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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.

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.

This invention describes materials and methods of detecting novel influenza virus in a sample. As highlighted by the recent H1N1 pandemic strain, influenza viruses are constantly evolving and novel reassortments can quickly spread around the world.

The technology relates to a protein-based nanoparticle platform that allows presentation of immunogenic molecules such as influenza virus antigens. This protein platform is made up of hepatitis B capsid/core proteins. The core proteins contain immunogenic loop c/e1, where other antigens can be inserted and the chimeric protein retains the ability to form capsid-like particles. The technology describes the insertion of one or more copies of influenza epitopes derived from the globular head or the stem region of hemagglutinin protein into or around the c/e1 loop of the core protein.

Details for this material are provided in the NIH AIDS Reagent Program Catalog (Catalog# 341): https://www.aidsreagent.org/reagentdetail.cfm?t=cell_lines&id=152.

There is a great need for broadly protective, “universal” influenza virus vaccines given the antigenic drift and shift of influenza viruses and the variable protective efficacy of the current influenza vaccines. This technology relates to a broadly protective, “universal” influenza vaccine candidate composed of a cocktail of different low pathogenicity avian influenza virus subtypes inactivated by betapropiolactone (BPL).

Available for licensing through a Biological Materials License Agreement are the murine MAbs described in Beeler et al, "Neutralization epitopes of the F glycoprotein of respiratory syncytial virus: effect of mutation upon fusion function," J Virol. 1989 Jul;63(7):2941-2950 (PubMed abs). The MAbs that are available for licensing are the following: 1129, 1153, 1142, 1200, 1214, 1237, 1112, 1269, and 1243. One of these MAbs, 1129, is the basis for a humanized murine MAb (see U.S.

This mouse has been generated by targeted gene disruption. The mouse provides a model to investigate the function of the chemokine receptor CX3CR1, which is a proinflammatory receptor for the leukocyte chemoattractant CX3CL1 (aka fractalkine). As an example, the mouse is in use in the study of atherosclerosis. Further, the mouse may serve as a model study the role of the immune system during infection with pathogens as well as other immunologically mediated diseases and responses to tumors.