82 results about "Mitochondrial protein" patented technology

Provided herein is a library of monoclonal antibodies specific for native proteins and native protein complexes of the oxidative phosphorylation (OXPHOS) system (for example, Complex I, II, III, IV, or V, or any protein subunit of any of such complexes). Hybridomas expressing such antibodies and antibodies that competitively inhibit the binding of any such antibody (e.g., antibodies that bind the same or a sterically overlapping epitope) are also contemplated. Methods of using, and kits including, the disclosed antibodies are also provided. Antibodies, methods and kits described herein address a need in the art by providing immunological reagents and assays useful, at least, for detecting mitochondrial diseases associated with deficiencies or alterations in OXPHOS Complexes I, II, III, IV and / or V.

A conjugate comprises: (a) a mitochondrial membrane-permeant peptide; (b) an active agent or compound of interest such as a detectable group or mitochondrial protein or peptide; and (c) a mitochondrial targeting sequence linking said mitochondrial membrane-permeant peptide and said active mitochondrial protein or peptide. The targeting sequence is one which is cleaved within the mitochondrial matrix, and not cleaved within the cellular cytoplasm, of a target cell into which said compound is delivered. Methods of use of such compounds are also described.

The invention discloses a method and system for determining mitochondria genome sequence information of various samples at the same time, wherein the various samples belong to different species. The method includes the following steps of: providing genome DNA of each of the various samples and mixing the genome DNA; performing library construction on the DNA mixture; performing sequencing on the DNA sequencing library; performing screening on the plurality of sequencing sequences to obtain a target sequence; performing sequence assembly on the target sequence to obtain the plurality of assembled sequences; performing morphological species taxonomy on each of the various samples to obtain morphological species taxonomy information of the various samples; performing species distribution on the assembled sequences based on the morphological species taxonomy information of the various samples and reference to a mitochondria protein gene database to determine the assembled sequence of each of the various samples; and respectively constructing a mitochondria genome of each of the samples based on the assembled sequence of each of the various samples, and determining the mitochondria genome sequence information.

The present invention relates generally to the mitochondrial protein, voltage-dependent anion channel (VDAC), polynucleotides encoding same and variants thereof, as well as peptide fragments, peptide derivatives and analogs. In particular, the present invention is directed to VDAC1 and specific amino acid and polynucleotide sequences thereof useful in inducing or regulating apoptosis and to pharmaceutical compositions comprising same useful in the treatment of diseases associated with aberrant apoptosis.

The invention relates to a cosmetic composition comprising at least one extract from the orchid Dendrobium chrysotoxum as an active agent and at least one cosmetically acceptable excipient.The invention relates to the use in a cosmetic composition of an extract from the orchid Dendrobium chrysotoxum as an active agent for preventing or delaying the appearance of the signs of skin ageing or for slowing or attenuating the effects thereof, or else also for promoting cell or tissue longevity.The invention in particular relates to an orchid extract inhibiting the expression and / or the activity of the mitochondrial protein Smac / DIABLO.

Assays are disclosed for identifying peptides and peptidomimetics for promoting apotosis in cells, through a pathway involving the Inhibitor of Apoptosis Proteins (IAPs), exemplified by XIAP, and the mitochondrial protein Smac / DIABOLO (hereinafter Smac) and homologs thereof. Also disclosed are IAP-binding peptides and peptidomimetics identified through the use of the assay.

The present invention relates generally to the mitochondrial protein, voltage-dependent anion channel (VDAC)5 polynucleotides encoding same and variants thereof, as well as peptide fragments, peptide derivatives and analogs. In particular, the present invention is directed to VDAC1 and specific amino acid and polynucleotide sequences thereof useful in inducing or regulating apoptosis and to pharmaceutical compositions comprising same useful in the treatment of diseases associated with aberrant apoptosis.

An obese mouse model was developed by overexpressing the mitochondrial protein prohibitin (PHB) in white adipose tissue (WAT) specific manner driven by adipocyte protein 2 (aP2) promoter. These mice begin to develop obesity as a result of mitochondrial remodeling (upregulation of mitochondrial biogenesis and function) in WAT.

