This technology includes transgenic mice to be used in the study of melanocyte stem cells (MSCs) for utilization in regenerative medicine. Using the melanocyte system as a model, we investigated establishment of MSCs in the hair bulge - the stem cell compartment of the hair. During embryogenesis, all melanoblasts express SOX10, but this expression is downregulated during hair follicle morphogenesis and MSC differentiation. To further study the role of SOX10, we generated transgenic mice overexpressing SOX10 in melanoblasts.

This technology includes a therapy and companion diagnostic which can be used for the early diagnosis and treatment of sepsis and sepsis-induced acute kidney injury (AKI). Mitochondrial damage plays a key role in sepsis-induced acute kidney injury BAM15 [2-ftuorophenyl){6-[(2- fluorophenyl)am ino]{1 ,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine] is a mitochondrial uncoupler that protects mitochondria with more specificity and less cytotoxicity than other uncouplers. Mitochondrial DNA (mtDNA) is a damage associated molecular pattern that is increased in human sepsis.

This technology includes a compound for use as a selective agonist of the A1 adenosine receptor (AR) for therapeutic hypothermia and other conditions. We have examined various synthesized nucleosides in a model of mouse hypothermia, in conjunction with AR knockout mice, to characterize the biological profiles. In trying to identify novel highly selective A1AR agonists that have superior in vivo activities, we have adapted a means of rigidifying the ribose moiety of adenosine in the form of a bicyclic (N)-methanocarba ring.

This technology includes microRNAs for use in cell lines for protein production and potentially future treatments of cancer or diseases related to metabolism. Mmu-miR-466h was identified as a major apoptotic regulator in suspension adapted Chinese Hamster Ovary cells. Mmu-miR-466h was found to have the pro-apoptotic activity by targeting some anti-apoptotic genes for degradation during the exposure of CHO-S cells to the nutrients depleted media.

This technology includes a method using ionophores to reduce sickling in patients with sickle cell disease. Sickle cell disease is caused by polymerization of a hemoglobin mutant, and the only approved treatment acts by replacing sickle hemoglobin with fetal hemoglobin, thereby increasing the delay time prior to polymerization. This drug is only partially successful because it does not induce fetal hemoglobin synthesis in all cells.

This technology includes compounds that are selective agonists of the A3 receptor for the treatment of various disorders such as cancer and autoinflammatory diseases. Structurally, these compounds extend the class of (N)-methanocarba derivatives that are selective agonists of the A3 receptor.

This technology includes mice which are intended to be bred with mice that have the tetracycline-response element promoter driving a gene of interest, for the study of kidney diseases. When the dual transgenic mice are fed tetracycline or doxycycline, the transgene is activated in glomerular podocytes.

This technology includes a class of A3AR-selective agonists to be used therapeutically to treat a variety of conditions, including chronic pain, cancer, and inflammatory diseases. This class of compounds produced full agonists of the human A3AR of nanomolar affinity that were consistently highly selective (>1000-fold vs. A1AR and A2AAR). The selectivity at mouse A3 receptors is smaller, but the compounds are still effective in vivo in reducing or preventing development of neuropathic pain.

This technology includes antibodies to apolipoprotein L1 (ApoL 1) to be used in basic science laboratory studies. ApoL 1 is a protein that is present within cells and circulates as component of high-density lipoprotein. Its functions are not well understood. Recently APOL 1 genetic variants have been shown to be highly associated with kidney disease in African Americans.

This technology includes the use of the (N)-methanocarba phosphonate analogues of 5’-AMP as cardioprotective agents for use in conditions such as cardiomyopathy and heart failure. We previously found a compound, MRS2339 (a phosphate derivative that can be slowly cleaved in vivo and lose potency), which activates the appropriate receptors and is protective in models of heart failure in several species (mouse, dog). MRS2339 is a phosphate derivative that can be slowly cleaved in vivo and lose potency. We now extend this technology to more stable derivatives, i.e.