18 results about "STAT5" patented technology

The present disclosure relates to an antibody or antigen-binding portion thereof that binds to TSLP protein, and methods of making and using the same. The antibody can bind to human TSLP and / or cynomolgus monkey TSLP with high affinity, can block the binding of TSLP to TSLPR, and can inhibit the transduction of TSLP-stimulated signals through the STAT5 pathway.

The invention relates to the technical field of biological medicine, in particular to application of targeted DBC1 in treatment of systemic lupus erythematosus. The application for knocking out or inhibiting the expression of the DBC1 gene as shown in SEQ ID NO.1, or blocking or inhibiting the active function of the DBC1 protein as shown in SEQ ID NO.2 comprises the following applications: 1) inhibiting the transcription of STAT5 and inhibiting the activation of an STAT5 signal channel; 2) the differentiation of Treg cells is promoted, and the differentiation of Tfh and Th2 cells is inhibited; according to the application, DBC1 in DCs is inhibited or knocked out, STAT5 signal activity is lowered, then Treg differentiation is promoted, Tfh and Th2 differentiation is inhibited, and finally the SLE treatment effect is achieved.

Disclosed herein is a T helper ("T H - GM" cell) that is regulated by IL-7 / STAT5 and secretes GM-CSF / IL-3. Also disclosed are methods and compositions for modulating T H - GM function to treat, for example, inflammatory disorders. Also provided are methods for specifically identifying T H - GM-mediated (e.g., TNF-a mediated) inflammatory disorders that are different from and / or in addition to non-T H - GM-mediated (e.g., TNF-a mediated) inflammatory disorders. Also provided are diagnostic and prognostic methods for T H - GM-mediated inflammatory disorders (e.g., rheumatoid arthritis).

The invention provides application of the STAT5 inhibitor and / or the creatine transporter inhibitor, and provides a new thought for clinical prevention and treatment of tumor metastasis.

The application discloses application of SGI-7079 in treating FLT3 mutant acute myeloid leukemia. The application research shows that SGI-7079 can be stably combined with FLT3, inhibit the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK, and induce G1 phase arrest and cell apoptosis. In vitro, SGI-7079 has strong inhibitory effect on FLT3-ITD and drug-resistant mutant cells; in a FLT3-ITD mouse model, SGI-7079 can significantly reduce leukemia load and prolong survival, and shows better curative effect than existing drugs on drug-resistant mutations such as F691L and D835Y. Meanwhile, SGI-7079 also has significant inhibitory effect on primary cells of FLT3-ITD positive patients. It is shown that SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and provides a new direction for optimizing targeted therapy strategy.

The invention discloses a preparation method and application of a mesenchymal stem cell exosome which is enriched with Foxp1 protein and has immune organ targeting property. The method comprises the following steps: acquiring a single-cell suspension of the mesenchymal stem cells, performing suspension culture on the single-cell suspension of the mesenchymal stem cells in an exosome removal culture medium to induce the mesenchymal stem cells to aggregate to form a compact cell cluster, and then collecting the exosome through differential centrifugation. According to the method disclosed by the invention, the mesenchymal stem cells are induced to aggregate through a suspension culture technology, so that the exosome with high yield and immune targeting is obtained. The Foxp1 protein is specifically enriched in the exosome, the exosome has the characteristics of high yield, immune organ targeting and strong immune regulation capability, Treg cell differentiation is regulated through the Foxp1 / STAT5 / Foxp3 axis, the limitation in the application of the existing exosome is solved, and a new strategy is provided for the treatment of autoimmune diseases.

The present application provides a kind of regulated γδT cell and its intervention regulation method and application, it is related to the field of biotechnology, the intervention regulation method includes the inhibition to the JAK1-STAT5 signal path of γδT cell, to reduce the secretion of IL-5 and / or IL-13 induced by IL-18.The intervention regulation method inhibits the JAK1-STAT5 path of γδT cell, can significantly reduce the secretion of IL-5 and IL-13 induced by IL-18, which has the effect of promoting tumor migration invasion.This eliminates the negative regulation of γδT cell, thereby enhancing its overall anti-tumor ability and improving safety.

