47 results about "Notch signaling pathway" patented technology

The invention provides generally a method of monitoring, diagnosing, prognosing and treating glioma. Specifically, the invention provides for three (3) prognostic subclasses of glioma, which are differentially associated with activation of the akt and notch signaling pathways. Tumor displaying neural or proneural PN lineage markers (including notch pathway elements) show longer median patient survival, while the two remaining tumor markers Prolif and Mes are associated with shortened survival. Tumors classified in this manner may also be treated with the appropriate PN- Prolif- or Mes-therapeutic corresponding to the subclassification in combination with anti-mitotic agents, anti-angiogenic agents, Akt antagonists, and neural differentiation agents. Alternatively, the invention also provides for method of prognosing and diagnosing glioma with a two-gene model based on the expression levels of PTEN and DLL3.

The present invention provides small molecule inhibitors of BMP signaling. These compounds may be used to modulate cell growth, differentiation, proliferation, and apoptosis, and thus may be useful for treating diseases or conditions associated with BMP signaling, including inflammation, cardiovascular disease, hematological disease, cancer, and bone disorders, as well as for modulating cellular differentiation and/or proliferation.

This invention provides methods of preventing, reducing, delaying or inhibiting the proliferation, growth, migration and/or metastasis of cancer by administering an effective amount of an inhibitor of the Hippo-YAP signaling pathway.

The invention provides a reagent for detecting a Notch signal path as well as a PCR (Polymerase Chain Reaction) detecting method and application thereof. The detecting reagent comprises PCR reaction primers for detecting an ADAM10 gene, an ADAM17 gene, an AES gene, a CBL gene, a CCND1gene, a CD44 gene, and the like, and primers of corresponding internal-reference regulatory genes GAPDH (Reduced Glyceraldehyde-Phosphate Dehydrogenase), ACTB (Beta-Actin) and B2M (Beta-2-Microglobulin). The invention provides the reagent for detecting core molecule changes of the NOTCH signal channel; by virtue of the detecting reagent, genes associated with the NOTCH channel can be quickly detected on transcriptional level by virtue of real-time fluorescent quantitative PCR; on this basis, core molecules and a mechanism of action of a tumor NOTCH signal channel are analyzed and researched, so that an NOTCH regulatory channel of tumor-associated medicaments is quickly and accurately found, and therefore, a powerful tool is provided for screening anti-tumor medicaments, discussing the mechanism of a novel targeted medicament, and the like.

The invention discloses a construction method for a conditional overexpression Yap1 gene mice model at an H11 locus. The construction method comprises the steps: firstly, obtaining an inducible Yap1 overexpression transgenic vector; then, obtaining transgenic F0-generation mice; next, enabling the F0-generation mice to mate with wild-type mice, carrying out passage and line establishment, and thusobtaining F1-generation mice; and carrying out expanding propagation of positive F1-generation mice, then mutually mating, and thus obtaining the conditional overexpression mice Yap1 animal model. The transgenic mice model constructed by the method can be used for studying the function of Yap1 in different tissues and different developmental stages and the action mechanism of Hippo signaling pathways, can also be used for studying the function of the Hippo signaling pathway in animal development, biotumorigenesis, regenerative medicine and other disciplines, and has important guiding significance on biological signal transduction studies.

The present invention relates to prevention of congenital deformations. The invention further relates to cancer inhibition and prevention. The invention further relates to methods and compositions to modulate, antagonize, or agonize disparate signaling pathways that may converge to regulate patterning events and gene expression during prenatal development, post-natal development, and during development in the adult organism. The invention also relates to activators or deactivators of pyruvate kinase M2 (PKM2) for the treatment, prevention, or amelioration of diseases related to PKM2 function.

The invention discloses 214 novel phosphorylation sites identified in signal transduction proteins and pathways underlying human carcinoma, and provides phosphorylation-site specific antibodies and heavy-isotope labeled peptides (AQUA peptides) for the selective detection and quantification of these phosphorylated sites/proteins, as well as methods of using the reagents for such purpose. Among the phosphorylation sites identified are sites occurring in the following protein types: Adaptor/Scaffold proteins, Cytoskeleton proteins, GTP Signaling proteins, Kinases, Metabolism proteins, Phosphatases/Phospho-diesterases/Proteases, Receptor proteins, RNA Processing proteins, Transcription proteins, Translation proteins, Transporter proteins, and Ubitquitin proteins, as well as other protein types.

