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Antibodies to UTA1, useful for immunoblotting and immunocytochemistry, are available to resell for research purposes. Urea Transporter 1 (UTA1) is activated by vasopressin and is responsible for urea transport across the apical membrane into the intracellular space within the renal inner medullary collecting duct. The inventor has developed rabbit polyclonal antibodies directed against a peptide sequence in human UTA1. Antibody also recognizes UTA3, another product of the same gene.

Parathyroid hormone receptors found on osteoblasts in bone and renal tubule cells in kidney elevate blood calcium levels when stimulated by parathyroid hormone (PTH) and PTH-related protein (PTHrP). Excessive secretion of PTH from the parathyroid gland results in primary hyperparathyroidism. Production of PTHrP by various tumors results in humoral hypercalcemia of malignancy. In both of these conditions, excessive blood calcium levels lead to clinically significant morbidity. A parathyroid hormone antagonist could therefore have therapeutic value.

JC Virus causes a fatal disease in the brain called progressive multifocal leukoencephalopathy (PML) that occurs in many patients with immunocompromised conditions. For example, more than five percent (5%) of AIDS patients develop PML. Additionally, these conditions include, but are not limited to, cancers such as leukemias and lymphomas, organ transplants such as kidney, heart and autoimmune conditions with treatment that modulates the immune system such as Multiple Sclerosis (MS), rheumatoid arthritis, psoriasis, and systemic lupus erythematosus.

This invention is directed to use of certain peptide analogs comprising multiple amphipathic helical domains that are able to promote cellular lipid efflux and stimulate lipoprotein lipase activity. As a result, administration of invention peptides lead to reduced incidences of hypertriglyceridemia without inducing toxicity. Existing peptides that stimulate efflux of lipids from cells exhibit unacceptably high toxicity. Invention peptides are superior to existing peptides and can also be used to treat or prevent a vast range of vascular diseases, and their dyslipidemic precursors.

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.

Cryopreservation using liquid nitrogen frozen polyvinyl bags allows for storing cellular materials for extended periods while maintaining their activity and viability. Such bags are commonly used in the clinic to store blood products including blood cells, plasma, hematopoietic stem cells, umbilical cord blood for future uses including transplantation. These materials, typically obtained in limited quantities, may be of great therapeutic value, as is the case of stem cells or cord blood derived cells which can be used to potentially treat a number of diseases.

This is a mouse model available to study T-cell differentiation. Growth factor independent 1 (GFi-1) is a transcriptional repressor that is transiently induced during T-cell activation. This knockout mouse line is a GFi-1[flox/flox] introduced into a mouse Cre controlled by a CD4 promoter, which allows selective removal of GFi-1 exclusively in T-cells. It has thus-far been used to demonstrate that GFi-1 plays a critical role in enhancing Th2 cell expansion and repressing induction of Th17 and CD103+ iTreg cells.

X-linked nephrogenic diabetes insipidus (XNDI) is a severe kidney disease caused by inactivating mutations in the V2 vasopressin receptor (V2R) gene that result in the loss of renal urine-concentrating ability. At present, no specific pharmacological therapy has been developed for XNDI, primarily due to the lack of suitable animal models. This technology provides a unique and viable animal model of XNDI. NIH investigators have generated mice in which the V2R gene could be conditionally deleted during adulthood by administration of 4-OH-tamoxifen.

Investigators at the National Heart, Lung and Blood Institute have developed modified defensins that are resistant to degradation, have improved characteristics compared to unmodified defensins, and are promising candidates for pulmonary disease therapeutics.

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.