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Sirt3 knockout: Sirt3 is a mitochondrial-localized tumor suppressor that maintains mitochondrial integrity and metabolism during stress.

Generation of floxed Sirtuin 6 for the construction of conditional knockout mice.

The Sirtuins (Sirt1-7), a family of seven proteins related to yeast Sir2, are histone deacetylases that regulate many critical biological processes including genomic stability, adaptation to calorie restriction and aging. Mice with a targeted disruption of Sirt6 had very low levels of blood glucose (and paradoxically, low insulin levels) and died shortly after weaning. Hypoglycemia, attributed to increased sensitivity to insulin, was the major cause for lethality.

Sirt1 knockout: Sirt1, a protein deacetylase, is a tumor suppressor that promotes genome stability and regulates proteins involved in energy metabolism.

Generation of floxed Sirtuin 1 Exon5-Exon6 for the construction of conditional knockout mice.

FGFR2 knockout is an embryonic lethal mutation and blocks limb bud initiation.

FGFR3 knockout. Complete knockout of the FGFR3 gene, the gene in which missense mutants cause short statue achondroplasia, fails to restrain cartilage growth at the bone growth plate, allowing bones to elongate excessively but fail to ossify.

This molecular probe may serve as a companion tool to identify and stratify patient populations based on the prevalence of the target A₃ adenosine receptors.

Small molecule drugs, A₃AR-selective agonists, are currently in advanced clinical trials for the treatment of hepatocellular carcinoma, autoimmune inflammatory diseases, such as rheumatoid arthritis, psoriasis, and dry eye disease, and other conditions.

The five Muscarinic Acetylcholine (ACh) receptors are G-protein coupled receptors (M1R-M5R). M3 muscarinic ACh receptors are present in the central nervous system and the periphery.

The invention is a STAT5 mutant mouse that can be used in research related to cancer, autoimmunity and infectious diseases as well as drug screening. The mouse model itself has multiple immunological defects resulting in formation of STAT5 dimers but not tetramers.

Researchers at NIDDK have developed polyclonal antibodies against the G protein, Gbeta5. Gbeta5 is a unique and highly specialized G protein that exhibits much less homology than other Gbeta isoforms (~50%) and is preferentially expressed in brain and neuroendocrine tissue. It is expressed prominently in the neuronal cell membrane, as well as in the cytosol and nucleus. Although this distribution pattern suggests that Gbeta5 may shuttle information between classical G protein-signaling elements at the plasma membrane and the cell interior, its function in the brain is largely unknown.