54 results about "Muscle actin" patented technology

The invention is directed to novel combinations of muscle-specific enhancers and promoter elements useful for achieving persistent expression in the muscle or myocyctes. The muscle-specific promoter elements are derived from a muscle creatine kinase promoter, a troponin I promoter, a skeletal alpha-actin promoter, or a desmin promoter. The muscle-specific enhancer elements are derived from either troponin I internal regulatory elements, muscle creatine kinase enhancers, or desmin enhancers.

Methods and compositions for reducing fibrosis and cirrhosis are provided in which an effective dose of an admixture of a polysaccharide compound and, for example, a compound selected from the group consisting of antibodies specific to intracellular or cell-surface: (i) beta-PDGF receptors; (ii) synaptophysin; (iii) zvegf3; (iv) CCR1 receptors; (v) connective tissue growth factor; (vi) alpha 1-smooth muscle actin; (vii) matrix metalloproteinases MMP 2 and MMP9; (viii) matrix metalloproteinase inhibitors TIMP1 and TMP2; (ix) integrins; (x) TFG-β1; (xi) endothelin receptor antagonists; and (xii) collagen synthesis and degradation modulating compounds; (xiii) actin synthesis and degradation modulating compounds; and (xiv) tyrosine kinases is administered to an animal in order to treat fibrosis.

The present invention provides methods of treating overproduction of cortisol in a subject by administering to the subject a peptide that antagonizes adrenocorticotropin hormone (ACTH) to block the activation of melanocortin 2 receptors.

The invention relates to methods for screening compounds for their ability to modulate actin polymerization. The invention is also related to compounds which modulate actin polymerization. More specifically, the invention is related to methods of screening compounds which modulate the interaction of cortactin or HS-1 with Arp2 / 3. The invention is also related to compounds which modulate the interaction of cortactin of HS1 with Arp2 / 3. Also provided are mutants of cortactin with decreased ability to interact with Arp2 / 3.

A method of treating or preventing tissue damage occurring subsequent to affecting an increase in blood flow through a blood vessel which is in communication with the tissue, by administering an effective amount of a composition including a tissue damage-reducing or -preventing polypeptide including at least one of Thymosin beta 4 (TB4), an isoform of TB4, an N-terminal fragment of TB4, a C-terminal fragment of TB4, TB4 sulfoxide, an LKKTET [SEQ ID NO: 1] peptide, an LKKTNT [SEQ ID NO: 2] peptide, an actin-sequestering peptide, an actin binding peptide, an actin-mobilizing peptide, an actin polymerization-modulating peptide, or a conservative variant thereof having tissue damage-reducing activity. The composition is administered to the tissue before, during and / or after affecting the increase in blood flow.

A method and system for predicting liver injury in vivo due to hepatocyte damage by a test compound are provided. The method includes acquiring images of fluorescently stained cells obtained from a cell culture in which the cells have been treated with a dose-range of at least the test compound and its vehicle. The cells may be hepatic cells including primary or immortalized hepatocytes, hepatoma cells or induced pluripotent stem cell-derived hepatocyte-like cells. The acquired images are segmented. The method further includes extracting and analyzing one or more phenotypic features from the segmented images, wherein the one or more phenotypic features are selected from the group of intensity, textural, morphological, or ratiometric features consisting of (a) features of DNA, (b) features of RELA (NF-KB p65), and (c) features of actin filaments at different subcellular regions and d) features of cellular organelles and their substructures in the segmented images. Finally, the method includes normalizing results from the treated samples to vehicle controls and predicting the probability of liver injury by the test compound based on test compound-induced normalized changes of the extracted and selected phenotypic features using machine learning methods.

Methods and compositions for reducing fibrosis and cirrhosis are provided in which an effective dose of an admixture of a polysaccharide compound and, for example, a compound selected from the group consisting of antibodies specific to intracellular or cell-surface: (i) beta-PDGF receptors; (ii) synaptophysin; (iii) zvegf3; (iv) CCR1 receptors; (v) connective tissue growth factor; (vi) alpha 1-smooth muscle actin; (vii) matrix metalloproteinases MMP 2 and MMP9; (viii) matrix metalloproteinase inhibitors TIMP1 and TMP2; (ix) integrins; (x) TFG-β1; (xi) endothelin receptor antagonists; and (xii) collagen synthesis and degradation modulating compounds; (xiii) actin synthesis and degradation modulating compounds; and (xiv) tyrosine kinases is administered to an animal in order to treat fibrosis.

The present invention concerns devices and methods for controlling actin filaments growth and organization with micro patterned nucleation sites, their uses for studying actin network formation, for screening of drugs or for preparing complex structures.

