50 results about "SMAD" patented technology

The instant application provides kits and methods for identifying agents which induce or inhibit the osteogenic effect of LMP or BMP proteins. The kits are directed to methods which measure either an amount of a complex between a Smurf protein or a fragment thereof and an LMP protein or a fragment thereof. Alternatively, the kits are directed to methods of measuring an amount of the ubiquitinated Smad protein or a fragment thereof.

<heading lvl="1">SUMMARY OF THE INVENTION < / heading> The use of gene therapy for the treatment of different kinds of fibrosis in human beings is disclosed. The purpose is the use of "therapeutic2 genes specifically directed to target organs to revert and / or prevent the development of the fibrosis process. The potential application of gene therapy to patients with fibrosis and / or cirrhosis will depend to a large extent on the successful delivery of genes which encode for therapeutic proteins to livers with severe fibrosis and that these genes which encode for proteins human MMP-8 active and latent, MMP-1, MMP-2, MMP-9 and MMP-13; human uPA wild type and / or modified (or its truncated version), the truncated receptor for TGF-beta type II and Smad-7 can be directed by adenovirus and / or other recombinant vectors that cannot transduce (infect) others organs. The recombinant adenoviruses (AdR) are vectors highly efficient for the transduction of therapeutic genes to diverse target cells. We have proved that they can carry genes to cirrhotic livers. The delivery of therapeutic genes through such adenoviral vectors and other recombinant vectors could also be performed using cationic and anionic liposomes (DOTMA). Therefore, we propose the use of this patent to be applied in the same manner to: Renal fibrosis Pulmonary fibrosis Hypertrophic and keloid scars (skin fibrosis), and Other kinds of fibrosis.

The invention relates to the application of BMP-7 in preparing drugs for preventing and / or treating hepatic fibrosis and belongs to the medical treatment technical field. The preparation comprises the steps of: preparing a hepatic fibrosis model of rats through an animal model experiment and a vitro cell experiment, separating liver cells and hepatic stellate cells of an animal to be tested, observing the affect of bone morphogenetic protein BMP-7 on experimental hepatic fibrosis. The results show that BMP-7 can restrain the activity of a signaling pathway protein Smad 1 / 3 of TGF-beta1 in cells and the expression of TGF-beta1.The results of the animal experiment show that BMP-7 can remarkably prevent and treat experimental hepatic fibrosis.

Cranial placodes are embryonic structures essential for sensory and endocrine organ development. The efficient derivation of cranial placodes from human pluripotent stem cells is disclosed where the timed removal of the BMP inhibitor Noggin, a component of the dual-SMAD inhibition strategy of neural induction, triggers placode induction at the expense of CNS fates. Further fate specification at the pre-placode stage enables the selective generation of placode-derived trigeminal ganglia capable of in vivo engraftment, mature lens fibers and anterior pituitary hormone-producing cells that upon transplantation produce hormones including, but not limited to, human growth hormone and adrenocortiocotropic hormone in vivo. Alternatively, anterior pituitary hormone-producing cells are generated in cell culture systems in vitro.

The method for producing a cell aggregate containing colloidal precursor cells according to the present invention comprises the steps of: (1) culturing pluripotent stem cells in suspension for 5-10 days in the absence of feeder cells in an embryoid formation medium containing one or more SMAD signaling inhibitors and one or more Wnt signaling activators, and then culturing the pluripotent stem cells in suspension in the culture medium for 5-10 days in the absence of feeder cells; thereby forming cell aggregates; (2) carrying out suspension culture on the cell aggregate obtained in the step (1) in an embryoid forming culture medium containing retinoic acid; a step (3) in which the cell aggregate obtained in the step (2) is subjected to suspension culture in an embryoid formation medium or a medium for neuroglial proliferation, said medium containing retinoic acid and one or more SHH signaling activators; and a step (4) in which the cell aggregate obtained in the step (3) is suspended and cultured in a culture medium for neuroglial proliferation, said culture medium not containing retinoic acid and containing one or more SHH signaling activators.

A method for producing a cerebral organoid having amyloid plaques is provided by the invention. The method comprises step (a) for forming, in the presence of an SMAD inhibitor, a germ layer body from a pluripotent stem cell having a mutation in an Alzheimer's disease-related gene; step (b) for, after step (a), embedding the germ layer body in an extracellular matrix, and three-dimensionally culturing the germ layer body in the presence of the SMAD inhibitor and a glycogen synthase kinase 3beta (GSK3beta) inhibitor, to form an organoid; and step (c) for, after step (b), removing the organoid from the extracellular matrix, and culturing the organoid in a culture medium while stirring same, wherein at least a portion of step (c) is performed in the presence of leukemia inhibitory factor (LIF).

The invention provides an application of a compound kushen (radix sophorae flavescentis) injection in preparing a medicine for treating chronic hepatic fibrosis. The compound kushen injection can also be applied in repairing liver injury, and liver tissues are recovered to be normal by inhibiting the deposition of collagen in the liver; in addition, the compound kushen injection can also inhibit activation of hepatic stellate cells, and the medicine is prepared by inhibiting activation of the hepatic stellate cells to treat chronic hepatic fibrosis; the medicine for treating chronic hepatic fibrosis is prepared by down-regulating the expression of hepatic stellate cell activators; the medicine for treating chronic hepatic fibrosis is prepared by selectively inhibiting hepatic stellate cell activation; and the medicine for treating chronic hepatic fibrosis is prepared by intervening activation of a TGF-beta / Smad signal axis in hepatic stellate cells. Compared with the lack of approved drugs for treating hepatic fibrosis in clinic at present, the application of the compound kushen injection disclosed by the invention shows that the compound kushen injection can be used as a promising candidate drug for preventing or treating hepatic fibrosis and preventing the progression of hepatic fibrosis in clinical application.

Methods are provided, in some aspects, for differentiating pluripotent cells into midbrain dopaminergic (DA) neurons using a mono-SMAD inhibition or inhibition of SMAD signaling with only one SMAD inhibitor. In some embodiments, mono-SMAD inhibition utilizes a single inhibitor of bone morphogenic protein (BMP) for differentiating pluripotent cells into midbrain DA neurons.