Several Gsα knockout mouse models have been generated in order to study the role of Gsα in vivo. The mouse models with universal Gsα disruption will be discussed below in the context of human diseases that are caused by heterozygous inactivating mutations within one of the 13 exons encoding this protein. In addition, Gsα has been conditionally ablated, through the use of the Cre-Flox technology, in specific tissues including liver, cartilage, bone, and glomerulus, confirming the absolute requirement of Gsα in the proper function of these tissues [48-51].
