43 results about "APOPTOGENIC PROTEIN" patented technology

The invention discloses a novel BH3 analogue targeted to Bcl-2 family anti-apoptotic protein and application of the novel BH3 analogue. The structural general formula of the BH3 analogue is as shown in the general formula A (the general formula A can be found in specification). A thought and method of peptidomimetics is adopted, the structure of a natural BH3 peptide fragment is simplified or modified, and the novel BH3 analogue is obtained. It is proved by experiments that the compound as shown in the general formula A and the Bcl-2 family anti-apoptotic protein represent excellent binding activity on the aspect of the molecular level; and it is shown by in-vitro carcinoma cell growth inhibition experiments that the compound has a certain in-vitro growth inhibition function on the human chronic myeloid leukemia cell K562, the human promyelocytic lenukemia cell HL-60 and the human tissue cell lymphoma cell U937. It is prompted by research results that the compound can be used as a candidate drug for preventing or treating related diseases caused by expression abnormality of anti-apoptotic protein in the Bcl-2 family protein.

The invention discloses a new method for diagnosing and reversing drug resistance of tumor cells to etoposide (also known as VP-16 and vepeside) by revealing a mechanism that the tumor cells generate drug resistance to a chemotherapy drug namely the etoposide. By detecting expressions of miRNA and apoptosis-related proteins in the tumor cells with different sensitivities to the etoposide, the inventor discovers that miR-17-5p and miR-20a show low expression in the cells with high sensitivities to the etoposide, but garget gene Bim-S pro-apoptotic proteins of the miR-17-5p and miR-20a show high expression. On the contrary, in the cells with drug resistance to the etoposide, the expression quantities of the miR-17-5p and miR-20a are high, but the Bim-S proteins show low expression. An inhibitor using the miR-17-5p and/or miR-20a can be used for effectively reversing the drug resistance of the tumor cells to the etoposide. The invention provides a brand-new simple and effective method for detection and/or prognosis of drug resistance of cancers to the etoposide, and provides a means of reversing the drug resistance of the tumor cells, which has great potential application values in clinical diagnosis and personalized treatment of tumors.

The invention discloses 432 novel acetylation sites identified in signal transduction proteins and pathways underlying human protein acetylation signaling pathways, and provides acetylation-site specific antibodies and heavy-isotope labeled peptides (AQUA peptides) for the selective detection and quantification of these acetylated sites/proteins, as well as methods of using the reagents for such purpose. Among the acetylation sites identified are sites occurring in the following protein types: Acetyltransferases, Adaptor/Scaffold proteins, Actin binding proteins, Adhesion proteins, Apoptosis proteins, Calcium-binding proteins, Cell Cycle Regulation proteins, Cell Surface proteins, DNA binding proteins, DNA replication proteins, Channel proteins, Chaperone proteins, Cellular Metabolism enzymes, Cytoskeletal proteins, DNA repair proteins, Endoplasmic reticulum proteins, Enzyme proteins, G protein and GTPase Activating proteins, Guanine Nucleotide Exchange Factors, Helicase proteins, Isomerase proteins, Extracelluar matrix proteins, Hydrolases, Ligase proteins, Lipid kinases, Inhibtor proteins, Lipid Binding proteins and Lyases.

The invention relates to use of Ruxolitinib in preparation of a drug for treating M2 type acute myeloid leukemia with t (8; 21) chromosome translocation, and the in-vitro effective concentration is 1 * 10<-6>-1 *10<-5>M. Drug Ruxolitinib is not only itself has the effect of inhibiting growth and inducing apoptosis on leukemia cell Kasumi-1, and enhances the drug sensitivity of the leukemia cell Kasumi-1 on rsTRAI by up-regulation of mRNA and protein expression level of DR4, up-regulation of cell apoptosis protein Bax expression, activation of apoptosis protein caspase-3 and inhibition of NF-kappa B protein activity. The drug can be used for treating the M2 type acute myeloid leukemia with t (8; 21) chromosome translocation, the new drug for treating the M2 type acute myeloid leukemia with t (8; 21) chromosome translocation is provided, and a new approach for overcoming TRAIL resistance in leukemia cells can be provided.

