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104 results about "Cellular Autophagy" patented technology

Beta-carboline ruthenium compound as well as preparation method and application thereof

The invention discloses a beta-carboline ruthenium compound. The molecular formula of the beta-carboline ruthenium compound is [Ru (N^N) 2 (Nh) XClY] (A^A)z, wherein N^N is selected from bpy or phen; A^A is selected from PF6 or SO3CF3; X is equal to 1 or 2, Y is equal to 2-X, and Z is equal to 1 or 2; or the molecular formula of the beta-carboline ruthenium compound is [Ru (N^N) 2 (1-Py-betaC)] (PF^)2, wherein N^N is selected from bpy, phen or DIP. On a molecular mechanism, the invention proves that the beta-carboline ruthenium compound can be used for treating cancers and has a better effectthan the effects of that of the traditional metal compound cisplatin with wide application and ruthenium compounds NAMI-A in clinical tests; . Thethe beta-carboline ruthenium compound for treating the cancers as an autophagic cell inducer fills the blank of the prior art and develops a new line for developing a new generation of high-efficiency medicaments for treating malignant tumors.
Owner:SUN YAT SEN UNIV

Novel autography regulators atg14l and rubicon

InactiveUS20120041175A1Decreased long-lived protein degradationSlow cell growthSugar derivativesDepsipeptidesKinase activityClass iii
The present invention provides for up- and down-regulation of cellular autophagy, e.g., for treating cancer or neurological disease. The invention results, in part, from discovery of two novel proteins, ATG14L (previously called “BISC”) and Rubicon (previously called “BIRC”), which bind to a Class III phophatidylinositol 3′-kinase (PI3K) / Vps34-Beclin 1 autophagic complex. ATG14L and Rubicon each regulate autophagic activity in an opposing manner. ATG14L and Rubicon can be used, for example, to increase / decrease autophagic activity, to increase / decrease PI3K / Vps34 kinase activity, and in so doing, treat diseases and disorders, such as cancer, neurodegenerative disease, stroke, metabolic disease, and age-related disease. ATG14L can increase autophagic activity and PI3K / Vps34 kinase activity; and Rubicon can decrease autophagic activity and PI3K / Vps34 kinase activity.
Owner:THE ROCKEFELLER UNIV +1

Chimeric molecule for mediating Tau protein degradation based on autophagy mechanism and application of chimeric molecule

ActiveCN111410695APromote degradationOvercome the defect of not being able to efficiently degrade intracellular macromolecular componentsAntibody mimetics/scaffoldsPeptide preparation methodsProtein targetMolecular binding
The invention discloses a chimeric molecule for mediating Tau protein degradation based on an autophagy mechanism, and the amino acid sequence is shown in SEQ ID NO:5 or 7. The invention also discloses a nucleic acid molecule and an expression vector; and the nucleic acid molecule is used for encoding the chimeric molecule for mediating Tau protein degradation based on the autophagy mechanism, andthe expression vector comprises the nucleic acid molecule. The invention also discloses an application of the chimeric molecule for mediating Tau protein degradation based on the autophagy mechanism,the nucleic acid molecule and the expression vector in degradation of Tau protein. The novel targeted chimeric molecule is developed in the invention, and the chimeric molecule is bound to the surface of the aggregate protein Tau, so that the Tau protein is recruited into cell autophagosome and is promoted to be degraded through the cell autophagy pathway. The novel protein targeted degradation technology provided by the invention is expected to be applied to different target proteins, so as to overcome the defect that a current ubiquitin-proteasome pathway-based protein targeted degradationtechnology cannot efficiently degrade intracellular macromolecules.
Owner:CHONGQING UNIV

Pharmaceutical composition for mild photothermal therapy of tumors as well as preparation method and application of pharmaceutical composition

The invention provides a pharmaceutical composition for mild photothermal therapy of tumors as well as a preparation method and application of the pharmaceutical composition. The pharmaceutical composition is composed of a dual-targeting amphiphilic glucan derivative carrier, a material (PTA) with photo-thermal conversion performance and an autophagy inhibitor. The dual-targeting amphiphilic glucan derivative carrier can be self-assembled in water to form nano-micelles, and is physically loaded with PTA and an autophagy inhibitor for tumor photothermal therapy. The preparation is mainly characterized in that: 1) the preparation has active dual-targeting capability of tumor cells and tumor-related fibroblasts, and can efficiently enter the cells through the action of receptor ligands, so that the transfer efficiency of the preparation is improved; 2) under the irradiation of 808nm laser, PTA absorbs light energy and efficiently converts the light energy into heat, and the autophagy inhibitor inhibits the autophagy behavior of tumor cells and sensibilizes photo-thermal, so that an excellent mild photo-thermal treatment effect is realized, and the physical barrier of a tumor matrix can be weakened; tumor photothermal can further induce tumor cells to generate immunogenic cell death, generated tumor fragments can further activate an immune system, and the tumor photothermal treatment effect is greatly improved.
Owner:CHINA PHARM UNIV

