Microglia activation leads to inflammation mediated dopaminergic degeneration in the brain of patients with Parkinson and Alzheimer's Disease. Thus Identification of drugs that reduce microglia activation could prevent or reverse neuronal degeneration in these diseases and other degenerative CNS disorders.

The disclosed invention provides materials and methods to treat granulocytopenia (low white cell count in the blood) which is characterized by a reduced number of granulocytes (relative) or an absence of granulocytes (absolute). This condition is commonly associated with cancer chemotherapy, but is seen less frequently in a number of conditions including the use of propylthiouracil, radiotherapy for marrow ablation for bone marrow transplantation, aplastic anemia, systemic lupus erythematosus, AIDS and a variety of other situations.

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.

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.

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).

The zinc finger protein ZFP36L2 has been shown by the inventors to play an essential role in hematopoiesis, a process that is dysregulated in hematological cancers, anemia, and other conditions. Thus, ZFP36L2 has promise for use in a diagnostic test to detect abnormal hematopoiesis, or as a target for the development of therapeutics to treat abnormal hematopoiesis.