The invention relates to the technical field of life beauty, and discloses a mole removing paste which is prepared from the following raw materials by weight: 0.25 milligram of radix sophorae flavescentis, 0.25 gram of golden cypress, 0.15 milligram of gallnut, 0.15 milligram of honeycomb and 0.2 milligram of borneol. The raw materials are uniformly mixed, and CAS apoptosis protease is extracted. When in use, the product can quickly decompose and soften cutin and decompose melanin, so that the mole scabs and falls off along with metabolism of a human body, and no scar is left.

The invention discloses application of bitter gourd exosomes in radiation heart injury protection, the bitter gourd exosomes and rat myocardial cells (H9C2) are co-cultured and subjected to radiation treatment, MTT experiments show that 5-25 [mu] g/ml of the bitter gourd exosomes can promote the cell viability of the radiated H9C2 myocardial cells, and 10 [mu] g/ml of the bitter gourd exosomes are selected as the use concentration of the bitter gourd exosomes. Under the condition that the bitter gourd exosome is 10 [mu] g/ml, Ki-67 fluorescent staining proves that the bitter gourd exosome can promote proliferation of radiated H9C2 myocardial cells. An Annexin V-PE/7-AAD flow apoptosis experiment and an apoptosis protein cleaved-caspase3 immunoblotting test prove that the bitter gourd exosome can be used for reducing the apoptosis of H9C2 myocardial cells after radiation. Immunofluorescence staining and protein immunoblotting of a DNA damage marker gamma-H2A. X show that the bitter gourd exosome can reduce DNA damage of H9C2 myocardial cells after radiation.

The invention discloses an apoptotic protein fusion type anti-HER-2 single-chain antibody as well as a preparation method and application thereof. The apoptotic protein fusion type anti-HER-2 single-chain antibody is formed by coupling an anti-HER2 single-chain antibody with apoptotic protein in different series modes, and the apoptotic protein is a cytochrome C or DNA fragmentation factor 40, canbe specifically coupled with the anti-HER-2 single-chain antibody to form a DFF40-scFv fusion type single-chain antibody and an nCytc (series)-scFv fusion type single-chain antibody. The apoptotic protein fusion type anti-HER-2 single-chain antibody is inserted into the upstream of scFv through a cDNA sequence of the apoptotic protein and cloned into an expression vector to construct recombinantplasmids, the recombinant plasmids are transferred into cells to induce expression of the apoptotic protein fusion type anti-HER-2 single-chain antibody, the preparation method is easy to construct and express, the constructed apoptotic protein fusion type anti-HER-2 single-chain antibody can specifically target HER-2 high-expression malignant tumors and mediate cancer cell apoptosis, and can be used for preparing drugs for targeted therapy of HER-2 high-expression cancers.

The invention discloses preparation of a compound of Au and an anti-apoptotic protein antagonistic peptide and application of the compound in synergistic induction of tumor cell apoptosis, and relates to the field of anti-tumor drugs. Mixing a gold salt solution with the anti-apoptotic protein antagonistic peptide containing sulfydryl; under the conditions of certain temperature and pH, redox reaction is carried out, high-valence Au ions are reduced into Au atoms or monovalent Au ions, and Au acts on sulfydryl of polypeptide to form a compound AuP; the sulfydryl-containing anti-apoptotic protein antagonistic peptide is selected from polypeptides with an intracellular anti-apoptotic protein antagonistic function. The AuP compound has broad-spectrum anti-tumor activity, and compared with a common peptide-gold compound or gold compound, the AuP compound can inhibit the activity of thioredoxin reductase and antagonize the function of high-expression anti-apoptotic protein at the same time, the single-drug double-target synergistic effect is achieved, and the curative effect is remarkably improved. The compound can be used for treating various malignant tumors such as chronic lymphocytic leukemia, acute monocytic leukemia and non-Hodgkin lymphoma.

