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M5 muscarinic receptor knockout: Deficiency of M5Rs reduces drug-seeking behavior.

The five Muscarinic Acetylcholine (ACh) receptors are G-protein coupled receptors (M1R-M5R). M1R, M3R and M5R selectively couple to Gq/G11; M2R and M4R selectively couple to Gi/Go. M5R knockout mice are viable and fertile, and have no major morphological abnormalities.

Conditional knockout of Stat5a and Stat5b: Combined deletion of conserved Stat5a and Stat5b in mammary epithelium at different times during pregnancy reveal multiple distinct functions.

Generation of a floxed Gnsa gene for the G-protein Gs alpha (G_salpha) for the construction of conditional knockout mice. The heterotrimeric G protein G_salpha couples many receptors to adenylyl cyclase and is essential for hormone-stimulated cAMP generation. Previous mouse models with germ-line mutations in Gnas, the gene that encodes G_salpha had limited usefulness in trying to decipher the role of G_salpha pathways in specific tissues since only heterozygotes were viable and could be analyzed.

Stat 5a Knockout: Stat5a deficiency results in the loss of prolactin-dependent mammary gland development and lactogenesis.

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.