107 results about "Akt signalling" patented technology

The invention discloses the application of an IL-11 monoclonal antibody in inhabiting a PI3K / Akt signal channel. The concentration of the IL-11 monoclonal antibody is 8 mug / mL, and the dosage of the IL-11 monoclonal antibody is 10 mug. The safe and efficient PI3K / Akt signal channel inhibitor, namely the IL-11 monoclonal antibody is found, and can be specifically combined with IL-11 secreted by cells to induct PTEN transcription, up-regulate PTEN expression and inhibit the expression of AKT on the downstream portion of the PI3K / Akt signal channel, and then the whole signal channel is inhibited. The inhibitor is a natural antibody, so that toxic and side effects are reduced and safety and efficiency are high.

The invention provides 3-(2-amino-ethyl)-5-(3-cyclohexyl-propylidene)-thiazoline-2,4-diketone and derivatives thereof. The compounds can be used as a dual inhibitor for Raf / MEK / ERK and PI3K / Akt signaling pathways, and can be used for treating cancer.

The invention discloses new application of a 2-(4-fluorophenyl)-3-nitro-8-O-ethyl-2-hydro-benzopyran compound, in particular application of the compound serving as phosphatidylinositol-3-kinase (PI3K) inhibitor. The PI3K inhibitor can inhibit PI3K and disturb a PI3K / AKT signal channel, has good treatment effect on multiple tumors, particularly malignant hematological diseases, can effectively control the propagation of tumor cells and induce the apoptosis thereof, and has the effect of inhibiting and treating the tumors; and meanwhile, the PI3K has low toxicity.

The invention discloses a purpose of a polyether compound in medicine preparation and an anti-tumor medicine screening method. The medicine is used for regulating and controlling at least one of the following signal channels: a calcium ion signal channel, a Wnt signal channel, a Hippo signal channel, a TNF signal channel, a VEGF signal channel, a p53 signal channel, an NF-kappa B signal channel, an Ras signal channel, an mTOR signal channel, an RNA degradation signal channel, a PPAR signal channel, a cAMP signal channel, an HIF-1 signal channel, an Insulin signal channel, an AMPK signal channel, an Rap1 signal channel, an apoptosis signal channel, a cell cycle signal channel, a cGMP-PKG signal channel, a DNA copying signal channel, an MAPK signal channel, a PI3K-Akt signal channel and an autophagy signal channel. The polyether compound provided by the invention can cause the tumor cell death through regulating and controlling various signal channels; and a better anti-cancer effect isachieved.

The invention discloses an application of Cornulin as a target in preparation of a drug for preventing and treating psoriasis. Cornulin is taken as the drug target on the gene level and / or the protein level for the drug. Cornulin is positively correlated with development of psoriasis, when a Cornulin antibody with proper concentration is used for treating an imiquimod mouse model of psoriasis, scales and skin lesion thickness can be improved, and AKT signals can be inhibited to inhibit development of psoriasis and inhibit skin lesion for returning to normal; compared with other psoriasis treating drugs, and the Cornulin antibody has the advantages that the intervention target is clearer, that is, AKT signal related molecular pathways in inflammatory pathways for psoriasis incidence are targeted.

The invention discloses application of rabdocetsin in preparing a product for inhibiting proliferation of esophageal squamous carcinoma cells. Proofed by experiment, the application has the advantages that the rabdocetsin can effectively inhibit the proliferation of the esophageal squamous carcinoma cells, the cloning formation of the esophageal squamous carcinoma cells, affecting the cycle progress of the esophageal squamous carcinoma cells, inducing the retardation of the cycle of the esophageal squamous carcinoma cells, inhibiting the DNA (deoxyribonucleic acid) restoration of the esophageal squamous carcinoma cells, inducing the withering of the esophageal squamous carcinoma cells, regulating up the expression amount of cleaved-caspase-9, regulating up the expression amount of cleaved-caspase-3, regulating up the expression amount of cleaved-PARP, inhibiting Akt signal pathways, inhibiting NF-kappa B signal pathways, and inhibiting the growth of tumors caused by the esophageal squamous carcinoma cells; the important application value is realized.

