SPINK2 mutant peptide conjugates are provided that inhibit KLK5. The KLK5 inhibitory peptide conjugates are Fc fusion peptides in which, in certain embodiments, the Fc region of the fusion peptides are the Fc region of human IgG1 or a fragment thereof. The KLK5 inhibitory peptide conjugates include an amino acid sequence of one of SEQ ID NOs: 34, 36, 38, 40, 42, 44, 46, 48, 96, 50, 52, 54, 56, 58, or 60. Pharmaceutical compositions that include the KLK5 inhibitory peptide conjugates useful for treating KLK5-related diseases are also provided.

SPINK2 mutant peptide conjugates are provided that inhibit KLK5. The KLK5 inhibitory peptide conjugates are Fc fusion peptides in which, in certain embodiments, the Fc region of the fusion peptides are the Fc region of human IgG1 or a fragment thereof. The KLK5 inhibitory peptide conjugates include an amino acid sequence of one of SEQ ID NOs: 34, 36, 38, 40, 42, 44, 46, 48, 96, 50, 52, 54, 56, 58, or 60. Pharmaceutical compositions that include the KLK5 inhibitory peptide conjugates useful for treating KLK5-related diseases are also provided.

The present invention provides methods for modulating SET activity by contacting SET with a binding agent such as an ApoE peptide derivative. In one embodiment of the invention, a pharmaceutical composition capable of modulating SET activity is administered to a patient for the treatment of an inflammatory or neurological condition. In another embodiment of the invention, compounds efficacious for the treatment of inflammatory and neurological conditions are identified by screening for a binding agent capable of competing with or inhibiting the binding of an ApoE derivative to SET.

Disclosed herein are inventive polypeptides (e.g., comprising a thermal sensitive ion channel or variant thereof and a domain 5 of kininogen 1 or variant or fragment thereof) and nucleic acid molecules encoding inventive polypeptides. Also disclosed are methods for modulating a cell comprising administering certain compositions (e.g., pharmaceutical compositions of the nucleic acid molecule) and applying a static magnetic field or an electromagnetic field. Methods for treating diseases or disorders in an animal (e.g., a human) comprising administering certain compositions (e.g., pharmaceutical compositions of the nucleic acid molecule) and applying a static magnetic field or an electromagnetic field, are further disclosed.

Compositions having a combination of specific biological components have been found to exert a number of useful effects in mammalian cells, including modulating TGF β signaling, apoptosis, and proliferation of mammalian cells, as well as decreasing inflammation in mice. These components can be obtained commercially, or can be prepared from biological tissues such as placental tissues. Placental amniotic membrane (AM) preparations described herein include AM pieces, AM extracts, AM jelly, AM stroma, and mixtures of these compositions with additional components. The compositions can be used to treat various diseases, such as wound healing, inflammation and angiogenesis-related diseases.

Provided are modified virus-like particles (VLPs) of paramyxoviruses, compositions containing them, methods of using the VLPs for delivery of any particular protein of interest to any of a variety of cells, kits that contain expression vectors for making, using and detecting VLPs, and methods for screening for anti-viral compounds using the VLPs. The modified VLPs contain a contiguous recombinant polypeptide that contains i) all or a segment of a C-terminal domain of a paramyxovirus nucleocapsid protein and ii) a polypeptide sequence of a distinct protein. Non-covalent complexes of paramyxovirus M protein and fusion proteins that contain a C-terminal domain of a paramyxovirus nucleocapsid protein and a polypeptide sequence of a distinct protein are provided, as are non-covalent complexes of cells, and cell receptors, with modified VLPs.

The present invention relates to novel chimeric molecules of ficolin-associated polypeptides, such as fusion polypeptides for the use in the treatment of conditions associated with inflammation, apoptosis, autoimmunity, coagulation, thrombotic or coagulopathic related diseases. The present invention further relates to nucleic acid molecules encoding such fusion polypeptides, vectors and host cells used in the production of the fusion polypeptides.

The present invention provides a method for diagnosing and detecting diseases associated with pancreas. The present invention provides one or more proteins or fragments thereof, peptides or nucleic acid molecules differentially expressed in pancreatic diseases (PCAT) and antibodies binds to PCAT. The present invention provides that PCAT is used as targets for screening agents that modulates the PCAT activities. Further, the present invention provides methods for treating diseases associated with pancreas.

The present invention relates to methods of producing recombinant plasminogen in a mammalian expression system. A method for producing plasminogen, the method comprising (i) providing a host cell comprising a first recombinant polynucleotide encoding plasminogen and a second recombinant polynucleotide encoding a plasminogen activation inhibitor; (ii) culturing said host cell in a suitable culture medium under conditions to effect expression of plasminogen from the first polynucleotide and plasminogen activation inhibitor from the second polynucleotide.

This disclosure provides SERPIN B1 polypeptides that possess neutrophil or pancreatic elastase inhibitory activity, and the elastase inhibition activity is resistant to oxidation by free radicals. The free radicals may a reactive oxygen species, or a reactive nitrogen species, or both. In some embodiments, the SERPIN B1 polypeptide comprises an amino acid substitution at residue 344 as compared to SEQ ID NO: 1. The SERPIN B1 polypeptides disclosed herein can be used to treat a patient having a disease or a genetic condition that is associated with the increased production of free radicals as compared to a normal individual or increased exposure to free radicals in environmental sources.