The invention relates to human umbilical cord mesenchymal stem cell membrane granules, preparation and applications thereof. The surfaces of the cell membrane granules express surface markers of human umbilical cord mesenchymal stem cells and wrap biomacromolecules and organelles; the biomacromolecules comprise mRNA products of dry genes of the human umbilical cord mesenchymal stem cells; the organelles comprise mitochondria, proteasome, lysosome and autophagosome; and the cell membrane granules does not contain cell nucleuses, cell nucleuse DNA and nucleoproteins as well as virus glycoproteins VSV-G. 1-5mum cell membrane granules can be formed by a filtering membrane with the pore diameter of 3mum in mechanical extrusion, are larger, can be used for delivering the biomacromolecules and the organelles in vitro and delivering the biomacromolecules and the organelles to the liver and the spleen, and has a function of repairing aged cells and injured cells. The human umbilical cord mesenchymal stem cell membrane granules, the preparation and the applications have the advantages that due to no containing of the VSV-G, the generation of immunoreactions for viral proteins is avoided; and due to no containing of nuclear DNA, the probability of inducing canceration of target cells is almost zero.

Disclosed are novel fusion protein constructs comprising a functional mitochondrial protein, that can enter mitochondria within intact cells. Further disclosed are methods of treating mitochondrial disorders by the disclosed fusion proteins and compositions therefor.

Disclosed herein is a recombinant nucleic acid, comprising: a mitochondrial targeting sequence; a mitochondrial protein coding sequence, wherein said mitochondrial protein coding sequence encodes a polypeptide comprising a mitochondrial protein; and a 3′UTR nucleic acid sequence. Also disclosed is a pharmaceutical composition comprising the recombinant nucleic acid and a method of treating Leber's hereditary optic neuropathy (LHON) using the pharmaceutical composition.

The invention discloses a kit for in-vitro single base damage repair detection through real-time quantitative PCR (Polymerase Chain Reaction). The kit comprises a 10X detection buffer solution, a 5X low-salt cell lysis solution, a 2X cell nucleoprotein or mitochondrion protein extract, a 20X detection substrate and a 2XqPCR damage repair buffer solution, wherein the repair buffer solution comprises taq enzyme, dNTP (Deoxyribonucleotide Triphosphate), probes and primers. In the kit, primers of an amplification internal reference and damage base qPCR (quantitative PCR) templates are the same, the amount of damage base repair can be calculated according to the amount of the internal reference. Since a complementary template only has 14 bases which are complementary with the primer 2, annealing of the complementary template and the primer 2 is not produced in a qPCR process, and specificity of damage repair detection is guaranteed. A 3' tail end of the complementary template is dideoxyoligonucleotide, so that extension of the template per se is avoided. The probe for detecting the damage template and the probe for detecting the internal reference template are marked with different fluorescent groups, so that absolute quantification of repair of the damage template is realized through detection in the same qPCR system.

The invention provides fusion protein constructs comprising a functional mitochondrial protein and methods of treating mitochondrial disorders by the fusion proteins and compositions thereof.

Provided is a recombinant nucleic acid, comprising: a mitochondrial targeting sequence; a mitochondrial protein coding sequence, wherein said mitochondrial protein coding sequence encodes a polypeptide comprising a mitochondrial protein; and a 3'UTR nucleic acid sequence. Also provided are a pharmaceutical composition comprising the recombinant nucleic acid and a method of treating Leber's hereditary optic neuropathy (LHON) using the pharmaceutical composition.

Methods for delivering non-mitochondrial proteins to mitochondria are provided. Also provided are nucleic acid constructs comprising a coding sequence encoding a DNA-binding polypeptide, fused to a mitochondrial targeting sequence (MTS) and a nuclear export signal (NES), and the encoded proteins. The construct successfully delivers DNA binding proteins to the mitochondrion. A chimeric methylase based on the above construct is successfully delivered to mitochondria, resulting in modification of mtDNA.

Provided is a recombinant nucleic acid, comprising: a mitochondrial targeting sequence; a mitochondrial protein coding sequence, wherein the mitochondrial protein coding sequence encodes a polypeptidecomprising a mitochondrial protein; and a 3'UTR nucleic acid sequence. Also provided are a pharmaceutical composition comprising the recombinant nucleic acid and a method of treating Leber's hereditary optic neuropathy (LHON) using the pharmaceutical composition.

