81 results about "Mitochondrial protein" patented technology

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.

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.

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.

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.

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 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 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.