148 results about "Myostatin" patented technology

The present invention provides novel activin IIB5 receptor polypeptides capable of binding and inhibiting the activities of activin A, myostatin, or GDF-11. The present invention also provides polynucleotides, vectors and host cells capable of producing the receptor polypeptides. Compositions and methods for treating muscle-wasting, metabolic and other disorders are also provided.

In certain aspects, the present invention provides compositions and methods for treating fatty liver disease by administering an antagonist of an ActRIIB signaling pathway. Examples of such antagonists include ActRIIB polypeptides, anti-ActRIIB antibodies, anti-myostatin antibodies, anti-GDF3 antibodies and anti-activin A or B antibodies. A variety of hepatic and metabolic disorders may be improved by treating fatty liver disease.

There are disclosed selective myostatin antagonists (including antibodies), nucleic acids encoding them, and methods of making and using them. Neutralizing antibodies recognizing the conformational epitope near position 21 to 31 and position 50 to 60.

The present invention provides variant activin IIB soluble receptor polypeptides and proteins capable of binding and inhibiting the activities of activin A, myostatin, or GDF-11. The present invention also provides polynucleotides, vectors and host cells capable of producing the variant polypeptides and proteins. Compositions and methods for treating muscle-wasting and other diseases and disorders are also provided.

It has been determined that metalloprotease cleavage of a myostatin pro peptide results in activation of a latent inactive myostatin to an active form. Accordingly, methods of identifying agents that modulate metalloprotease mediated activation of myostatin are provided, as are agents identified using such methods. Also provided are methods of modulating muscle growth in an organism by increasing or decreasing metalloprotease mediated cleavage of a myostatin pro peptide.

The invention relates to methods and materials for enhancing muscle mass or for the treatment of muscle disease in a subject, comprising introducing a cell which has a lower than normal level of myostatin signalling, into the subject.

The present invention provides variant activin IIB soluble receptor polypeptides and proteins capable of binding and inhibiting the activities of activin A, myostatin, or GDF-11. The present invention also provides polynucleotides, vectors and host cells capable of producing the variant polypeptides and proteins. Compositions and methods for treating muscle-wasting and other diseases and disorders are also provided.

Certain disclosed oligomers induce exon skipping during processing of myostatin pre-mRNA. The oligomers may be in a vector or encoded by the vector. The vector is used for inducing exon skipping during processing of myostatin pre-mRNA. A therapeutically effective amount of the oligomer may be administered to a subject patient such that exon skipping during processing of myostatin pre-mRNA is induced. The administration to a subject may be used in order to increase or maintain muscle mass, or slowing degeneration of muscle mass in the subject. The administration to a subject may ameliorate muscle wasting conditions, such as muscular dystrophy. Examples of such muscular dystrophies which may be so treated include Becker's muscular dystrophy, congenital muscular dystrophy, Duchenne muscular dystrophy, distal muscular dystrophy, Emery-Dreifuss muscular dystrophy, facioscapulohumeral muscular dystrophy (FSHD), limb-girdle muscular dystrophy, myotonic muscular dystrophy, and oculopharyngeal muscular dystrophy

The invention relates to a CRISPER-Cas9-system-mediated sheep MSTN (myostatin) gene knock-out and exogenous gene site-specific integration method. The method comprises the following steps: establishing a CRISPER-Cas9-system-based gRNA (guide ribonucleic acid) expression vector according to a sheep MSTN gene sequence, establishing an exogenous-gene-containing donor plasmid capable of being integrated into a host genome according to the acting site of the gRNA, and transforming the optimized CRISPER-Cas9 vector, the gRNA expression vector and the linearized donor plasmid into sheep fibroblasts, thereby obtaining the sheep MSTN gene knock-out and exogenous gene site-specific integrated cells. The CRISPER-Cas9-mediated targeted vector provides a simple quick safe way for sheep MSTN gene knock-out and exogenous gene site-specific integration, thereby greatly enhancing the screening efficiency of the transgenic cell line. The method can screen the site-specific integrated exogenous gene cell line without adding any selection marker, thereby greatly enhancing the safety of the transgenic animals and having important value for sheep genetic breeding.

The present invention provides variant activin IIB soluble receptor polypeptides and proteins capable of binding and inhibiting the activities of activin A, myostatin, or GDF-11. The present invention also provides polynucleotides, vectors and host cells capable of producing the variant polypeptides and proteins. Compositions and methods for treating muscle-wasting and other diseases and disorders are also provided.

The present invention relates to a method of improving wound healing in a human or animal patient by inhibiting the activity of myostatin (GDF-8) using one or more myostatin antagonists. The present invention also relates to a method of treating fibrotic diseases or disorders comprising administering a myostatin antagonist.