The invention discloses a method for detecting entry of small molecule compounds into mitochondria at a cell in-situ level. The method particularly comprises the following steps: selecting suitable small molecule compounds to be incubated with cells; acquiring mitochondria with complete physiological structures without destroying cell mitochondria; collecting cytoplasm; incubating with the small molecule compounds and the acquired mitochondria; respectively pyrolyzing the obtained mitochondria after incubating the small molecule compounds and the cytoplasm collected before under non-denaturing conditions to acquire a mitochondrial protein lysate and a cytoplasmic protein lysate; and then, detecting whether the small molecule compounds enter the mitochondria at the cell in-situ level by combining with mass spectrum analysis. The method can be adopted to detect whether the small molecule compounds enter the mitochondria at the cell in-situ level, and can further detect a way in which the small molecule compounds enter the mitochondria, can be directly applied to target region verification of a pilot drug or screening of the pilot drug using the mitochondrion as an effector, and has the advantages of high reliability and high sensitivity.

The invention discloses a transhydrogenase-1 activity determination kit and a use method thereof. The kit comprises a mixed solution of a Tris-HCl buffer solution, sucrose and EDTA, a Tris-HCl buffersolution, NADH and AcPyADP. The method is based on the detection principle of replacing the NADP<+> with a synthetic substrate 3-acetylpyridine adenine dinucleotide phosphate (APADP<+>) and calculating TH-1 activity through measuring a light absorption increasing speed at 375nm of APADPH generated by the reduction of APADP<+> catalyzed by TH-1, can effectively eliminate the interference of NAD andhas high detection specificity. Through a simple work liquid, only through adding a sample and a work liquid into a microcuvette or a 96-well plate, the determination is finished and detection is convenient. The kit can effectively isolate cytoplasmic proteins and mitochondrial proteins and accurately determine TH-1 located in the mitochondrial inner membrane.

The invention discloses an application of hydroxytyrosol in preparation of healthy food and a drug for preventing and treating Alzheimer disease. Hydroxytyrosol can cross the blood brain barrier so as to remarkably improve cerebral nerve functions and learning and memory abilities of a mouse with the Alzheimer disease; besides, hydroxytyrosol can also reverse mitochondrial dysfunction and mitochondrial protein carbonylation abnormity in the brain of the mouse with the Alzheimer disease, SOD-2 protein expression is improved, and system steady states of two enzymes are improved. More importantly, due to the fact that the mouse with the Alzheimer disease has long-term inflammatory injury in the brain, the inflammatory injury in the brain of the mouse with the Alzheimer disease is remarkably relieved with JNK / MAPK (Jun N-terminal kinase / Mitogen-activated protein kinase) as a target under intervention of hydroxytyrosol, and the functions of preventing and treating occurrence and development of the Alzheimer disease are realized.

The present invention relates to mitochondrial protein that can be used as a marker for diagnosing stomach cancer. According to the present invention, the marker for diagnosing stomach cancer comprises mitochondrial enoyl coenzyme A hydratase 1.

The invention discloses a screening method and an application of uridine monophosphate modified protein in mitochondria. The method is characterized in that biotin-labeled UTP (Biotin-16-UTP) is usedas a raw material, under the action of uridine monophosphate transferase SelO, total mitochondrial protein is subjected to UMP modification reaction, and the protein modified by UMP further has a biotin label, subsequently, the modified protein is screened out by using a biotin-streptavidin Pull-down technology, and finally, the modified protein and a modification site are determined by mass spectrometry. The method is advantaged in that a simple and feasible experimental method is developed, proteins which can be modified by UMP are screened from mitochondrial total proteins, and an importantresearch means is provided for signal transduction mediated by SelO proteins and post-translational modification in mitochondria.

The Mito-Ob obese mouse model overexpresses the mitochondrial protein prohibitin (PHB). Mito-Ob male mice develop insulin resistance in addition to obesity and they do not develop overt diabetes. It has been discovered that these mice also spontaneously develop nonalcoholic steatohepatitis (NASH) and hepatocarcinogenesis over time. Also described is a mutant Mito-Ob mouse that develops lymphadenopathy and histiocytosis.

The invention is in the art of medical treatments, in particular the treatment of tumors with ionizing radiation. It provides means and methods for predicting whether a subject is likely to develop radiation damage upon radiotherapy. The invention provides tools that allow individualized and optimized radiation treatment of a subject in need of a radiation treatment. The invention also provides methods of determining the risk of developing severe dyspnea after radiation treatment. More in particular, the invention relates to an in vitro method for predicting the risk of developing radiation induced toxicity comprising the steps of obtaining mitochondrial DNA from a sample of a subject, determining the number of non-synonymous variations present in at least one gene encoding a mitochondrial protein, attributing a value to the number of non-synonymous variations, wherein a higher value corresponds to a higher risk of developing radiation induced lung toxicity.