197results about "Muscle proteins" patented technology

The present invention relates to pharmaceutical compositions comprising therapeutically effective amounts of troponin C, I or T subunits, fragments, or homologs thereof, for the treatment of diseases or disorders involving abnormal angiogenesis and methods of use thereof.

Pharmaceutical compositions containing therapeutically effective amounts of troponin C, I, or T, subunits, fragments, or analogs for the treatment of diseases or disorders involving abnormal angrogenesis.

The invention provides methods of diagnosing and treating heart diseases and conditions, methods for identifying compounds that can be used to treat or to prevent such diseases and conditions, and methods of using these compounds to treat or to prevent such diseases and conditions. Also provided in the invention are animal model systems that can be used in screening methods.

The invention provides a method for assaying for troponin I in a sample such as serum, the method comprising a determination of the troponin I concentration in a sample using a standard preparation that comprises a complete native troponin complex. One exemplary assay for troponin I concentration according to the invention is an immunoassay. Further contemplated in the method is a step comprising contacting the sample with a Ca2+-binding agent. Another aspect of the invention is the standard preparation comprising a complete native troponin complex. Yet another aspect of the invention is a kit for use in the assay method comprising the standard preparation, a detectable label, and a troponin I binding partner, such as an anti-troponin I antibody. All aspects of the invention are usefully practiced using human materials, such as a human troponin complex, and / or human sources for samples.

A non-human animal model is provided, particularly a mouse model for movement hyperactivity, excitoxicity disorders (e.g. myoclonic cramping) and neurodegeneration, in which modified cytoplasmic dynein heavy chain1 is expressed. Modified human and mouse cytoplasmic dynein heavy chain1 proteins and nucleic adds are also provided, including the corresponding recombinant proteins. The invention further provides uses for the non-human animal model and the modified cytoplasmic dynein heavy chain1 proteins and nucleic acids, in particular for the diagnosis and treatment of medical conditions associated with over-expression of cytoplasmic dynein heavy chain1.

The present invention provides compositions and methods for targeting an extracellular matrix derived (EMD) peptide predominantly to an injured tissue, as opposed to an uninjured tissue in vivo. The targeted EMD peptide facilitates the repair and / or regeneration of the injured tissue by providing a surface for cells to attach and grow, thereby facilitating the repair and / or regeneration of the injured tissue.

The invention provides a DNA element for high-throughput in vitro protein synthesis, and specifically discloses a novel DNA element capable of greatly enhancing protein translation efficiency. According to the present invention, with the application of the DNA element in a yeast in-vitro protein synthesis system, the relative light unit value of the activity of the synthesized luciferase is enhanced by about 22.3 times compared to the DNA element containing only the omega sequence.

Peptide antagonists of zonulin are disclosed, as well as methods for the use of the same. The peptide antagonists bind to the zonula occludens receptor, yet do not physiologically modulate the opening of mammalian tight junctions.

Disclosed herein are compositions and methods for repairing cell membranes. In addition, the invention relates to therapeutic compositions comprising nucleotides and / or polypeptides of the invention in combination with a pharmaceutically acceptable carrier, wherein the composition facilitates the repair of cell membranes. Moreover, the invention relates to the treatment and / or prevention of pathological conditions associated with cell membrane damage.

The present invention provides compositions and methods for targeting an extracellular matrix derived (EMD) peptide predominantly to an injured tissue, as opposed to an uninjured tissue in vivo. The targeted EMD peptide facilitates the repair and / or regeneration of the injured tissue by providing a surface for cells to attach and grow, thereby facilitating the repair and / or regeneration of the injured tissue.

A cardiac troponin I ultra-sensitive detection reagent kit, a preparation method, and a detection method. The reagent kit comprises at least one first anti-cardiac troponin I antibody marked with a trace marker and at least one second anti-cardiac troponin I antibody coated on magnetic microspheres, the first anti-cardiac troponin I antibody and cardiac troponin I binding site being different from the second anti-cardiac troponin I antibody and cardiac troponin I binding site. The reagent kit may further comprise a diluent capable of significantly reducing non-specific binding in a detection process, so as to further increase the detection accuracy and sensitivity. The method using the reagent kit to detect cardiac troponin I sensitively and accurately detects the amount of cardiac troponin I in a sample, and provides more timely and reliable information for the early diagnosis and treatment of AMI.

