Main Menu

This technology includes five microRNA mimics which were identified to improve the functional expression of hard-to-express membrane protein. These miRNAs are: hsa-miR-22-5p; hsa-miR-18a-5p, hsa-miR-22-3p, hsa-miR-429 and hsa-miR-2110. Improving expression level of recombinant mammalian proteins is vital, as the adequate supply of correctly folded proteins is the prerequisite for all structure and function studies.

This technology includes a sensitive and specific method to rapidly detect antibodies in biofluids. This assay has been used for the detection of antibodies in blood, urine, and saliva. Until now, no one has used LIPS to detect clinically relevant antibodies to SARS-CoV-2 Nucleocapsid (N) or Spike (S) in saliva. Briefly, LIPS employs recombinantly synthesized target proteins or peptides (e.g., S and N proteins) tagged with light-emitting proteins as targets to be captured by host produced immunoglobulins. These immunoglobulins can be captured by protein A/G beads and immobilized.

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 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 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 an alternative synthetic biotin-streptavidin replacement system for use in the development of clinical diagnostics. Peptide nucleic acids (PNA) when functionalized onto the surface of microspheres are capable of targeting short RNA targets from solutions. However, when the target nucleic acid becomes longer and complicated in structure, the PNA no longer efficiently binds due to steric hindrance from the microspheres and/or slow hybridization kinetics of larger nucleic acid targets.

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 an engineered HEK293 cell line expressing firefly luciferase by functionally knocking out the caspase 8 associated protein 2 (CASP8AP2) gene using CRIPSR/Cas9 genome editing for improved production efficiency. This engineered cell line possesses superior recombinant protein expression capabilities than the parental cell line from which it was created, while proliferating and metabolizing carbon at a comparable rate. Improved recombinant protein expression is mediated by growth arrest at the G0/G1 phase.

This technology includes a sphingosine kinase 1 (Sphk1) knockout mouse model for use in developmental biology research. Sphingosine-1-phosphate (S1P) is synthesized from sphingosine and ATP by the action of sphingosine kinase, and activates cell signaling. Two sphingosine kinases, SPHK1 and SPHK2, have been identified. To study the physiological function of SPHK1, Sphki null mice were generated. The mice were viable, fertile, with no obvious abnormalities. Total SPHK activity in most tissues was substantially reduced, suggesting the presence of other sphingosine kinases.

This technology includes a new method to induce recombinant protein expression in E. coli through the activating the SoxS promoter by molecular oxygen. We previously discovered that the SoxRS regulon of E. coli is activated in response to elevated dissolved oxygen concentration mainly to protect the bacteria from possible oxygen damage. We hypothesized that the 16-fold increase in the expression of this regulon make it possible candidate for inducing the expression of recombinant proteins.