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30 results about "PINK1" patented technology

PTEN-induced kinase 1 (PINK1) is a mitochondrial serine/threonine-protein kinase encoded by the PINK1 gene. It is thought to protect cells from stress-induced mitochondrial dysfunction. PINK1 activity causes the parkin protein to bind to depolarized mitochondria to induce autophagy of those mitochondria. PINK1 is processed by healthy mitochondria and released to trigger neuron differentiation. Mutations in this gene cause one form of autosomal recessive early-onset Parkinson's disease.

Target ZIP7 related to diagnosis, treatment, prevention and treatment of cardiovascular diseases and application of target ZIP7

The invention discloses a target ZIP7 related to diagnosis, treatment, prevention and treatment of cardiovascular diseases and application of the target ZIP7. The application of a substance for inhibiting or silencing ZIP7 gene expression or inhibiting ZIP7 protein activity in any one of the following conditions that a medicine for increasing the concentration of zinc ions in mitochondria is prepared; a medicine for reducing the mitochondrial membrane potential is prepared; a medicine for increasing aggregation of PINK1 in mitochondria is prepared; a medicine for increasing the aggregation of Parkin in mitochondria is prepared; a medicine for inducing mitochondrial autophagy is prepared; a medicine for reducing the release level of active oxygen in myocardial tissues is prepared; a medicine for reducing the myocardial infarction risk is prepared; a medicine for treating or adjunctively treating myocardial infarction is prepared; a medicine for improving the cardiac function after myocardial infarction is prepared; a medicine for inhibiting the enlargement of the infarction area after myocardial infarction is prepared; a medicine for inhibiting ventricular negative remodeling after myocardial infarction is prepared; a medicine for reducing damage of myocardial cells and myocardial tissues in the myocardial infarction process is prepared; and a medicine for reducing the death quantity of myocardial cells in a non-infarction region after myocardial infarction is prepared.
Owner:TIANJIN MEDICAL UNIV

Application of PINK1 as marker for predicting sensitivity of lung adenocarcinoma to MAPK inhibitor and recurrence of lung adenocarcinoma

The invention discloses application of PINK1 as a marker for predicting sensitivity of lung adenocarcinoma to an MAPK inhibitor and recurrence of lung adenocarcinoma. Through experiments, it is found that expression increase of PINK1 in tumors prompts that a lung adenocarcinoma patient has higher tumor dormancy and recurrence risks, so that dormancy and recurrence of lung adenocarcinoma can be predicted by detecting the expression level of PINK1 in the lung adenocarcinoma patient, and the blank of biomarkers for dormancy and recurrence of lung adenocarcinoma in the prior art is filled up; the expression level of PINK1 can be used as a judgment standard for lung adenocarcinoma dormancy and recurrence, and is used for developing a lung adenocarcinoma dormancy and recurrence prediction kit. Besides, for a lung adenocarcinoma patient receiving the MAPK pathway inhibitor, the increase of the expression of the PINK1 prompts that the risk of drug resistance and relapse is increased after the patient is treated, so that intervention measures can be taken in advance clinically, tumor relapse is prevented, and a new strategy and thought are provided for clinically treating the lung adenocarcinoma.
Owner:SUN YAT SEN MEMORIAL HOSPITAL SUN YAT SEN UNIV

Establishment of detection method of colon tissue PINK1/Parkin of rat dysbacteriosis diarrhea

PendingCN114480590AImprove disordered diarrheaActivate autophagyMicrobiological testing/measurementMaterial analysis by optical meansStainingRat model
The invention discloses establishment of a detection method of colon tissue PINK1 / Parkin of rat dysflora diarrhea, and the detection method comprises the following steps: preparing a rat model with dysflora diarrhea, treating the rat model with a Gegen Qinlian decoction, performing HE dyeing and RT-PAR detection, and detecting the PINK1 / Parkin in the rat model with PINK1 / Parkin. It is determined that the radix puerariae qinlian decoction can reduce the expression level of mitochondrial autophagy PINK1 / Parkin in colon tissue of a rat suffering from the dysflora diarrhea, and the radix puerariae qinlian decoction can activate mitochondrial autophagy and remove damaged mitochondria in the tissue by influencing expression of PINK1 and Parkin, so that the effect of treating the dysflora diarrhea is achieved.
Owner:贵州中医药大学

