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This technology includes an alpha-galactosidase-A knockout mouse model that can be used to study Fabry disease, an X-linked lysosomal storage disorder. Alpha-galactosidase-A is a crucial enzyme responsible for the breakdown of glycolipids, particularly globotriaosylceramide (Gb3), within lysosomes. In Fabry disease, a rare and inherited lysosomal storage disorder, mutations in the GLA gene lead to deficient or non-functional alpha-galactosidase-A enzyme activity.

This technology includes a mouse model of TRIOBP human deafness which can be used for research and treatment development for deafness. This model contains mutations altering the TRIOP-5 isoform.

Scientists at NIAID have developed two immortalized stable B cell lines from rhesus macaques that can have value as research tools for the discovery of neutralizing antibodies of simian origin against HIV and that may have value in the development of an HIV vaccine. These B cell lines encode human Bcl-6 and Bcl-xL proteins, which are major regulators of apoptosis. These B cell lines are derived from the lymph node of a rhesus macaque (RM) that was infected with SHIV.CH505.

There are five known Ebolavirus species: Ebola virus (Zaire ebolavirus); Sudan virus (Sudan ebolavirus or SUDV); Taï Forest virus (Taï Forest ebolavirus, formerly Cote d'Ivoire ebolavirus); Bundibugyo virus (Bundibugyo ebolavirus); and Reston virus (Reston ebolavirus). Last year an ebolavirus outbreak resulted in 164 cases and 55 deaths. While there is an FDA-approved Ebola virus vaccine authorized for use against Ebola virus infections, ERVEBO, this vaccine is not effective against SUDV due to the significant variation between Ebola virus and SUDV.

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of a targeted disruption of the Rpe65 gene in mice, a novel model for studying retinal diseases and testing potential therapies.

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of a transgenic mouse model for X-linked retinoschisis (XLRS).

Traf3ip2-/- C57/BL6 mice are a genetically modified mouse model in which the Traf3ip2 gene, responsible for encoding the CIKS adaptor protein essential for IL-17 cytokine signaling, has been disrupted. These mice offer a robust platform for research in autoimmune and inflammatory diseases, as well as potential applications in cancer studies. By eliminating IL-17 signaling and cross-interactions with other pathways, they provide a unique opportunity for drug discovery and proof-of-principle studies, shedding light on disease mechanisms and therapeutic development.

In this research endeavor, a multifaceted approach has been employed to investigate the intricate roles of CD300 family proteins in immunological processes. Lentiviral transduction of the L929 cell line with mouse and human CD300f genes, followed by puromycin selection, has established cellular models to examine the functions of these receptors. Concurrently, engineered constructs encoding extracellular domains of mouse CD300lb and CD300ld, fused with human IgG1, have been developed for the production of receptor extracellular domain proteins, facilitating studies on protein interactions.

This technology entails a novel vaccine design against malaria, employing an alphavirus Virus-Like Particle (VLP) system to present a critical epitope from the Plasmodium falciparum circumsporozoite protein (PfCSP). The vaccine targets the junctional region between the N-terminus and the central repeat domain of PfCSP, a segment previously identified as vital for generating protective immunity.