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SMAD7 conditional knockout mice are available for licensing. SMAD7 can be knocked out by breeding with CRE-recombinase transgenic mice with a variety of promoters to yield tissue or cell type-specific deletions of SMAD7. SMAD7 has been shown to play a role in bone morphogenesis, cardiovascular tissue generation, immune regulation and fibrosis. Therefore, these mice provide a unique model to examine the role of the SMAD7 gene in disease processes that involve immunological, fibrotic, or cardiovascular components.

Plasmodium vivax (malaria) is a significant health concern in many parts of Asia, Latin America, North Africa, and the Middle East. There is a lack of continuous culture systems for this pathogen. The subject technology is an erythroid progenitor continuous cell line (termed CD36E) identified by erythroid markers CD36, CD33, CD44, CD71, CD235, and globoside. These CD36E cells are heterozygous for Fya and Fyb (Duffy antigen). Due to recent evidence that Plasmodium vivax (P. vivax) can infect erythroid progenitor cells (reference: YX Ru et al.

This technology relates to specific (N)-methanocarba adenine nucleosides that have been developed and dendrimers that connect these compounds to create molecules with multiple targets. Dendrimers are essentially repeated molecular branches presenting the core receptor-binding molecules. The compounds synthesized function as agonists and antagonists of a receptor of the G-protein coupled receptor (GPCR) superfamily.

The inventors have isolated and characterized an alkaloid, phantasmidine, from the skin of the Ecuadoran poison frog E. anthonyi. Phantasmidine is selective for beta4-containing receptor subtypes, unlike many nicotinic receptor agonists currently in development, which target beta2-containing receptor subtypes.

This technology describes monoclonal antibodies against mouse chemokine (C-X-C motif) ligand 9 (CXCL9), also known as Monokine induced by gamma interferon (Mig). CXCL9 is a secreted protein that functions to attract white cells and increased expression of CXCL9 has been linked to several diseases. The inventors at the NIH generated over 100 anti-mouse CXCL9 antibodies from a CLXL9/Mig knockout mouse and further characterized several antibodies to show neutralization of CXCL9.

This invention discloses small molecule inhibitors of human 12-lipoxygenase (12-hLO). 12-lipoxygenase expression, activation, and lipid metabolites have been implicated in type 1 and type 2 diabetes, cardiovascular disease, hypertension, Alzheimer’s, and Parkinson’s disease. The development of 12-hLO inhibitors may be a potent intracellular approach to decreasing the ability of platelets to form large clots in response to vessel injury or activation of the coagulation pathway.

NIH Inventors have recently discovered a novel Leucine-rich repeat and calponin homology domain-containing protein 4 (Lrch4) in a proteomic screen of the plasma membrane of lipopolysaccharide (LPS)-exposed macrophages. Expression data by RT-PCR revealed that all Lrch family members (1-4) are expressed in macrophages, but only Lrch4 was recruited into lipid rafts (signaling microdomains of the plasma membrane) by LPS. Lrch4 is the most highly expressed Lrch family member in mouse tissues. It is a predicted single-spanning transmembrane protein that is encoded by the Lrch4 gene in humans.

Monitoring an immune system that has been depleted by infection (e.g., HIV), chemotherapy, or progenitor cell transplantation is vital to assessing individual’s recovery status. This technology provides a new plasmid standard to be used as part of the existing TREC assay. This new plasmid has a shorter insert than the commercially available one, which means it now matches the PCR product generated in the qPCR reaction in the TREC assay. Additionally, the new plasmid is easier to grow up than the existing standard.

The nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) encodes a protein that has anti-inflammatory, proapoptotic, and antitumor properties. It plays a pivotal role in antitumorigenesis induced by chemopreventive compounds. Transgenic mice expressing human NAG-1 have been developed by the NIH investigator and collaborator.

Cerebral Cavernous Malformation (CCM) is a brain disease affecting up to 0.5% of the worldwide population. CCM is characterized by grossly dilated vessels prone to leaking and hemorrhage which result in severe headaches, seizures, and strokes. Inherited forms of the disease are due to mutations in one of three loci, CCM1, CCM2, and CCM3. Prior efforts to develop mice with targeted null mutations in Ccm1, Ccm2, or Ccm3 have been unsuccessful, as such mutations result in embryonic death.