The invention discloses application of tartary buckwheat flavone in preparation of a medicine for treating pancreatic cancer, and finds that the tartary buckwheat flavone can obviously promote apoptosis of pancreatic cancer cells, inhibit proliferation of the pancreatic cancer cells and break DNA (deoxyribonucleic acid) in the aspect of researching the activity effect of the tartary buckwheat flavone on the pancreatic cancer cells, and has huge potential in the aspect of exerting tumor resistance. The tartary buckwheat flavone is prepared from tartary buckwheat powder through alcohol extraction and resin purification, the preparation method is simple, when the tartary buckwheat flavone is used for preparing the medicine composition for preventing, treating or improving pancreatic tumors, the tartary buckwheat flavones can promote the expression of apoptosis protein Caspase-3, Caspase-8, Cleave-Caspase-3, Cleave-Casspse8, Cleave-caspase9 and Bax and inhibit expression of anti-apoptosis protein Bcl-2, it is proved that the tartary buckwheat flavone has the activity function of promoting apoptosis of the pancreatic cancer cells, and then the activity effect of resisting pancreatic cancer is achieved.

The invention relates to a traditional Chinese medicine composition for treating lymphoma and a preparation method and application thereof. The traditional Chinese medicine composition is prepared from the following medicines in parts by weight: 10-30 parts of spica prunellae, 3-18 parts of edible tulip, 9-30 parts of salvia chinensis, 9-30 parts of herba violae, 3-18 parts of semen impatientis, 25-35 parts of raw semen coicis, 9-30 parts of rhizoma sparganii, 9-30 parts of curcuma zedoary, 10-30 parts of cortex lycii radicis, 3-18 parts of herba patriniae, 3-18 parts of turtle shell, 3-18 parts of rhizoma anemarrhenae, 3-18 parts of pericarpium citri reticulatae, 3-18 parts of ginger processed pinellia, 5-30 parts of white poria cocos and 3-9 parts of liquorice. The traditional Chinese medicine composition further comprises the following raw material medicine in parts by weight: 0.05-0.1 part of realgar. The traditional Chinese medicine composition has the advantages that the traditional Chinese medicine composition can effectively inhibit proliferation and growth of lymphoma cells Raji cells and Jeko-1 cells, and time and concentration dependence is shown. In addition, the detoxification and tumor elimination formula can also up-regulate expression of pro-apoptotic protein of lymphoma cells and inhibit expression of anti-apoptotic protein of the lymphoma cells at the same time, so that obvious apoptotic bodies are formed, apoptosis of the lymphoma cells is effectively promoted, and the detoxification and tumor elimination formula is concentration-dependent.

The invention discloses application and a method of E199L protein in promoting cell apoptosis. The invention provides an application of E199L in promoting cell apoptosis, the E199L competitively destroys the interaction between anti-apoptosis proteins and BAK and/or BAX through the wide interaction between the E199L and the anti-apoptosis proteins such as BCL-XL, MCL-1, BCL-W and BCL-2A1, and finally induces cell apoptosis.

The invention relates to the technical field of treatment of ocular tissue lesions, and particularly discloses application of ellagic acid in preparation of a medicine for relieving ocular tissue lesions, wherein the ellagic acid can regulate and control the rise of the expression level of LC3b/a protein and the reduction of the expression level of p62 protein in eyeball tissues of diabetic mice, improve autophagy disorder of diabetic ocular tissues, relieve diabetic mouse eye tissue pathological injury, inhibit eye tissue inflammation NLRP3 and IL-1beta protein expression, inhibit eye tissue apoptosis protein c-caspase1 expression, and inhibit mouse eye tissue pyroptosis protein GSDME, GSDME-N and GSDMD-N expression, so that GSDMD and GSDME mediated pyroptosis is inhibited, and an anti-inflammatory protection effect on cells is achieved. The ellagic acid provided by the invention can relieve pathological injury of eye tissues of diabetic mice and has a protective effect on retinas of the diabetic mice.

The invention provides an anti-apoptotic PTD-FNK protein and a method for preparing the same. Total RNA (ribonucleic acid) of the livers of rats is used as a template, prokaryotic expression vector pET28a(+)-PTD-FNK plasmids of PTD-FNK proteins are constructed by the aid of molecular cloning technologies and gene point mutation technologies, the prokaryotic expression vector pET28a(+)-PTD-FNK plasmids are transformed into Escherichia coli BL21(DE3), PTD-FNK soluble expression is induced at the low temperatures, and proteins are extracted from supernatants and precipitates.