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Q490L point mutation was introduced into the rat M3 muscarinic receptor cDNA to confer persistent, constitutive (ligand-independent) activity. Expression of the M3 receptor mutant was placed under the control of a 650 bp fragment of the rat insulin promoter II (RIP II) to limit expression to the islet beta cell.

Researchers at NIH have developed islet beta cell M3 muscarinic acetylcholine receptor knockout mouse. The mice were generated by crossing floxed mouse M3 muscarinic acetylcholine receptor mice with mice in which Cre recombinase was controlled by the beta-cell specific rat insulin promoter (RIP-Cre mice).

Researchers at NIH have generated transgenic mice in which the M3 muscarinic receptor is overexpressed in pancreatic beta cells. This was done by placing the receptor gene under the control of the 650 bp rat insulin promoter II (RIP II). The resulting mice show a pronounced increase in glucose tolerance and enhanced plasma insulin levels. Strikingly, these mutant mice were resistant to diet-induced glucose intolerance and hyperglycemia.

Two isoforms of sphingosine kinase, sphingosine kinase 1 (SphK1) and sphingosine kinase 2 (SphK2), convert sphingosine to sphingosine 1-phosphate (S1P) in mammalian cells. While the importance of SphK1 has been known for some time, information about SphK2 is still being revealed. Therefore, researchers at NIH have developed an antibody against mouse SphK2, which can be used to further understand the role of this enzyme.

The cleavage of sphingoid base phosphates by sphingosine-1-phosphate (S1P) lyase to produce phosphoethanolamine and a fatty aldehyde is the final degradative step in the sphingolipid metabolic pathway. Researchers at NIH injected rabbits with the C-terminal peptide of the mouse S1P lyase — 551-TTDPVTQGNQMNGSPKPR-568 — to develop an antibody that can be used in western blotting to study this pathway.

Type I interferons play a critical role in both innate and adaptive immunity through the stimulation of the IFNAR1 which initiates interferon signaling in response to viral and bacterial infections. However, abnormal interferon signaling is associated with human diseases, such as lupus. The present invention discloses six hybridomas that produce mouse monoclonal antibodies specific for the extracellular domain of human IFNAR1. Two of the monoclonal antibodies are able to bind IFNAR1 and reduce interferon signaling.

Our technology describes unique genetic signatures in patients with digestive diseases and liver disorders. Using comprehensive analysis of 735 microRNAs and 19,000 mRNAs, we have identified a unique set of microRNAs and/or mRNAs which predict disease phenotypes in patients with digestive and liver disorders. The identification of such point-of- care genetic signatures is significant for both personalized biomarkers and novel targeted biotherapeutics. These microRNAs and mRNAs function either together or separately thus modulating protein expressions in one or more signaling pathways.

The invention pertains to the use of glucan encapsulated non-immunostimulatory small interfering RNAs (siRNAs) to treat type-2 diabetes. Endocannabinoids (EC) are lipid signaling molecules that act on the same cannabinoid receptors that recognize and mediate the effects of endo- and phytocannabanoids. EC receptor CB1R activation is implicated in the development of obesity and its metabolic consequences, including insulin resistance and type 2 diabetes.

Strongyloides stercoralis is an intestinal nematode endemic that affects an estimated 30 to 100 million people worldwide. Many of these individuals may be asymptomatic for decades. The present invention discloses a NIE recombinant antigen that can be used in improved assays and diagnostics for S. stercoralis infection. The NIE antigen is the only one that is non-cross-reactive with sera from humans with other related filaria infections. The NIE antigen can be utilized as a skin test antigen for immediate hypersensitivity as well as for use in ELISA or other assays.

This invention relates to methods of rapidly detecting influenza, including differentiating between type and subtype. Unlike culture and serological tests requiring 5 to 14 days for completion, CDC researchers developed a rapid, accurate assay, which is easily adapted to kit form. This assay also requires less labor input than immunoassays. These methods can be used to quickly identify a broad variety of influenza types and subtypes, including viruses that may be involved in pandemics (such as H5N1, for example).