The present invention provides a fusion protein of an antigen-binding protein and a fluorescent protein or a fluorescence-labeled tag protein. The present invention provides a fusion protein of an antigen-binding protein and a fluorescent protein or a fluorescence-labeled tag, wherein the antigen-binding protein is an antigen-binding protein having a helix structure or a β-sheet structure at a terminus, the fluorescent protein or the fluorescence-labeled tag is a fluorescent protein or a fluorescence-labeled tag having a helix structure or a β-sheet structure at a terminus, and the helix at the terminus and the helix at the terminus are linked, or the β-sheet structure at the terminus and the β-sheet structure at the terminus are linked.

The invention discloses low molecular weight cysteine peptidase inhibitors of natural origin, which are several-amino acid oligopeptides of the molecular weight below 3 kDa, free of salts with a molecular weight below 700 Da, a method for isolation of the same from natural organic material selected from the group consisting of egg whites, casein or milk and homogenates of plants such as knotweed, especially of the species Fallopia japonica, Houtt, mistletoe, soy, pineapple, rice, potatoes and other substances of natural origin, as well as medical (first) use in human and veterinary medicine of the low-molecular cysteine peptidase inhibitors of natural origin, being several-amino acid oligopeptides of the molecular weight below 3 kDa and the knotweed cystatin, as well as their use in manufacturing medicaments useful in prevention and treatment of inflammations associated with overexpression of cysteine peptidase enzymes originating from infecting microorganisms, or with overexpression of cysteine peptidase enzymes, being autogenic cysteine cathepsins in the human body.

The present invention relates to a microorganism for drug delivery, which has been transformed with a gene construct including a therapeutically active peptide, is delivered safely into the intestines through oral administration, and expresses and secretes a cystatin in the gastrointestinal tract, and also relates to a pharmaceutical composition for prevention or treatment of gastrointestinal disease, which includes the same. The present invention demonstrates the safety and superiority of lactic acid bacteria as a system for delivering a protein-based drug, and thus it is expected the lactic acid bacteria will be widely used as an agent for treatment of gastrointestinal disease in the medical field.

The present disclosure relates to proteins including PD-L1 binding affimer polypeptide sequences, gene expression constructs encoded those proteins, cells expressing those proteins, and pharmaceutical preparations of those proteins, gene expression constructs and cells and use in the treatment of various human conditions including cancer.

Methods for differentiating full-length high molecular weight kininogen (HMWK) and cleaved HMWK in a sample are provided herein. Such methods may comprise treating a biological sample with a protease to generate a plurality of digested peptides, and measuring one or more signature peptides, which are indicative of cleaved HMWK and/or full-length HMWK.

Methods for differentiating full-length high molecular weight kininogen (HMWK) and cleaved HMWK in a sample are provided herein. Such methods may comprise treating a biological sample with a protease to generate a plurality of digested peptides, and measuring one or more signature peptides, which are indicative of cleaved HMWK and/or full-length HMWK.

Provided herein are fusion protein comprising: an effector domain comprising a catalytic domain of a deubiquitinase, or a functional fragment or functional variant thereof; and a targeting domain comprising a moiety that specifically binds a membrane protein. Also provided herein are methods of using the fusion proteins to treat a disease, including genetic diseases.

The disclosure provides compositions and methods for the detection of renal disease and periodontal disease in mammals.

It is disclosed herein that RPE degeneration in human cell culture and in mouse models is driven by a non-canonical inflammasome pathway that results in activation of caspase-4 (also known as caspase-11 in mouse) and caspase-1, and requires cyclic GMP-AMP synthase (cGAS)-dependent interferon- (IFN-) production and gasdermin D-dependent interleukin-18 (IL-18) secretion. Reduction of DICER1 or accumulation of Alu RNA triggers cytosolic escape of mitochondrial DNA, which engages cGAS. Collectively, these data highlight an unexpected role for cGAS in responding to mobile element transcripts, reveal cGAS-driven interferon signaling as a conduit for mitochondrial damage-induced NLRP3 activation, and expand the immune sensing repertoire of cGAS and caspase-4 to non-infectious human disease. Coupled with the unexpected result that caspase-4, gasdermin D, IFN-, and cGAS are elevated in the RPE of human eyes with geographic atrophy, these findings also identify new targets for a major cause of blindness.

The present invention includes a composition and method of modulating a dysregulated gut-derived inflammation following a thermal injury comprising: identifying a mammal in need of treatment for the dysregulated gut-derived inflammation following the thermal injury; and providing the mammal with a recombinant Cystatin 9 (CST9) and Cystatin C (CSTC) in a synergistic amount sufficient to restrain or prevent a life-threatening, unrestrained systemic dysregulated gut-derived inflammation in the mammal caused by the thermal injury.