Preparation method and application of nervous system neoplasm cell autophagosome to preparing vaccine

The invention belongs to the technical field of biologics and relates to a preparation method and application of nervous system neoplasm cell autophagosome to preparing a vaccine. Sirolimus and ammonium chloride are adopted to induce and culture nervous tumor cells, autophagosome generation is promoted, and autophagosome is extracted through repeated blowing and beating and high-speed centrifugation at different steps. A great deal of autophagosome can be rapidly prepared by using the method provided by the invention, after the autophagosome is carried by DCs (Dendritic Cells), DC maturation can be effectively promoted, T lymphocyte can be activated, proliferation of the T lymphocyte can be promoted, a remarkable killing function on tumor cells can be achieved, and the killing effect is remarkably better than tumor freeze thawing splitting antigen prepared in the prior art. The autophagosome prepared by using the method can be further adopted to prepare a nervous system tumor vaccine,and the vaccine is a dendritic cell tumor vaccine for nervous system derived tumor cell autophagosome.
Owner:AFFILIATED HUSN HOSPITAL OF FUDAN UNIV

Sorafenib drug-resistant marker and application thereof

The invention relates to a sorafenib drug-resistant marker and application thereof, and belongs to the technical field of biomedicine. The sorafenib drug-resistant marker is CCT6A. Research of the marker finds that on one hand, the relationship between CCT6A / B55 gamma pathway regulation and control of autophagy and liver cancer cell sorafenib drug resistance can be identified through deep research, and a scientific basis is provided for a new approach of targeting the pathway to treat liver caner. On the other hand, sorafenib drug-resistant people can be prompted, and the effects of personalized treatment and precise treatment are achieved in liver cancer treatment or cancer treatment.
Owner:THE THIRD AFFILIATED HOSPITAL OF SUN YAT SEN UNIV

3-hydrogenated pinicolic acid cyanide ethyl ester medicine and application thereof

The invention discloses a 3-hydrogenated pinicolic acid cyanide ethyl ester medicine and application thereof. The medicine comprises a compound with the following structure formula which is as shown in the description. The medicine also comprises pharmaceutically acceptable salts, 3-hydrogenated pinicolic acid cyanide ethyl ester as well as derivatives and pharmaceutically acceptable salts thereof, and pharmaceutically acceptable auxiliary materials or carriers. The 3-hydrogenated pinicolic acid cyanide ethyl ester is a PI3K / mTOR dual inhibitor; the invention also relates to application of the 3-hydrogenated pinicolic acid cyanide ethyl ester medicine to promotion of cell autophagy and application of the 3-hydrogenated pinicolic acid cyanide ethyl ester medicine to preparation of medicines for treating tumors such as gastric cancer, liver cancer, lung cancer, prostatic cancer and nasopharynx cancer and the like, neurodegenerative diseases such as presenile dementia and the like, and diabetes. The 3-hydrogenated pinicolic acid cyanide ethyl ester medicin provides a novel clinical medication choice.
Owner:CHINA THREE GORGES UNIV

Method for creating wheat seedling drought premature senility physiological phenotype by using cell autophagy inhibitor

The invention belongs to the field of botany, and relates to a method for creating a wheat seedling drought premature senility physiological phenotype by using a cell autophagy inhibitor. The method inhibits the activity of phosphoinositide 3 phosphokinase (PI3K) necessary for formation of an autophagy vesicle membrane structure by using the cell autophagy inhibitor, and the time for creating thewheat seedling drought premature senility phenotype only needs 3 days. Through the method provided by the invention, the autophagy function of wheat cells under drought stress can be simply and quickly verified, and an important methodological basis is also provided for carrying out autophagy research on other plants under drought stress.
Owner:CROP RES INST SHANDONG ACAD OF AGRI SCI

Method for identifying functional kinase for regulating cell autophagy

The invention discloses a method for identifying functional kinase for regulating cell autophagy, and belongs to the technical field of biological information. The method comprises the following steps: carrying out transcriptome, proteome and phosphorylated proteome analysis on a cell sample before and after autophagy inducer treatment to obtain gene expression data, protein expression data and phosphorylation site data of the cell sample before and after autophagy inducer treatment; normalizing the obtained phosphorylation site data to obtain kinase intensity information; according to the obtained kinase intensity information, calculating kinase which is remarkably changed in the cell sample before and after treatment of the autophagy inducer; according to the obtained kinase with significant change, carrying out the significant change analysis on transcriptional expression, protein expression and phosphorylation modification levels of the kinase, and acquiring the functional kinase for regulating and controlling cell autophagy by combining the autophagy regulation and control function of the known kinase. According to the method, the kinase screening range can be effectively reduced, the workload of experimental verification is reduced, and the functional kinase for regulating and controlling cell autophagy is accurately identified.
Owner:HUAZHONG UNIV OF SCI & TECH
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