The invention belongs to the technical field of biology, discloses a method for regulating the attack behavior of channa argus based on a prolactin PRL signal channel, provides a transcriptional regulation channel of an olfactory prolactin receptor (PRLR) for regulating the attack behavior of channa argus, and finds that a prl gene and caor24 olfactory receptor differential expression are screened from attack difference individuals before and after channa argus breeding. The transcriptional regulation and control effect of the snakehead PRL / PRLR / STAT5 signal channel on caor24 is verified. The method for regulating and controlling the attack behavior of the snakeheaded fish based on the PRL signal channel is established, and a new thought is provided for regulation and control of the attack behavior of the fish. The method provides a practical solution thought for aquaculture attack behavior regulation and control.

The described technology pertains to biotechnology, specifically methods and systems for modulating FOXP3 expression in human CD4+ T cells using CRISPR-based genomic editing techniques. FOXP3, a transcription factor essential for regulatory T cell (Treg) function, is constitutively expressed in Tregs but transiently expressed in conventional CD4+ T cells (Tconvs) upon activation. The approach addresses challenges in precise modulation of FOXP3 expression by identifying cis-regulatory elements, such as CNSO, NCNS, and PPP, and trans-regulatory factors, including GATA3, STAT5, and ETS1, that influence FOXP3 expression in Tconvs. Utilizing CRISPR interference (CRISPRi) and CRISPR nuclease (CRISPRn) screens, the methods enable targeted, cell-type-specific modulation of FOXP3 levels. Applications include engineered T cell therapies for autoimmune diseases, cancer, and transplantation. Advanced epigenetic editing tools, such as CRISPRoff, further enhance specificity by targeting DNA methylation states at regulatory loci. This approach offers scalable solutions for programming FOXP3 expression in diverse therapeutic contexts.

In one embodiment, a problem to be solved by the present invention is to provide a new agent the agent being for at least one selected from the group consisting of promoting breast milk secretion, enhancing breast milk secretion function, improving inhibition of breast milk secretion function, and inhibiting mammary gland involution, said agent comprising, as an active ingredient, a substance that has not heretofore been known to have a breast milk secretion promoting effect. The present invention provides an agent for at least one selected from the group consisting of promoting breast milk secretion, enhancing breast milk secretion function, improving inhibition of breast milk secretion function, and inhibiting mammary gland involution, said agent containing a starting material derived from at least one selected from the group consisting of oranges, aloe, carrots, American ginseng, figs, almonds, hyuganatsu, laurel, apples, soybeans, chrysanthemums, wheatgrass, pepper, ginger, ebi-imo, Japanese yams, kuugaimo, Nikko maple, poppies, and radishes.

The invention relates to an application of a chicken CISH gene and an encoding protein thereof in regulating and controlling the crude fat content of yolk. The regulation and control mechanism of the CISH gene on the liver and the relation between the CISH gene and the yolk crude fat content are defined, namely, CISH expression is reduced, a GH / PRL-JAK2-STAT5 negative feedback mechanism is weakened, synthesis of substances such as yolk precursors in the liver is enhanced, and then the substances are transported into the yolk through blood, so that the yolk lipid content is increased. The method for verifying the expression quantity of the CISH gene in the laying hen is adopted, and the lipid deposition level in the egg can be simply and rapidly evaluated. The method not only can provide a new thought for researching yolk lipid deposition, but also lays a foundation for increasing the content of crude fat in the yolk in subsequent production practice.

The invention discloses an application of a small-molecule inhibitor PZ1 in treatment of KIT mutation positive acute myelogenous leukemia. Researches show that PZ1 can significantly inhibit proliferation of multiple KIT mutation positive leukemia cells and promote apoptosis at the cellular level, and the effect is significantly superior to that of existing TKI drugs; a further research shows that the PZ1 can be stably combined with KIT protein and inhibit the phosphorylation level of KIT and downstream STAT5, AKT, ERK and other signal channels. In-vivo research results show that PZ1 can reduce the proportion of mouse peripheral blood leukemia cells, significantly reduce infiltration of leukemia cells in bone marrow and spleen, and reduce the weight of spleen. Therefore, the invention discloses the treatment effect of the PZ1 in the KIT mutation positive leukemia, can effectively overcome the TKI drug resistance of the existing KIT mutation positive leukemia, solves the current treatment difficulty of the drug resistance of the KIT mutation positive leukemia, and provides a new strategy for the treatment of the disease.