The invention discloses CXCL13 oncoprotein and an application of targeted medicine for the CXCL13 oncoprotein in the tumor aspect. A method for preparing the tumor targeted medicine includes the steps of screening antibodies capable of effectively reducing the high expression of the CXCL13 oncoprotein or neutralizing the activity of the CXCL13 oncoprotein; preparing the corresponding tumor targeted medicine through the antibodies. According to the CXCL13 oncoprotein and the application, the anti-CXCL13 monoclonal antibodies can achieve the good anti-tumor effect by suppressing a p-AKT signal channel, a p-ERK signal channel and an EMT signal channel and accordingly suppressing growth, invasion and metastasis of tumor cells.

The invention belongs to the technical field of functional analysis methods of disease metabolism biomarkers, and provides a biomarker metabolic pathway and an analysis method. The metabolic biomarker is stearic acid, phytosphingosine, glycine, glutamine and phospholipids; an acting target spot of the metabolic biomarker is a target protein related to a depression nervous system, immune response and endocrine; and the metabolic pathway is a PI3K-Akt signaling pathway, an mTOR signaling pathway, an MAPK signaling pathway, an erbB signaling pathway, a neurenergen signaling pathway, an Rap1 signaling pathway and an Ras signaling pathway. A functional network analysis method suitable for depression characteristics is established, and the clinical application of these biomarkers helps to optimize the diagnosis of depression, and can provide some valuable clues for the subsequent depression network function researches.

The present invention discloses the use of selenate or its pharmaceutically acceptable salts, especially in supranutritional amounts, in methods and compositions for inhibiting the growth or proliferation of tumor cells. The present invention also discloses the use of selenate or its pharmaceutically acceptable salts in combination with one or both of a hormone ablation therapy and a cytostatic agent or cytotoxic agent, for inhibiting the growth or proliferation of tumor cells. In certain embodiments, the methods of the invention are useful for treating or preventing cancers, especially cancers in which the Akt signaling pathway is activated, such as prostate cancer. Additionally, the present invention discloses the use of selenate or its pharmaceutically acceptable salts in combination with a hormone-ablation therapy and optionally a cytostatic agent or cytotoxic agent in methods and compositions for treating hormone- dependent cancers.

Provided herein are methods of detecting or inhibiting melanoma growth based on Gab2 protein expression. Gab2 protein was found to be either amplified and / or overexpressed in melanoma. Gab2 protein expression correlated with clinical melanoma progression and higher levels of expression were seen in metastatic melanomas compared to primary melanoma and melanocytic nevi. Over-expression of Gab2 potentiates, whereas silencing of Gab2 reduces, migration and invasion of melanoma cells. Gab2 mediated hyperactivation of Akt signaling in the absence of growth factors and inhibition of the PI3K-Akt pathway decreased Gab2-mediated tumor cell migration and invasive potential. Gab2 over-expression resulted in enhanced tumor growth and metastatic potential in vivo. These results demonstrate a previously undefined role for Gab2 in melanoma tumor progression and metastasis.

The invention discloses a function and application of SH2B adapter protein 3(SH2B3) for treating cardiac hypertrophy. By virtue of the SH2B adapter protein 3(SH2B3), interrelation between the expression of SH2B3 gene and cardiac hypertrophy is determined; when the cardiac hypertrophy occurs, the expression of SH2B3 is obviously increased; activation of an Akt signal channel is suppressed by SH2B3 gene defect, the cardiac hypertrophy and fibrosis are also suppressed, and the heart function is protected; the activation of the Akt signal channel is remarkably accelerated by over expression of the SH2B3 gene, the cardiac hypertrophy and fibrosis are improved, and the heart function is deteriorated. Therefore, the SH2B3 gene can be used as a medicine target mark for screening medicines for protecting the heart function and / or preventing, relieving and / or treating the cardiac hypertrophy; the SH2B3 gene can be used as a target gene in gene treatment for designing and preparing medicines and / or biological reagents for protecting the heart function and / or preventing, relieving and / or treating the cardiac hypertrophy, so that an effective novel way is provided for the treatment of the cardiac hypertrophy.

