609 results about "Signalling pathways" patented technology

The present invention provides immunosuppression compounds capable of inhibiting the programmed cell death 1 (PD1) signalling pathway. The present invention further provides peptide based compositions for treatment of cancer or treatment of infections via immunopotentiation caused by inhibition of immunosuppressive signaling induced by PD-1, PD-L1, or PD-L2 and therapies using them, immunopotentiative substrates included as the active ingredient. Further, the invention provides an application of the compositions containing the peptide moieties for preventive and/or therapeutic agents for cancer, cancer metastasis, immunodeficiency, an infectious disease or the like and an application of peptide moieties as a testing or diagnostic agent or a research agent for such a disease.

Indazole-3-carboxamide compounds for treating various diseases and pathologies are disclosed. More particularly, the present invention concerns the use of an indazole-3-carboxamide compound or analogs thereof, in the treatment of disorders characterized by the activation of Wnt pathway signaling (e.g., cancer, abnormal cellular proliferation, angiogenesis and osteoarthritis), the modulation of cellular events mediated by Wnt pathway signaling, as well as genetic diseases and neurological conditions/disorders/diseases due to mutations or dysregulation of the Wnt pathway and/or of one or more of Wnt signaling components. Also provided are methods for treating Wnt-related disease states.

The activity of multiple proteins in a single living cell, portion of a cell or in a group of cells is simultaneously measured by introducing reporter molecules. The reporter(s) is chemically modified by the enzyme of interest. In some cases the enzyme(s) is affected by the addition of a stimulus or a pharmaceutical compound to the cell. The reactions between the enzymes and the reporters are diminished or terminated, and the reporter and modified reporter are removed. The activity of the enzyme(s) is determined by measuring the amount of reporter remaining, the amount of altered reporter produced, or by comparing the amount of reporter to the amount of altered reporter. A database is compiled of the activities of the different proteins. By performing a series of experiments at different time points, conditions, and varieties of cell types, a database is developed for molecular cellular mechanisms in health and disease states. By exposing cells to a variety of compounds data for drug development and screening is provided.

The invention discloses a method for improving the efficiency of CRISPR mediated homologous recombination. The method includes the steps of: inhibiting the expression of Lig4, DNA-PK and XRCC6 by shRNA so as to inhibit the non-homologous end joining (NHEJ) repair pathway; conducting fusion expression on sgRNA and shRNA at targeting genome specific positions to form shRNA-sgRNA polycistron; and placing the polycistron at the RNA polymerase II or RNA polymerase III promoter downstream. The carrier constructed by the method provided by the invention has a concise structure and is convenient to use, also enhances the homologous recombination efficiency by dozens of times, greatly expands the function and application of the CRISPR carrier, and is a good tool for functional gene and signal pathway research, medical research, and recombinant protein expression.

The present invention makes available a method for inducing neuronal differentiation and preventing the death or degeneration of neuronal cells both in vitro and in vivo. The subject method stems from the unexpected finding that, contrary to traditional understanding of neural induction, the default fate of ectodermal tissue is neuronal rather than mesodermal and/or epidermal. In particular, it has been discovered that preventing or antagonizing a signaling pathway in a cell for a growth factor of the TGF-β family can result in neuronal differentiation of that cell.

A programmable logic device having logic block that can be selectively placed in a reduced power consumption mode is provided. The PLD includes a plurality of logic array blocks (LABs) and a plurality of interconnects defining signal pathways between the plurality of LABs. Sleep control logic of the PLD issues a sleep control signal for placing at least a portion of the plurality of LABs in a sleep mode. Bias control logic of the PLD is in communication with the sleep control logic. The bias control logic is triggered by the sleep control signal to issue a first bias control signal and a second bias control signal. The first and second bias control signals are transmitted to corresponding transistors of the LABS. The first and second bias control signals apply a reverse bias to corresponding transistor wells to increase threshold voltages for the respective transistors.

The invention provides a method and device of realizing parallel receiving of GNSS multimode by adopting a single-pass radio frequency front-end and belongs to the radio frequency communication technical field. The method comprises: after RF frequency signal received entering the single-pass radio frequency front-end, a sampling period of a signal pathway is divided into N short time segments according to the number N of the modes of receiving signals, the RF signals is down converted into IF signals by a Mixer and a LPF low pass filter controlled by a time division multiplexed signal to shift the time division multiplexed signal, the single-pass radio frequency front-end receives a mode of signal within every short time segment and realizes parallel receiving signals of N modes at the single-pass radio frequency front-end in such periodic alternating repetition. The invention can realize the parallel receiving of GNSS multiple modes (including BD-2, GPS, Galileo and GLONASS) with only a single-pass radio frequency front-end under the control of the time division multiplexed system.

