickling process are estimated through the appearance state of the preserved egg; the preserved eggs are graded and marked according to the abnormal solidification area and the metal salt accumulation area, the preserved eggs are subjected to appearance visual recognition to determine the pickling quality of the preserved eggs, the preserved eggs are quickly and accurately recognized and screened, and the production efficiency and quality of the preserved eggs are improved.

The invention belongs to the technical field of biology, and particularly relates to a composition for improving the developmental potential of oocytes, an in-vitro maturation culture solution and an optimized culture method. And a CCR5 / CXCR3 antagonist. The preparation for in-vitro embryo production contains an Ephrin ligand family and a CCR5 / CXCR3 antagonist, the microenvironment for maturation culture of oocytes is synergistically optimized, further, sesquiterpenol compounds and / or phenylpropane compounds can be added on the basis, and therefore the preparation can be used for preparing the embryos in vitro by means of the synergistic effect of the components. The composition can effectively inhibit the formation of abnormal protein aggregates in oocytes, enhance the ability of proteasomes to remove error protein aggregates, significantly reduce the level of reactive oxygen species (ROS) and increase the content of endogenous antioxidant substances such as glutathione (GSH), so as to reduce the protein toxicity stress, oxidative stress and other dimensions, and thus, the composition can be used for preparing an anti-inflammatory drug. The quality and the fertilization rate of oocytes after in-vitro maturation and the development potential of subsequent embryos are remarkably improved, and the application prospect is wide.

The invention discloses a synthetic lethal screening method based on a DED1 phase separation defect cell model and application, and belongs to the technical field of biotechnology, genetic engineering and drug screening. The DED1 mutant provided by the invention loses phase separation capability through extreme asymmetric RGG motif distribution specificity, but maintains the stress function of protein. A DED1-based phase separation defect cell model constructed by introducing the mutant can be used for identifying complementary cell pathways and researching the action mechanism of abnormal protein aggregation related diseases, and has important application in the aspect of developing drugs or combination therapies for some neurodegenerative diseases.

Disclosed herein is a method of treating neurodegenerative diseases involving accumulation of abnormal proteins in the central nervous system (CNS) of a user. The method includes utilizing an intraoral device to apply photobiomodulation and vibration to specific points on hard and soft palates of the user to stimulate the user's glymphatic system and decongest hyperphosphorylated tau and amyloid proteins and toxins, and simultaneously with the utilization of the intraoral device, applying a transcranial device to exert vasopneumatic compression and photobiomodulation on the user's head and neck to stimulate the user's lymphatic system and enhance the flow of lymphatic fluid towards the subclavian lymphatic pathway.

Disclosed is a method of treatment of a disease associated with abnormal protein aggregation comprising parenterally administering pharmaceutical formulations comprising trehalose. Also disclosed is an injectable aqueous pharmaceutical formulation comprising a therapeutically effective amount of trehalose.

The invention discloses an engineered exosome for removing intestinal abnormal protein to treat nervous system diseases, which is prepared by the following steps: carrying out competent ice bath on abnormal protein degrading peptide, plasmids of a fluorescent protein sequence and escherichia coli for a first time, immediately transferring into a 42 DEG C metal bath for a second time, and then immediately transferring into an ice-water mixture for an ice bath for a third time; the preparation method comprises the following steps: adding an antibiotic-free liquid culture medium into a culture medium, carrying out mild shaking culture in a shaking table at 37 DEG C for a fourth time to obtain a bacterial solution, and collecting exosomes from the bacterial solution to obtain the engineered exosomes for removing intestinal abnormal proteins to treat nervous system diseases, by combining the engineered exosome with the core design of colon precise delivery, intelligent colonization support and treatment function programmed coupling, multiple bottlenecks of oral delivery and efficacy regulation of the exosome therapy for central nervous system diseases are systematically solved.