The study is different from other studies in the prior art, and a biological method is used to explore the mechanism of action of AdipoRon on the treatment of type 2 diabetes. Liver cells are used asan experimental subject for construction of an experimental group blocking a P13 / Akt signaling pathway, then the AdipoRon acts, and expression of related carbohydrate genes of the liver cells is analyzed to investigate the cellular mechanism of the AdipoRon on the treatment of the type 2 diabetes. At present, the study is not reported at home and abroad. Almost all methods for treating the type 2diabetes require proper diet and exercise, and produce adverse effects such as hypoglycemia and weight gain, by oral administration of the AdipoRon, excess calorie intake can be safely reduced, and consequence caused by a sedentary lifestyle can be reduced, so that the AdipoRon provides a novel treatment method, a lot of money for purchase of db / db mice and double gene knockout mice can be saved.

The invention provides a polypeptide for targeting a liver cancer vascular endothelial cell and application thereof. The polypeptide is characterized by comprising an amino acid sequence of SPSCALP. The polypeptide SPSCALP provided by the invention can target the liver cancer vascular endothelial cell, is used for mainly inhibiting a PI3K-AKT signal path of the liver cancer vascular endothelial cell and inhibiting the biological function of the liver cancer vascular endothelial cell, but has no remarkable influence on normal liver tissue endothelial cells.

The invention discloses a function and an application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy and belongs to the field of gene functions and applications. The mutual relation between expression of TRIM32 and myocardial hypertrophy is determined, a research result proves that in a model where myocardial hypertrophy occurs, the expression of TRIM 32 is remarkably reduced than that of a normal group; if expression of TRIM 32 is inhibited, activation of an AKT signal path is remarkably promoted, myocardial hypertrophy and fibrosis are promoted, and the cardiac function is deteriorated; if overexpression of TRIM 32 is promoted, activation of the AKT signal path is remarkably inhibited, myocardial hypertrophy and fibrosis are inhibited, and the cardiac function is protected. Therefore, TRIM32 can be taken as a target gene and used for screening or preparing a drug for protecting the cardiac function, preventing cardiac fibrosis and / or preventing, relieving and / or treating myocardial hypertrophy, and a new effective way is provided for treatment of myocardial hypertrophy.

The invention provides an application of inhibitor of histone deacetylase HDAC 6 in preparing drugs for preventing and treating acute kidney injury. Furthermore, the histone deacetylase HDAC 6 is Tubastatin A. The selective inhibitor of HDAC 6 can lighten the renal pathology damage of acute kidney injury induced by cis-platinum and improve the kidney function. The HDAC6 inhibitor TA can lower the release of inflammatory factors and lighten the oxidative stress reaction through regulating an AKT signal access, an NF-KB inflammation access, an autophagy level and an E-cadherin expression; thus the apoptosis of kidney tubule cell and necrosis of tubule expansion are reduced, the renal pathology damage and kidney function are improved; the inhibitor can protect the kidney structure and function in the acute kidney injury. Therefore, HDAC6 is likely to be an important target point to prevent and treat the acute kidney injury.

The invention belongs to the fields of biotechnology and medicine, and in particular relates to an application of an SET gene in preparing a product for diagnosing and / or treating gastric cancer. It is provided that the SET achieves frequent high expression (80%) in gastric cancer tissues, and the increase in SET expression is significantly correlated to aggressive phenotype and worse prognosis of a patient with the gastric cancer (P is less than 0.05). The low expression of the SET can obviously inhibit the migration and the invasion of gastric cancer cells. In addition, the SET, by virtue of a PP2A / Akt signaling pathway, can promote tumor malignant transformation. Furthermore, the gastric cancer tissues are obviously higher than para-carcinoma tissues in SET protein level. Therefore, the SET gene can serve as a specific marker gene for diagnosing the gastric cancer, so that it is more accurate and rapid to diagnose the gastric cancer. The SET gene provided by the invention provides a novel therapeutic target for the prevention and the treatment of the gastric cancer.

The invention belongs to the technical field of medicines, and relates to new medicinal application of andrographolide, in particular to new application of the andrographolide in preparation of medicines for treating spongioblastoma. The andrographolide can restrain the growth of human spongioblastoma cells in vivo and in vitro, the mechanism of the andrographolide relates to down regulation of activation of a PI3K / Akt signal, and then human andrographolide cell cycles are induced to be retarded in a G2 / M period. The andrographolide can be used for preparing intestinal canal and parenteral administration dosage forms and is used for treating human spongioblastoma.