The invention relates to a cell model obtained after targeted knockout of a rabbit BMP2 gene based on CRISPR/Cas9 and application thereof, belonging to the technical field of molecular biology and biomedicine. According to the invention corresponding oligos are synthesized for three targeting sites of the rabbit BMP2 gene on the design principles of CRISPR/Cas9 and are constructed on px458 vectors; and a CRISPR/Cas9 system is constructed directed at the three targeting sites in rabbit mesenchymal stem cells, and the CRISPR/Cas9 system can effectively knock out the rabbit BMP2 gene, is easy to operate and has high rabbit BMP2 gene knockout efficiency. The cell model disclosed in the invention can greatly promote research related to the functions and signaling pathways of the BMP2 gene.

Disclosed are compounds of Formula I, including steroisomers, geometric isomers, tautomers, solvates, metabolites and pharmaceutically acceptable salts thereof, that are useful in modulating PIKK related kinase signaling, e.g., mTOR, and for the treatment of diseases (e.g., cancer) that are mediated at least in part by the dysregulation of the PIKK signaling pathway (e.g., mTOR).

The invention involves the treatment, prevention, and reduction of immunoinflammatory disorders involving the combination of an agent that increases the signal activity of a glucocorticoid receptor (e.g., glucocorticoid receptor agonist) and an agent that modulates the signaling activity of one or more signaling pathways selected from the NF-κB pathway, NFAT pathway, AP-1 pathway, and Elk-1 pathway such that proinflammatory cytokine secretion or production, or any other inflammatory response, is reduced. Further, screening methods are provided for identifying candidate compounds and strategies useful for treating, preventing, or reducing such conditions.

The present invention includes compositions, methods and kits for non-nuclear transfer reprogramming an adult differentiated cell obtained from an adult tissue into an ES-like cell. The reprogrammed cell can be converted into an ES-like cell which can be re- or trans-differentiated into various differentiated cell types. The present invention further relates to identification of a novel signaling pathway, and components thereof, which effect reprogramming of a cell. The present invention further comprises compositions, methods and kits for regulating the mammalian cell cycle and cellular proliferation, as well as for treating diseases and for identifying components that affect the cell cycle, and reprogram cells, among other things.

The invention includes compositions and methods for regulating PI3K p110 delta as an anti-retroviral therapy. The invention includes inhibiting p110 delta, a component of PI3K p110 delta signaling pathway, or any combination thereof in a cell as an anti-retroviral therapeutic approach for treating a retroviral infection, for example HIV. The invention includes a method of modulating PI3K p110 delta in a cell infected with a retrovirus by contacting the cell with an effective amount of a composition comprising an inhibitor of PI3K p110 delta.

The present invention relates to compositions and methods for identifying abnormalities in TSC signaling pathways. In particular, the present invention relates to methods of diagnosing and treating disorders such as tuberous sclerosis, which are caused by mutations in the TSC genes. The present invention further relates to methods and compositions for treating cancers mediated by TSC signaling disorders.

The invention belongs to the technical field of biology, and discloses a polypeptide containing two chimeric antigen receptor structures, nucleic acid for coding the polypeptide, a modified T lymphocyte, and a preparation method and application of the T lymphocyte. The polypeptide provided by the invention contains the two chimeric antigen receptor (CAR) structures, wherein one chimeric antigen receptor structure specifically targets a tumor cell, and the other one specifically targets a normal B lymphocyte, so that a CAR-T cell is effectively amplified through recognizing the B lymphocyte ofa blood circulation system, and more CAR-T cells arrive at a solid tumor part so as to specifically kill the tumor cell for improving a treatment effect on the solid tumor. The polypeptide further comprises an ScFv structure of an anti-PD-L1 monoclonal antibody, and the CAR-T cells can simultaneously secrete a PD-L1 monoclonal antibody which interdicts an immunosuppressive action medicated by a PD1/PDL1 signal pathway and T cell failure, so that the treatment effect on the solid tumor is improved, the functional activity of immune cells in vivo is prolonged at the same time, and finally the tumor recurrence is retarded and even avoided.

The present invention relates to cyclic compounds of formula (I) and their use to inhibit the programmed cell death 1 (PD-1) signaling pathway and/or for treatment of disorders by inhibiting an immunosuppressive signal induced by PD-1, PD-L1 or PD-L2.

A method for communicating data in a network environment is provided that includes receiving a request from an end user for a communications link, the request being used to initiate a communication session. A response is then received that is communicated to the end user in order to establish the communication session, the response being generated by a network node that was selected as a result of a loadbalancing decision. Port-level filtering for the communication session may then be invoked after the response such that separate data and signal pathways are established for selected information associated with the communication session.