Disclosed are materials and methods for treating diseases of the mammalian eye, and in particular, Usher syndrome 1B (USH1B). The invention provides AAV-based, dual-vector systems that facilitate the expression of full-length proteins whose coding sequences exceed that of the polynucleotide packaging capacity of an individual AAV vector. In one embodiment, vector systems are provided that include i) a first AAV vector polynucleotide that includes an inverted terminal repeat at each end of the polynucleotide and a suitable promoter followed by a partial coding sequence that encodes an N-terminal portion of a full-length polypeptide; and ii) a second AAV vector polynucleotide that includes an inverted terminal repeat at each end of the polynucleotide and a partial coding sequence that encodes a C-terminal portion of a full-length polypeptide, optionally followed by a polyadenylation (pA) signal sequence. In another embodiment, the vector system includes i) a first AAV vector polynucleotide comprising an inverted terminal repeat at each end, a suitable promoter followed by a partial coding sequence that encodes an N-terminal portion of a full-length polypeptide followed by a splice donor site and intron and ii) a second AAV vector polynucleotide comprising an inverted terminal repeat at each end, followed by an intron and a splice-acceptor site for the intron, followed by a partial coding sequence that encodes a C-terminal portion of a full-length polypeptide, optionally followed by a polyadenylation (pA) signal sequence. The coding sequence or the intron sequence in the first and second AAV vectors preferably includes a sequence region that overlaps.

A molecular motor in which multiple concentric cylinders (or nested cones) rotate around a common longitudinal axis. Opposing complementary surfaces of the cylinders or cones are coated with complementary motor protein pairs (such as actin and myosin). The actin and myosin interact with one another in the presence of ATP to rotate the cylinders or cones relative to one another, and this rotational energy is harnessed to produce work. The concentration of ATP and the number of nested cylinders or cones can be used to control the rotational speed of the motor. The length of the cylinders can also be used to control the power generated by the motor. In another embodiment, the molecular motor includes at least two annular substrates wherein one annular substrate is coated with a first motor protein and the other annular substrate is coated with a second motor protein. The first and second motor proteins interact with each other to move the second annular relative to the first annular substrate.

Efficient and muscle-specific gene expression can be obtained with constructs containing two or more copies of USE and / or ΔUSE fused to the minimal promoter of the TnISlow gene. USE is a small (about 160-bp) upstream enhancer of the TnISlow gene that confers slow-twitch muscle fiber specificity. ΔUSE is generated from a 100-bp deletion at the 5′ end of USE. ΔUSE confers expression in slow- and fast-twitch muscle fibers. The strength and relatively small size (less than 600-bp) of these constructs make them useful for gene therapy applications.

The present invention relates to pharmaceutical compositions comprising therapeutically effective amounts of recombinant troponin C, I or T subunits for the treatment of diseases or disorders involving abnormal angiogenesis.

The present invention provides a method for producing systemic red fluorescent zebrafish. The present invention also provides a new gene fragment and a systemic red fluorescent zebrafish.

Polypeptides corresponding to stable, circulating degradation products of troponin I (TnI) are described. The fragments comprise a sequence of the N-terminus of native cardiac TnI with 95-115 amino acid and additionally include fragments lacking about the 20-30 N-terminal amino acids. Utilities of these fragments and antibodies thereto include sensitive detection of myocardial infarction and purification of antibodies sensitive to the detection of troponin I degradation products.

A water soluble peptide composition derived from animal muscle tissue proteins is provided. The peptide composition contains less than about 1 weight percent fats and oils based upon the weight of the peptide composition and less than about 2 weight percent ash based on the weight of the peptide composition.

The invention pertains to methods for detecting the presence or absence of a mutation associated with hypertrophic cardiomyopathy (HC). The methods include providing DNA which encodes a cardiac myosin binding protein and detecting the presence or absence of a mutation in the amplified product which is associated with HC. The invention further pertains to methods for diagnosing HC in a subject. These methods typically include obtaining a sample of DNA which encodes a cardiac myosin binding protein from a subject being tested for FHC and diagnosing the subject for FHC by detecting the presence or absence of a mutation in the sarcomeric thin filament protein which causes FHC as an indication of the disease. Other aspects of the invention include kits useful for diagnosing HC and methods for treating HC.

The subject invention relates to antibodies to troponin I as well as methods of use thereof. In particular, such antibodies may be used to detect Troponin I in a patient and may also be used in the diagnosis of, for example, a myocardial infarction or acute coronary syndrome.

The invention provides isolated nucleic acids that encode LCP, including two isoforms, and fragments thereof, vectors for propagating and expressing LCP nucleic acids, host cells comprising the nucleic acids and vectors of the present invention, proteins, protein fragments, and protein fusions of the novel LCP isoforms, and antibodies thereto. The invention further provides transgenic cells and non-human organisms comprising human LCP nucleic acids, and transgenic cells and non-human organisms with targeted disruption of the endogenous orthologue of the human LCP gene. The invention further provides pharmaceutical formulations of the nucleic acids, proteins, and antibodies of the present invention, and diagnostic, investigational, and therapeutic methods based on the LCP nucleic acids, proteins, and antibodies of the present invention.