A kind of protective agent for mitochondrial function of weaned piglets

The invention discloses a protective agent for mitochondrial function of weaned piglets, which comprises the following components: 0.3-1.5 parts by weight of ellagic acid, 0.3-2 parts by weight of curcumin, 0.3-1.3 parts by weight of syringin, and 3-3 parts by weight of sodium montmorillonite 15 parts by weight. Compared with the single addition of ellagic acid, curcumin, syringin and sodium montmorillonite in the feed, the protective agent for mitochondrial function of weaned piglets of the present invention significantly improves the content of mitochondrial DNA in the intestinal tract and liver of post-weaned piglets, and the mitochondrial respiratory chain. Complex IV activity, expression of mitophagy marker proteins PINK1, Parkin, and LC3II / LC3I. Ellagic acid, curcumin, syringin, and sodium montmorillonite have significant interactions in improving intestinal and liver mitochondrial function and mitophagy levels, and have a positive synergistic combination effect. The protective agent for mitochondrial function of weaned piglets of the present invention can significantly improve the mitochondrial autophagy levels of the intestinal tract and liver after weaning through the synergistic effect of various components, and greatly improve the mitochondrial functions of the intestinal tract and liver after weaning.
Owner:ZHEJIANG UNIV

A mitophagy regulator that relieves oxidative stress in pigs

ActiveCN109673857BReduced production of reactive oxygen speciesReduce contentAccessory food factorsBiotechnologyPig liver
The invention discloses a mitophagy regulator for relieving pig oxidative stress, which comprises the following components: 6-13 parts by weight of butyrate, 1-3 parts by weight of Achyranthes knuckle polysaccharide, 5-10 parts by weight of betaine, sodium-based 30-60 parts by weight of montmorillonite. Compared with the addition of butyrate, achyranthes bidentata polysaccharide, betaine and sodium montmorillonite alone in the feed, the present invention can significantly reduce the production of reactive oxygen species in the mitochondria of the liver and intestinal tract and the content of peroxidation product malondialdehyde, and promote oxidation stress. The expression of mitophagy marker proteins PINK1, Parkin, and LC3II / LC3I in pig liver and intestine after stimulation significantly increased the content of mitochondrial DNA and the activity of mitochondrial oxidative respiratory chain complex IV in pig liver and intestine. Moreover, Na-based montmorillonite has a controlled-release effect on butyrate, Achyranthes bidentata polysaccharide, and betaine, making it easy to mix with feed, forming a uniform dispersion system, and easy to use. Through the synergistic effect of each component, the invention significantly improves the level of pig mitophagy, protects the function of mitochondria, and then significantly relieves the oxidative stress of pigs.
Owner:ZHEJIANG UNIV

Chimeric molecule for mediating mitochondrial targeted degradation based on autophagy mechanism and application thereof

ActiveCN111471111ARealize regulationAchieving regulation of intracellular organelles is feasible regulationNervous disorderPeptide/protein ingredientsNeuro-degenerative diseaseAmino acid
The invention discloses a chimeric molecule for mediating mitochondrial targeted degradation based on autophagy mechanism. The amino acid sequence of the chimeric molecule is shown by SEQ ID NO: 1 or2 or 3 or 4. The invention also discloses a nucleic acid molecule for encoding the chimeric molecule for mediating mitochondrial targeted degradation based on, an expression vector containing the nucleic acid molecule, and applications of the chimeric molecule, the nucleic acid molecule and the expression vector in targeted degradation of mitochondria. According to the chimeric molecule for mediating mitochondrial targeted degradation, through targeted degradation of intracellular mitochondria, it is proved that regulation and control of intracellular organelles at the cellular level are feasible, and reference is provided for targeted degradation of other organelles; the chimeric molecule disclosed realizes degradation of the intracellular mitochondria at a cellular level, and provides adrug research and development thought for treatment of diseases; and particularly, a certain treatment thought can also be provided for neurodegenerative diseases caused by PINK1-Parkin pathway mutation.
Owner:CHONGQING UNIV
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