The invention provides a method for enhancing the secretion function of mesenchymal stem cells and application, and belongs to the technical field of biology. Research shows that by using Hyaluronic acid sodium (HA) to pretreat umbilical cord mesenchymal stem cells in vitro, the secretion function of the umbilical cord mesenchymal stem cells can be significantly promoted, secretion of HGF, SCF, EGF, VEGF and other factors is promoted, activation of a PI 3K-AKT signal channel is further promoted, and the repair effect on damage is enhanced. The method is simple, convenient, low in cost and highin safety, and therefore the method HAs good practical application value.

The present disclosure includes methods and compositions for treating any condition or disorder that benefits from activation of the Akt signaling pathway. These methods and compositions involve the use of valproic acid, derivatives, analogs and compositions including the same for treating muscular disorders, such as muscular dystrophy.

The invention discloses application and a detection method of an LINC02085 gene, and belongs to the technical field of molecular biology of rheumatism. According to the invention, a specific PCR primer is designed and synthesized according to the extracted total RNA sequence, and an Rt-qPCR technology is utilized to find that the expression of LINC02085 in peripheral blood mononuclear cells of a rheumatoid arthritis (RA) patient is significantly increased, which proves that the LINC02085 can be applied to the preparation of a preparation for auxiliary diagnosis, treatment or prognosis evaluation of rheumatoid arthritis. The pcDNA3.1-LINC02085 sequence for specific overexpression of the gene and the si-LINC02085 sequence for small interference of the gene are designed and synthesized at thesame time, proliferation of synovial fibroblasts (FLS) and inflammatory response of FLS induced by TNF-alpha can be remarkably inhibited by regulating and controlling a PI3K / AKT signal channel, and the gene can become a molecular targeted therapy tool for RA.

Aspects of the invention relate to methods and compositions for treating Alzheimer's disease (AD). In some embodiments, the invention provides methods for screening and identifying compounds that selectively inhibit the targeting of the insulin-Akt signaling pathway by Aβ oligomers.

The invention relates to application of an extracellular acidic environment in delaying apoptosis of granulocytes. Through inhibiting generation of intracellular active oxygen, the extracellular acidic environment reduces the level of glutathionylation of intracellular globular actin and promotes formation of fibrous actin, thereby activating an Akt signal path and leading to delaying of cell apoptosis. According to the invention, the important role of a microenvironment pH value in immunoloregulation is revealed; a novel path and novel targets revealed in the invention are expected to provide novel ideas and strategies for designing a novel blood transfusion medical storage scheme, a novel neutrophile granulocyte infusion scheme and a novel treatment scheme for diseases and tumors related to inflammations in clinical practice in the future.

The invention relates to the technical field of biological pharmaceuticals, in particular to a fusion protein and an application thereof. According to the fusion protein, a plasma membrane positioningsequence, a Dab1 protein, a light-sensitive protein and a fluorescent protein are in fusion to be positioned to a lipid raft region or a non lipid raft region of a cytoplasmic membrane, and through illumination, quick activation and adjustment and control of a PI3K / Akt signal channel can be realized locally at a high time and space resolution. The fusion protein has great important significance in quick effective specific opening and closing control of the signal channel, contributing to understanding a cascade transmission rule of signals and researching diseases closely related to the signal channel.

There is provided a method for promoting epithelium repair in a subject, the method comprising administering to the subject a therapeutically effective amount of an activator of PI3K / Akt signalling.

The invention discloses a drug composition for treating B cell lymphoma. The drug composition comprises a PI3K / AKT signal pathway inhibitor and a chemotherapeutic drug, and further comprises targetedCD20 infliximab, such as rituximab. The drug composition provided by the invention is especially suitable for treating relapsed or refractory B cell lymphoma. In view of the key effect of a CSC (cancer stem cell) in the transferring and drug resisting process, the invention provides a new pro-differentiation therapy strategy for the CSC, that is, a decisive signal conduction pathway for maintaining the dryness of the stem cell is determined, and then the pathway is interfered to promote CSC differentiation. The differentiation cell is finally sensitive to a routine treatment method (such as chemotherapy). Under the condition, the PI3K / AKT signal pathway inhibitor is combined with an R-CHOP scheme to exert a good effect of treating drug-resisting DLBCL (diffuse large B cell lymphoma).

