Our lab studies the genetic regulation, chemical processes, and functional role of the Gsα protein, which is required for accumulation of the chemical messenger cyclic adenosine monophosphate (cAMP) inside cells. Our lab studied both a human disease (Albright hereditary osteodystrophy, or AHO) that is associated with mutations in the Gsα-subunit gene and a mouse model with an intentionally inactivated Gsα-subunit gene. Through these studies our lab demonstrated that, in some tissue, the copy of the Gsα-subunit gene inherited from the father is inactive due to a process called genomic imprinting. This explains why maternal inheritance leads to a form of AHO that is associated with obesity and resistance to multiple hormones (pseudohypoparathyroidism type 1a, or PHP1a), while paternal inheritance is not. We are continuing to study these patients in great detail and are developing various genetically engineered mouse models with deletion of the gene in order to understand its role in the development of obesity and diabetes.