Novel tetrahydroisoquinoline derivative compounds are disclosed herein that may be used as an active ingredient for a pharmaceutical composition, and in particular, for a pharmaceutical composition useful for preventing or treating a disease or condition responsive to modulation of the contractility of the skeletal sarcomere. This may be accomplished, for example, by modulation of the troponin complex of the fast skeletal muscle sarcomere through one or more of fast skeletal myosin, actin, tropomyosin, troponin C, troponin I, and troponin T, and fragments and isoforms thereof. The tetrahydroisoquinoline derivative compounds can thus be used as an agent for preventing or treating 1) neuromuscular disorders, 2) disorders of voluntary muscle, 3) CNS disorders in which muscle weakness, atrophy, and fatigue are prominent symptoms, 4) muscle symptoms stemming from systemic disorders, and 5) dysfunctions of pelvic floor and urethral / anal sphincter muscle.

The invention provides a new medical application of the thiazolopyrone analog, that is, its application in the preparation of anti-hepatic fibrosis or anti-acute liver injury drugs. The general structural formula of the thiazolopyrone analogue is: Classical pharmacological experiments have confirmed that the thiazolopyrone analogue can down-regulate smooth muscle actin α-SMA and transforming growth factor TGF-SMA of human hepatic stellate cells LX-2 β1 expression, thereby inhibiting the proliferation and transformation of human hepatic stellate cells LX‑2. in CCl 4 In the induced mouse liver fibrosis / acute liver injury model experiment, thiazolopyrone analogs can inhibit the up-regulation of ALT and AST in mouse serum, and can inhibit the expression of α-SMA and TGF-β1 related to liver fibrosis , a variety of pathological section analysis and immunoomics experiments also confirmed that this analogue can effectively treat acute liver injury and liver fibrosis in mice. Therefore, this type of thiazolopyrone compound can be used as an active substance for the preparation of anti-hepatic fibrosis or anti-acute liver injury drugs.

A method and system for predicting liver injury in vivo due to hepatocyte damage by a test compound are provided. The method includes acquiring images of fluorescently stained cells obtained from a cell culture in which the cells have been treated with a dose-range of at least the test compound and its vehicle. The cells may be hepatic cells including primary or immortalized hepatocytes, hepatoma cells or induced pluripotent stem cell-derived hepatocyte-like cells. The acquired images are segmented. The method further includes extracting and analyzing one or more phenotypic features from the segmented images, wherein the one or more phenotypic features are selected from the group of intensity, textural, morphological, or ratiometric features consisting of (a) features of DNA, (b) features of RELA (NF-KB p65), and (c) features of actin filaments at different subcellular regions and d) features of cellular organelles and their substructures in the segmented images. Finally, the method includes normalizing results from the treated samples to vehicle controls and predicting the probability of liver injury by the test compound based on test compound-induced normalized changes of the extracted and selected phenotypic features using machine learning methods.

The present invention is directed to practical high-yielding synthetic processes for preparing 3,4-disubstituted-thiazolidin-2-ones, which do not compromise the absolute stereochemical integrity of the compounds. The present invention is also directed to novel compounds of 3,4-disubstituted-thiazolidin-2-ones. The compounds prepared by the present invention are useful in the synthesis and manufacture of compounds (such as latrunculins and / or their analogs) for treating diseases or conditions associated with inhibiting actin polymerization.

The present invention provides the use of Cimicifugae rhizoma triterpenoid saponin extract, Cimicifugae rhizoma, actein, deoxyactein, or a composition formed by actein and deoxyactein in the preparation of a medicament or a functional health product for autoimmune diseases. The present invention also provides a pharmaceutical composition for autoimmune diseases and a pharmaceutical composition for inhibiting inflammatory cytokines. The invention provides new applications of Cimicifugae rhizoma triterpenoid saponin extract, Cimicifugae rhizoma, actein, deoxyactein, etc., and widens the application field of medicines or functional health products for autoimmune diseases. The raw materials source is plenty, the cost is low, and it has a broad market application value.

The invention belongs to the field of pharmaceutical chemistry, and in particular relates to an imidazole heterocyclic diphosphonic acid compound as well as a preparation method and application thereof. The imidazole heterocyclic diphosphonic acid compound has a larger non-toxic concentration range for an osteoclast precursor, and can significantly inhibit the formation of osteoclasts at the same time; the imidazole heterocyclic diphosphonic acid compound can damage actin ring to the utmost extent, thus having an obvious inhibiting effect on the osteoclasts and further being used as an osteoclast inhibitor; the imidazole heterocyclic diphosphonic acid compound solves the problems that diphosphonate in the prior art is low in inhibiting effect on the osteoclasts, high in toxicity and large in side effects.