54 results about "STAT5" patented technology

Compounds, compositions and methods are provided for modulating the expression of STAT5. The compositions comprise oligonucleotides, targeted to nucleic acid encoding STAT5. Methods of using these compounds for modulation of STAT5 expression and for diagnosis and treatment of diseases and conditions associated with expression of STAT5 are provided.

Compounds, compositions and methods are provided for modulating the expression of STAT5. The compositions comprise oligonucleotides, targeted to nucleic acid encoding STAT5. Methods of using these compounds for modulation of STAT5 expression and for diagnosis and treatment of diseases and conditions associated with expression of STAT5 are provided.

The invention is directed to diagnostic and monitoring methods (assays) for cancer and kits that may be used in such methods. More particularly, an aspect of the invention relates to the use of activated Stat5 for diagnosing and monitoring breast cancer and predicting the effectiveness of cancer treatment. The invention also relates to the use of screening assays for discovering compounds that effect levels of activated Stat5.

The present invention relates to novel compounds, compositions containing same and methods for inhibiting STAT3 and / or STAT5 activity or for the treatment of a STAT3 or STAT5-dependent cancer using said compounds; or a pharmaceutically acceptable salt, solvate or prodrug thereof.

The invention discloses application of PPM1A in the treatment and diagnosis of asthma. To be specific, the invention relates to application of the PPM1A as a detection target in preparation of a diagnostic reagent for bronchial asthma, application of a regent detecting the PPM1A in preparation of a diagnostic reagent for bronchial asthma, application of the PPM1A as a therapeutic target in preparation or screening of a drug for treating bronchial asthma, and application of a substance suppressing PPM1A expression in preparation of a drug for treating bronchial asthma. The invention discloses the application of PPM1A in detecting the plasma of the bronchial patient; expressions of the PPM1A in an asthma patient and a normal person are discovered to be different for the first time; and the indicator can be used as the molecular marker of the bronchial asthma. Besides, the PPM1A acting as a miR-1165-3p target gene is discovered to be able to promote Th2 differentiation through the STAT1,STAT5, and Akt accesses to cause the asthma, so that the PPM1A can used as a therapeutic target for asthma.

The present invention relates to a method and substance for maintaining the pluripotency and self-replication ability of a stem cell, such as a hematopoietic stem cell, while keeping it undifferentiated. Specifically, the present invention provides a composition for maintaining the expansion or pluripotency of a stem cell, comprising active STAT5, and a method using the same. STAT5 may be in the form of a protein or a nucleic acid. The composition may contain a cellular physiologically active substance (e.g., SCF, TPO, Flt-3L, etc.). The present invention also relates to a cell, a tissue and an organ prepared from the stem cell.

The invention discloses development and an application of a therapeutic agent for TSLP-related diseases, and relates to an antibody binding to TSLP protein or an antigen binding part thereof as well as a preparation method and an application of the antibody. The antibody can be combined with human TSLP and / or cynomolgus monkey TSLP with high affinity, can block the combination of the TSLP and TSLPR, and can inhibit the transduction of a TSLP stimulating signal through an STAT5 pathway.

The invention relates to cytokine receptor-like factor 2 (CRLF2), and particularly certain mutant forms of CRLF2, as prognostic and therapeutic targets in precursor B-cell acute lymphoblastic leukemia (B-ALL). Mutant CRLF2 with a Phe232-Cys (F232C) mutation is overexpressed and constitutively activates STAT5 in a subset of B-ALL patients with particularly poor prognosis. Methods and compositions useful for identifying, inhibiting expression, and inhibiting activity of the mutant CRLF2 are provided. Also provided are methods and compositions useful for treating B-ALL.

Single nucleotide polymorphic sites at positions 3117, 12195, 13244, 13319, and 13516 of the bovine STAT5 gene are associated with improved fertilization rate and / or improved embryo survival rate. Also disclosed are nucleic acid molecules, kits, methods of genotyping and marker assisted bovine breeding methods.

The activity of a number of therapeutic antibodies is mediated in part by antibody-dependent cell-mediated cytotoxicity (ADCC). An engineered effector cell line expressing the low affinity Fc receptor, FcγR111a (CD16), that responds to ligation of the Fc moiety of antibody bound to the specific antigen expressed on target cells by activation of a NFAT responsive reporter gene is described. In this cell line the firefly luciferase (FL) reporter gene is regulated by a novel synthetic chimeric promoter containing binding sites for NF-AT, AP1, NFkB, and STAT5 that confers improved sensitivity, an improved dynamic range, an improved tolerance to human serum and a reduced incubation time, relative to engineered effector cell lines that express a NFAT regulated reporter-gene, when used in an ADCC assay together with engineered target cells. The target cells have been engineered to over-express a constant high level of the specific antigen recognized by the therapeutic antibody, and homologous control cells have been developed in which the gene encoding the specific drug target has been invalidated by genomic editing. Target cells that have been engineered to over-express a constant level of CD20 together with homologous control cell line, in which the gene encoding CD20 has been invalidated, have been used to quantify the ADCC activity of Rituxan with a high degree of precision and with minimal interference from human serum.