The present invention belongs to the technical field of medicines, specifically relates to an application of ebracteolatain A (EA) in preparing drugs for treating breast cancer and reveals for the first time that the ebracteolatain A can inhibit expression of PKD1 protein in breast cancer cells in a dose-dependent manner. At the same time, the overexpression of PKD1 can significantly restore an inhibitory effect of the ebracteolatain A on proliferation of breast cancer cells. Finally, through mechanism research and analysis, the ebracteolatain A is confirmed to inhibit the proliferation of thebreast cancer cells by inhibiting MEK / ERK and PI3K / AKT signaling pathways mediated by the specific target PKD1. The research finds that the PKD1 plays a very important role in process of inhibiting the proliferation of breast cancer by the ebracteolatain A and is a key target in treatment process of the breast cancer.

The invention belongs to the technical field of drug preparation, and particularly relates to an application of an excreted factor GREM2 to 2-type diabetic therapy drug preparation. The research proves that a GREM2 transgenic mouse has obviously improved sugar tolerance and obviously increased insulin sensitivity. Further experiments show that a hepatic insulin downstream P-AKT signal path of the transgenic mouse is remarkably enhanced, prompting that the hepatic insulin sensitivity is increased. An ob diabetic mouse model is used to find that after adenovirus overexpression GREM2 protein is given to an ob mouse, blood glucose is obviously improved, fatty liver is obviously improved, and insulin sensitivity is remarkably increased. Therefore, the GREM2 can be applied to preparation of sugar-reducing drugs and drugs for improving 2-type diabetes, and provides a new drug target for clinically curing the 2-type diabetes.

The invention discloses application of CD82 / TIMP1 in preparation of medicine for inhibiting migration of human pancreatic cancer cells, and belongs to the technical field of biological engineering. CD82 and TIMP1 are directly combined to trigger the intracellular transport and circulation of TIMP1, block cytoskeleton remodeling, reduce lamellipodia / filopodia projecting formation and inhibit cell viability and migration. TIMP1 enhances an Akt signaling pathway by CD82 on a pancreatic cancer cell membrane, blocks cytoskeleton remodeling, reduces lamellipodia / filopodia projecting formation, inhibits cell viability and migration, and has no effect on the growth of cancer cells. The deep explanation on a TIMP1 / CD82 axis as a new signaling pathway for inhibiting tumor metastasis helps us more clearly know and understand the process of cancer metastasis, and helps find a critical juncture of prevention and control of cancer metastasis.

The invention discloses a traditional Chinese medicine preparation, and preparation and application thereof. The traditional Chinese medicine preparation is prepared from the following raw materials in proportion by mass: 10 to 30 parts of prepared rehmannia roots, 10 to 30 parts of radix rehmanniae, 3 to 6 parts of cortex cinnamomi, 10 to 20 parts of radix salviae miltiorrhizae, 10 to 20 parts of radix angelicae sinensis, 10 to 20 parts of seeds of Chinese dodder, 10 to 20 parts of fructus psoraleae, 10 to 20 parts of herba epimedii, 9 to 30 parts of radix pseudostellariae, 10 to 15 parts of radix polygoni multiflori preparata, 8 to 15 parts of radix paeoniae rubra, 9 to 15 parts of cortex moutan, 9 to 15 parts of poria cocos, 9 to 15 parts of bighead atractylodes rhizome, 15 to 30 parts of Chinese yam and 3 to 6 parts of liquorice roots. The traditional Chinese medicine preparation has the advantages that the bone marrow mesenchymal stem cell multiplication of an AA patient can be promoted; by activating an SDF-1 / CXCR4-PI3K / AKT signal path, the aplastic anemia MSCs function restoration can be effectively promoted; the mRNA expression of MSCs VEGF, SDF-1, CXCR4 and Akt of mice can be effectively improved; the hemopoietic microenvironment can be improved.