The application provides a preparation method of paeonol glycoside for inhibiting GM-CSF + The application belongs to the technical field of biological medicine, and relates to application of Th cell differentiation in a medicine for preventing and / or treating rheumatoid arthritis (RA). + Abnormal activation of Th cells is obviously earlier than appearance of clinical symptoms of RA in a time axis, is an early key initiating factor for driving occurrence of the RA disease, and is a core target point for implementing an early blocking strategy. + Further, it is found that paeonol glycoside (Alb) can block a gamma c / JAK3 / STAT5 signal path by targeting and combining with an interleukin-2 receptor gamma chain, down-regulate CSF2 gene transcription and GM-CSF protein expression, thereby inhibiting differentiation of Th cells, and finally achieving an effect of preventing occurrence of CIA arthritis and not rebounding after drug withdrawal. The application provides a new intervention medicine which is high in safety, suitable for long-term use, can effectively regulate immune abnormalities in a pre-RA stage, prevents rheumatoid arthritis, and has a wide application prospect.

The application discloses application of SGI-7079 in treating FLT3 mutant acute myeloid leukemia. The application research shows that SGI-7079 can be stably combined with FLT3, inhibit the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK, and induce G1 phase arrest and cell apoptosis. In vitro, SGI-7079 has strong inhibitory effect on FLT3-ITD and drug-resistant mutant cells; in a FLT3-ITD mouse model, SGI-7079 can significantly reduce leukemia load and prolong survival, and shows better curative effect than existing drugs on drug-resistant mutations such as F691L and D835Y. Meanwhile, SGI-7079 also has significant inhibitory effect on primary cells of FLT3-ITD positive patients. It is shown that SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and provides a new direction for optimizing targeted therapy strategy.

The invention provides a gamma delta T cell subjected to regulation treatment as well as an dry regulation method and application thereof, and relates to the technical field of biology, and the dry regulation method comprises the step of inhibiting a JAK1-STAT5 signal channel of the gamma delta T cell so as to reduce secretion of IL-5 and / or IL-13 induced by IL-18. According to the dry regulation method, a JAK1-STAT5 pathway of gamma delta T cells is inhibited, and secretion of IL-5 and IL-13 which are induced by IL-18 and have the effect of promoting tumor migration and invasion can be remarkably reduced. The negative regulation on gamma delta T cells is eliminated, so that the overall anti-tumor capability of the gamma delta T cells is enhanced, and the safety is improved.

Provided herein are novel synthetic pathway activators comprising transmembrane domains and tiled intracellular signaling domains comprising a combinatorial signaling domain comprising two or more Signal Transducer and Activator of Transcription (STAT)1, STAT3, STAT4, STAT5 and / or Toll-like receptor (TLR) / IL-1R (TIR) signaling domains(s).

The application discloses application of a small molecule inhibitor PZ1 in treating KIT mutation positive acute myeloid leukemia. Researches of the application show that PZ1 can significantly inhibit the proliferation of a plurality of KIT mutation positive leukemia cells and promote cell apoptosis at a cell level, and the effect is significantly better than that of an existing TKI drug; further researches show that PZ1 can stably combine with KIT protein and inhibit the phosphorylation level of KIT and downstream STAT5, AKT, ERK and other signal paths. In-vivo research results show that PZ1 can reduce the proportion of leukemia cells in peripheral blood of mice, significantly reduce the infiltration of leukemia cells in bone marrow and spleen, and reduce the weight of spleen. Therefore, the application discloses the treatment effect of PZ1 in KIT mutation positive leukemia, and can effectively overcome the TKI drug resistance of the existing KIT mutation positive leukemia, solve the treatment difficulty of the current KIT mutation positive leukemia drug resistance, and provide a new strategy for the treatment of the disease.