Here, the inventors disclose the treatment of imatinib mesylate resistant chronic myelogenous leukemia cells with a cotreatment of vorinostat (SAHA, suberoylanilide hydroxamic acid) and dasatinib, a dual Abl / Src kinase (TK) inhibitor. Combined treatment of cultured human CML and BaF3 cells with vorinostat and dasatinib induced more apoptosis than either agent alone, as well as synergistically induced loss of clonogenic survival, which was associated with greater depletion of Bcr-Abl, p-CrkL and p-STAT5 levels. Co-treatment with dasatinib and vorinostat also attenuated the levels of Bcr-AblE255K and Bcr-AblT315I and induced apoptosis of BaF3 cells with ectopic expression of the mutant forms of Bcr-Abl. Finally, co-treatment of the primary CML cells with vorinostat and dasatinib induced more loss of cell viability and depleted Bcr-Abl or Bcr-AblT315I, p-STAT5 and p-CrkL levels than either agent alone.

The invention is directed to diagnostic and monitoring methods (assays) for cancer and kits that may be used in such methods. More particularly, an aspect of the invention relates to the use of activated Stat5 for diagnosing and monitoring breast cancer and predicting the effectiveness of cancer treatment. The invention also relates to the use of screening assays for discovering compounds that effect levels of activated Stat5.

The present invention provides nucleic acid molecules that inhibit STAT5 expression. Methods of using the nucleic acid molecules are also provided.

The invention discloses application of a vaccaria segetalis seed extract in promotion of cow lactation. The application of the vaccaria segetalis seed extract protected by the invention comprises at least one of the following from (1) to (6): (1) promoting cow lactation; (2) promoting cow mammary epithelial cells to secrete lactose; (3) promoting the cow mammary epithelial cells to secrete beta-casein; (4) promoting the cow mammary epithelial cells to secrete triglyceride; (5) promoting Stat5 gene expression in the cow mammary epithelial cells; (6) improving the expression quantity and / or activity of Stat5 proteins in the cow mammary epithelial cells. The invention lays a foundation for deeply developing application of vaccaria segetalis seeds in preparation of a feed additive.

The invention provides a method for detecting fowl PRL based on a JAK-STAT 5 signal transduction pathway.The method comprises the specific steps that A, a CDS region sequence of a fowl PRL acceptor is extracted and inserted into an eukaryotic expression vector to form a signal reception vector; B, a signal response sequence STAT5 is inserted into the eukaryotic expression vector containing a reporter gene to form a signal response vector; C, human embryo kidney 293T cells are added into an improved DMEM culture medium for culture, transfection of the signal expression vector and the signal response vector is performed, and PRLs of different final concentrations are added in sequence; D, the activity of the reporter gene is detected, and a curve of the reporter gene activity along with PRL changes is obtained; E, the steps A-C are repeatedly executed, the activity of the reporter gene in a sample is detected, and the PRL concentration in the sample is obtained through calculation according to the curve of the reporter gene activity along with PRL changes.The method is high in operability, low in using cost, high in sensitivity, good in stability and repeatability and capable of meeting the requirement for scientific research and fowl breeding detection.

The invention relates to a method for determining the biological activity of recombinant human growth hormone Fc fusion protein through a luciferase reporter gene method. The method utilize a STAT5 reaction element (SGG1) and GHR plasmid to obtain a SGG1 luciferase reporter gene with stable expression and a cell strain of GHR after the transfection of a HEK293 cell; the expression of the downstream luciferase report gene of the SGG1 reaction element can be activated after growth hormone Fc fusion protein is added; and the biological activity of the growth hormone Fc fusion protein can be determined according to a fluorescence signal value fitting four-parameter curve. The detection method which is easy in operation, high in sensitivity, small in variable coefficient and high in accuracy can be established for the biological activity determination of the growth hormone Fc fusion protein; and the method has important guidance effects on the research and development of the growth hormoneFc fusion protein and the quality control in production.

