Fragile X syndrome (FXS) is the most common inherited form of human intellectual disability. FXS is caused by loss of function of the FMR1 gene which results in significant behavioral deficits in spatial learning and memory tests. FMR1−/− knockout mice share many of the learning deficits and decreased synaptic function encountered in FXS patients. Anecdotal evidence indicates a reduction in the amount of Reelin, a large extracellular signaling protein important for normal hippocampal synaptic plasticity, may play role in the etiology of FXS. Disclosed herein is a rAAV9 Reelin viral vector expressing a REELIN repeat R3+R6 fusion protein that is shown to rescue cognitive deficits in FMR1−/− mice as evaluated in the Hidden Platform Water Maze, Open Field and Fear Conditioning. Reelin gene therapy is therefore potentially a novel therapeutic for the treatment of Fragile X Syndrome.

The invention relates to antibody conjugates (e.g., a bispecific antibody), drug and nanoparticle compositions and methods and compositions for generating them. This invention further relates to methods of using these compositions for imaging, diagnosing or treating a disease.

The invention relates to antibody conjugates (e.g., a bispecific antibody), drug and nanoparticle compositions and methods and compositions for generating them. This invention further relates to methods of using these compositions to image, diagnose or treat a disease.

The present invention is based on the seminal discovery of a panel of targeting peptides and antibodies that can recognize AD brains at different stages of the disease, starting from early to advanced stage. The peptide probes described here are unique in the field and can be expected to advance understanding on early neurodegenerative changes associated with AD and improve the therapeutic outcomes by early detection and intervention in AD. Further, the invention provides antibodies that can be used to treat AD.

The present disclosure relates to the field of biotechnology. In particular, provided are a ligase fusion protein and an immobilized ligase comprising the same. Also provided is use of the ligase fusion protein or the immobilized ligase in the preparation of conjugates. Further provided is a process for the preparation of conjugates using a ligase or a ligase unit.

Compositions and methods are provided for depletion of pluripotent cells. In one embodiment of the invention, methods are provided for depletion of pluripotent cells from a mixed population of differentiated cells and stem cells, to provide a population of cells substantially free of pluripotent stem cells.

Disclosed herein are methods, compositions, kits, and systems for rapid multiplex detection of a microorganism of interest. Recombinant bacteriophages encoding capture moiety-indicator protein fusion products allow for the capture of indicator proteins on a surface. Cocktail compositions of recombinant bacteriophages can be used to detect potentially harmful bacteria. The specificity of recombinant bacteriophages for binding microorganisms allows targeted and highly specific detection of a microorganism of interest.

The present invention is situated in the field of multimers used for targeted therapies. More particularly, the invention relates to methods for preparing multifunctional heteromultimeric protein complexes with a defined ratio of functional components and to multifunctional heteromultimeric protein complexes for directing complement-dependent cytolysis, optionally comprising a scaffold, which display three or more different functional components present in a defined relative ratio, of which one is a tracking component.

A voltage indicator includes a polypeptide sequence comprising a voltage-sensitive opsin domain and a capture protein domain arranged and disposed to capture a fluorescent dye ligand. When the fluorescent dye ligand is captured and the voltage indicator is bound to a cell membrane, an increase in voltage across the cell membrane causes an increase in fluorescent emission.

Disclosed is means which enables simple and rapid detection of the presence or absence of mismatch repair activity, and which is useful for diagnosis and treatment of mismatch repair-deficient cancers. In an integrated-type nucleic acid construct provided by the present invention, [promoter region], [5′-side region+first homologous region], and [second homologous region+3′-side region] are placed in the same nucleic acid molecule. In a divided-type nucleic acid construct, [promoter region], [5′-side region+first homologous region], and [second homologous region+3′-side region] are placed in two different nucleic acid molecules. The nucleic acid construct of the present invention can be used as a therapeutic agent for mismatch repair-deficient cancer, as a diagnostic agent for mismatch repair-deficient cancer, or as a companion diagnostic agent for predicting an effect of an anticancer drug for mismatch repair-deficient cancer, containing the nucleic acid construct.