This disclosure provides a method for treating a subject afflicted with a cancer comprising administering to the subject a combination of therapeutically effective amounts of an antibody or an antigen-binding portion thereof that binds specifically to Programmed Death-1 (PD-1) or to Programmed Death Ligand-1 (PD-L1), and an antibody or an antigen-binding portion thereof that binds specifically to C-X-C Chemokine Receptor 4 (CXCR4) or to C-X-C motif chemokine 12 (CXCL12). The disclosure also provides a kit for treating a subject afflicted with a cancer, the kit comprising one or more dosages of an antibody or an antigen-binding portion thereof that binds specifically to PD-1 or to PD-L1, one or more dosages of an antibody or an antigen-binding portion thereof that binds specifically to CXCR4 or to CXCL12, and instructions for using the antibodies or portions thereof for treating the subject.

The use of luteinizing hormone receptor (LHR) as a treatment target in cancer is provided. Data demonstrates that LHR plays an important role in androgen synthesis and signaling pathways critical for prostate cancer progression. When LHR is silenced, there is a significant downregulation of androgen receptor (AR) mRNA and protein expression with a subsequent suppression of PSA expression. Data suggesting that the LH-LHR signaling cascade may be an upstream and viable therapeutic target in castration-resistant prostate cancer (CRPC) is presented.

This invention relates to novel endothelin receptor antagonists, derivatives, acceptable acid addition salts thereof. The invention also provides compositions comprising a compound of this invention and the use of such compositions in methods of treating diseases and conditions that are beneficially treated by compounds that block the endothelin signaling pathway that leads to vasoconstriction and in particular those diseases or conditions beneficially treated by endothelin receptor antagonists.

The invention discloses an application of a chlorogenic acid in activation of an immune related signaling pathway of an organism and a research method of the chlorogenic acid, belongs to the field of biological medicines, and provides a new application of the chlorogenic acid for regulating and controlling the organism immunoreaction from gene and molecular level, namely an application of the chlorogenic acid in activation of the immune related signaling pathway of the organism. A molecular contact between the immune related signaling pathway and the anti-cancer function of the chlorogenic acid is established. A method for accurately regulating and controlling the immune related signaling pathway of the organism through the chlorogenic acid is provided. Through the application, the chlorogenic acid can be further used for guiding treatment of tumors, and can also be used for building related research models for the specific action principle of the immune related signaling pathway or other related applications.

The invention relates to the field of crude drugs, specifically relates to a medical application of camptothecin and its derivative in resisting Alzheimer disease. Pharmacological experiments prove that: the camptothecin and its derivative have significant effect on inhibiting production of A beta, the IC50 is within the range of 0.1-10 nM, and the molecular weights of the compounds are all less than 500 Dalton, which mean the compounds has latent capacity of permeating a blood cerebral barrier. More importantly, the camptothecin and its analogues have no influence on cytotoxicity and apoptosis in inhibiting the concentration range of A beta, and simultaneously have no side effect on Notch signal passages.

The invention discloses a method for inducing fetal hepatic stem cells to differentiate into mature hepatic cells in a three-step sequential mode, and belongs to the technical field of biology. The method comprises the following steps that (1) the fetal hepatic stem cells are obtained and identified, specifically, (a) the fetal hepatic steam cells are separated and amplified, and (b) the fetal hepatic stem cells are identified; (2) the fetal hepatic steam cells are induced to differentiate, specifically, (a) a tissue suspension prepared from normal hepatic tissue which is ground and homogenized is collected on dry ice at a low temperature, supernatant is collected after centrifuging and added into a Williams'E cell culture medium, and the fetal hepatic stem cells in the step (1) are cultivated to obtain hepatic progenitor cells, (b) the cells obtained in the step (a) are continuously cultivated through the Wiliams'E culture medium added with a Notch signal channel inhibitor to obtain hepatocyte-like cells, and (c) the cells obtained in the step (b) are cultivated through a rapid cell expansion culture medium added with HGF to obtain functional hepatic cells. Through the method, thefetal hepatic stem cells obtained early can be induced into the functional hepatic cells rapidly, accurately and efficiently.

Methods and compositions are provided for inhibiting the responsiveness of CD4⁺ T cells that have been sensitized to antigen, i.e. CD4⁺ memory, or effector T cells. It is shown herein that such effector T cells will fail to proliferate in response to antigen when inhibited by two compounds, which act on two distinct signaling pathways, the mTOR pathway and the MAPK (MEK) pathway. A synergistic combination of inhibitors is required to achieve effector T cell inactivation because a single inhibitor can provide for inactivation of naïve CD4⁺ T cells, but will not by itself inactivate the sensitized effector T cells.