The present invention relates to compositions and methods for the treatment of prostate cancer. In certain embodiments, the invention relates to compositions and methods for the inhibition of prostate cancer cell growth, comprising inhibiting the activity of Stat5 in prostate cancer cells.

Disclosed herein is a T-helper cell (“TH-GM” cell) that is regulated by IL-7 / STAT5 and which secrete GM-CSF / IL-3. Also disclosed are methods and compositions for modulating TH-GM function for the treatment of, e.g., inflammatory disorders. Diagnostic and prognostic methods for specifically identifying TH-GM-mediated inflammatory disorders (e.g., rheumatoid arthritis), as distinct from and / or in addition to non-TH-GM-mediated (e.g., TNF-α-mediated) inflammatory disorders, are also provided.

Here, the inventors disclose the treatment of imatinib mesylate resistant chronic myelogenous leukemia cells with a cotreatment of vorinostat (SAHA, suberoylanilide hydroxamic acid) and dasatinib, a dual Abl / Src kinase (TK) inhibitor. Combined treatment of cultured human CML and BaF3 cells with vorinostat and dasatinib induced more apoptosis than either agent alone, as well as synergistically induced loss of clonogenic survival, which was associated with greater depletion of Bcr-Abl, p-CrkL and p-STAT5 levels. Co-treatment with dasatinib and vorinostat also attenuated the levels of Bcr-AblE255K and Bcr-AblT315I and induced apoptosis of BaF3 cells with ectopic expression of the mutant forms of Bcr-Abl. Finally, co-treatment of the primary CML cells with vorinostat and dasatinib induced more loss of cell viability and depleted Bcr-Abl or Bcr-AblT315I, p-STAT5 and p-CrkL levels than either agent alone.

The present invention relates to compositions and methods for the treatment of prostate cancer. In certain embodiments, the invention relates to compositions and methods for the inhibition of prostate cancer cell growth, comprising inhibiting the activity of Stat5 in prostate cancer cells.

Cells are genetically modified to express a luminophore, e.g., a modified (F64L, S65T, Y66H) Green Fluorescent Protein (GFP, EGFP) coupled to a component of an intracellular signalling pathway such as a transcription factor, a cGMP- or cAMP-dependent protein kinase, a cyclin-, calmodulin- or phospholipid-dependent or mitogen-activated serine / threonin protein kinase, a tyrosine protein kinase, or a protein phosphatase (e.g. PKA, PKC, Erk, Smad, VASP, actin, p38, Jnk1, PKG, IkappaB, CDK2, Grk5, Zap70, p85, protein-tyrosine phosphatase 1C, Stat5, NFAT, NFkappaB, RhoA, PKB). An influence modulates the intracellular signalling pathway in such a way that the luminophore is being redistributed or translocated with the component in living cells in a manner experimentally determined to be correlated to the degree of the influence. Measurement of redistribution is performed by recording of light intensity, fluorescence lifetime, polarization, wavelength shift, resonance energy transfer, or other properties by an apparatus consisting of e.g. a fluorescence microscope and a CCD camera. Data stored as digital images are processed to numbers representing the degree of redistribution. The method can be used as a screening program for identifying a compound that modulates a component and is capable of treating a disease related to the function of the component.

The invention discloses a PCV2 strain with GAS-like motif mutation as well as a preparation method and application of the PCV2 strain. A GAS-like motif in PCV2DNA is mutated, so that the mutated PCV2DNA cannot be combined with STAT5 protein in virus replication, and a mutant strain of which the replication capacity is far lower than that of a wild PCV2 strain is obtained through virus rescue. The mutant strain can be used for researching a PCV2 replication mechanism and attenuated live vaccines, so that a new thought is provided for prevention and control of PCV2.

The invention discloses application of an STAT3 inhibitor and an STAT5 activator in enhancing lethality of an NK (Natural Killer) cell to a tumor cell. Persons skilled in the art know that by inhibiting STAT3 in a tumor microenvironment, the killing function of immune cells such as NK cells to tumor can be promoted; STAT5 is capable of promoting both growth and development of tumor cells and development and cell toxicity of the NK cells, and by inhibiting STAT5 levels of the NK cells, not only are normal functions of the NK cells damaged, but also growth of tumor can be promoted, so that promotion of expression of STAT5 in the NK cells is beneficial to treatment on tumor. The invention finds that Flexilarin F or Flexilarin G can be used as an STAT3 inhibitor and an STAT5 activator, and byinhibiting expression of STAT3 and activating expression of STAT 5 with the Flexilarin F or Flexilarin G, the lethality of the NK cell to the tumor cell can be improved, and by contrast, diterpene Lobocrassin E has no such function.