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This technology includes the creation and use of a mouse anti-Atlastin-1 monoclonal antibody (3194, IgG1). Mutations in Atlastin-1 are commonly found in hereditary spastic paraplegia, SPG3A. In addition, this protein is conserved in all eukaryotes, and it mediates fusion of endoplasmic reticulum tubules in cells, giving it its characteristic polygonal appearance. Thus, this protein is of interest to both those interested in disease pathogenesis and those studying basic cell biology.

This invention includes the generation and use of a polyclonal antibody for synapse-associated protein 102 (SAP102) and a polyclonal antibody that binds to mGluR7 when phosphorylated at Serine 862. Peptides of the sites were generated and injected into rabbits to create an immune response. Serum was collected from the rabbits that was then affinity purified. The specificity of the resulting polyclonal antibodies was then determined using biochemical techniques.

This invention includes human induced pluripotent stem cell (iPSC) lines that harbor a single copy dCas9-BFP-KRAB at the CLYBL safe harbor locus (mediating CRISPR inhibition of human gene expression) and/or a single copy of dox-inducible NGN2 at the AAVS1 locus (enabling the differentiation of the iPSCs into neurons). The CRISPR-mediated inhibition of human gene expression is maintained into the differentiated neurons, permitting functional studies of targeted genes in neurons.

This invention includes the generation and use of polyclonal antibodies that specifically recognize the glutamate receptor 1 protein that has been phosphorylated at Serine 567 (GluA1 pS567). Glutamate receptors are ligand-gated ion channels and are the predominant excitatory neurotransmitter receptor type in humans. A peptide sequence on the gene was selected surrounding the phosphorylation site. This peptide was then generated and injected into rabbits to create an immune response. Serum was then collected from the rabbit and the antibodies were affinity purified.

This invention includes the generation and use of monoclonal antibodies that specifically recognize either arginine vasopressin (AVP) or oxytocin (OT) when bound to neurophysins. The neurophysins (NPs) are a family of proteins that bind to hormones as they are released from the hypothalamus and make their way to the pituitary gland. Monoclonal antibodies were generated that specifically recognize vasopressin bound to a neurophysin (NP-AVP) or oxytocin bound to a neurophysin (NP-OT). Seven monoclonal antibodies were characterized.

This technology relates to the creation and use of newly identified ligands to the D1 dopamine receptor (D1R). The D1 dopamine receptor is linked to a variety of neuropsychiatric disorders and represents an attractive drug target for the enhancement of cognition in schizophrenia, Alzheimer disease, and other disorders. These ligands are positive allosteric modulators (PAMs) that bind to the dopamine receptor at a site other than where dopamine binds and causes the receptor to have an increased response.

The technology relates to therapeutic approaches that inhibit and block the replication of the endogenous HERV-K retrovirus. Previous work has shown that patients with Amyotrophic Lateral Sclerosis (ALS) can have HERV-K activation. In animal models, activation of HERV-K can lead to neurodegenerative symptoms similar to those exhibited by ALS patients. Work in these animal models has allowed the identification of the responsible transcription factor (TDP-43) as well as the corresponding positions of the HERV-K promoter binding sites.

The technology includes USP30 knockout HeLa cells that were generated using CRISPR technology. Parkin and Pink1 are key master genes for triggering the degradation of mitochondria (mitophagy). In contrast, USP30 has been found to be localized in the mitochondria and have a role in antagonizing Parkin function, thereby impeding mitophagy.

This invention relates to methods and algorithms that incorporate information from multiple imaging modalities to identify, estimate the size, and track the time course of brain lesions. Subjects develop brain lesions over the natural course of a disease. Currently, lesions are measured and tracked by a trained neuroradiologist using slice-by-slice inspection, a slow process that is prone to human error and hard to generalize to large observational studies.

This technology includes a cell line that stably expresses YFP-Parkin and mt-mKeima that can be used to study mitochondrial degradation, mitophagy, using flow cytometry (FACS). Compromised mitophagy is implicated in Parkinson disease. The effects of any compounds or genetic alteration on Parkin-mediated mitophagy can be monitored.