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This technology includes a transgenic reporter mouse that expresses a fluorescent protein called mt-Keima, to be used to detect and quantify in vivo mitophagy. This fluorescent protein was originally described by a group in Japan and shown to be able to measure both the general process of autophagy and mitophagy. We extended these results by creating a living animal so that we could get a measurement for in vivo mitophagy. Our results demonstrate that our mt-Keima mouse allows for a straightforward and practical way to quantify mitophagy in vivo.

This technology includes a generated polyclonal antibody in rabbit that detects the mitochondrial uniporter (MCU) protein. This antibody was created by immunizing rabbits with a synthesized sequence of the MCU protein and can be used to identify and quantify MCU protein in various tissues. The polyclonal nature of the antibody ensures it recognizes multiple epitopes on the MCU, enhancing detection reliability. This technology is crucial for understanding MCU's role in mitochondrial function and mammalian physiology.

This technology includes monoclonal antibody was raised in mice against amino acids 703-1074 of ZFR. Antibody specificity was confirmed by immunoblotting lysates from cells depleted of ZFR using shRNAs.

This technology includes the method of blocking CD38 in expanded natural killer (NK) cell therapy in combination with daratumumab in patients with multiple myeloma. Our in vitro studies have already confirmed the addition of NK cells to myeloma cells that have been exposed to daratumumab enhances myeloma killing compared to single agent treatment.

This technology includes three distinct cell lines of motor neuron progenitors, derived from different sources: human induced pluripotent stem cell (iPSC) line BC1, human iPSC line X1, and human embryonic stem cell (hESC) line H14. These cell lines hold significant potential for multiple diagnostic and therapeutic applications. A key advantage of these cell lines is the commercial availability of their starting materials (iPSC-BC1, iPSC-X1, and hESC-H14), which are not restricted in terms of usage of their derivatives.

This technology includes a neural stem cell (NSC) line derived from a Niemann Pick C (NPC) patient, aimed at advancing research and drug development for NPC, an inherited neurodegenerative disorder characterized by the accumulation of cholesterol in neurons. The NSCs, which serve as a crucial intermediate cell type, can be differentiated into any neuronal or glial cell of the brain or spinal cord under appropriate culture conditions. These cells originate from fibroblasts reprogrammed into induced pluripotent stem cells.

This technology includes a novel plasmid design for cell immortalization. It uniquely combines the conditional activation of human telomerase and c-myc genes through cumate addition, a method distinct from traditional immortalization techniques which commonly use SV40 T-antigen, telomerase, or c-myc. This plasmid also includes a GFP reporter and a puromycin resistance gene, enhancing the efficiency of the immortalization process.

This technology includes antibodies for TMC1 protein as a treatment for hearing loss. TMC1 is one of the common genes causing hereditary hearing loss. Our laboratory used synthetic peptides corresponding to the TMC1 protein to immunize rabbits. The resulting antisera were shown to bind to TMC1 protein expressed in heterologous expression systems. TMC1 protein is required for the transduction of sound into electrical impulses in inner ear sensory cells.

This technology includes six human monoclonal antibodies (mAbs) that target tumor antigens derived from the CT-RCC HERV-E (human endogenous retrovirus type E) to generate Chimeric Antigen Receptor (CAR) T cells to treat patients with advanced clear cell renal cell carcinoma (ccRCC). These mAbs were identified from Adagene Inc’s human antibody phage library, and data show that majority of these mAbs only bind to CT-RCC HERV-E+ ccRCC cells, which express TM but not CT-RCC HERV-E non-expressing ccRCC cells nor non-RCC cells.

This technology includes the method of blocking CD38 in expanded natural killer (NK) cell therapy in combination with daratumumab in patients with multiple myeloma. Our in vitro studies have already confirmed the addition of NK cells to myeloma cells that have been exposed to daratumumab enhances myeloma killing compared to single agent treatment.