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Cystic fibrosis (CF) is a common genetic disease that affects the entire body, producing thick, sticky mucus that clogs the lungs, pancreas, and other organs. It is the most common fatal genetic disease in the United States, and is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR).

Calcium is a key element in the regulation of many cellular processes, including muscle contraction, hormone excretion from gland cells, neurotransmitter release from nerve synapses, and the regulation of cellular metabolism. Elevated calcium levels are found in a number of diseases.

Human immunodeficiency virus type-1 reverse transcriptase (HIV-1 RT) gene encodes 560 amino acids. In the virus, however, HIV-1 RT occurs as a dimer of two related polypeptides, p66 and p51 subunits at a molar ratio of 1:1. The p51 subunit is derived from a C-terminal proteolytic cleavage of the p66 subunit. This invention describes a simplified protocol to purify large quantities of histidine-tagged and untagged heterodimeric forms of human immunodeficiency virus type-1 reverse transcriptase (HIV-1 RT) from Escherichia coli.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of inflammatory disease, and their anti-inflammatory effects are believed to result from their ability to inhibit the formation of prostaglandins by prostaglandin H synthase (COX). Two forms of prostaglandin H have been identified, COX-1 and COX-2. The former seems to be constitutively expressed in a variety of tissues while the high expression of the latter has been reported in colorectal tumors. NSAIDs have been shown to be effective in reducing human colorectal cancers and possibly breast and lung cancers.

This technology relates to novel animal models of several human bone diseases that have been linked to enhanced BMP signaling. More specifically, this mouse model expresses a mutant receptor for BMP, known as Alk2 that is always actively signaling. This receptor is under the control of the Cre-loxP system, which allows control of expression of the mutant Alk2 in both a developmental and tissue-specific manner. As a result, the enhanced signaling conditions exhibited in multiple human bone-related diseases can be studied with the same animals.

Oxidative stress resulting in the formation of biological radicals has been implicated in a number of human diseases, such as cancer as well as aging. There is, however, a paucity of reliable methods for in vivo or ex vivo detection of radical formation. Until now the only general technique that allowed for the detection of these highly reactive species was electron spin resonance (ESR) using spin traps. One of the most popular of these spin traps is 5,5-dimethyl-1-pyrroline N-oxide (DMPO).

TTP has been implicated in autoimmune and inflammatory diseases through its role as a regulator of the transcripts encoding several pro-inflammatory cytokines, including tumor necrosis factor alpha. However, it has been difficult to study endogenous TTP in man and other animals because it is expressed at very low levels in most cells and tissues, and because of the lack of mouse monoclonal antibodies directed at the human protein.

The retinoid-related orphan receptor gamma (RORgamma) is a member of the nuclear receptor superfamily. NIH investigators used homologous recombination in embryonic stem cells to generate mice in which the RORgamma gene was disrupted. RORgamma deficient mice lack peripheral and mesenteric lymph nodes and Peyer's patches indicating that ROR expression is indispensable for lymph node organogenesis. In addition, RORgamma is required for the generation of Th17 cells which play a critical role in autoimmune disease.

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.

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.