Searchable abstracts of presentations at key conferences in endocrinology

ea0015oc23 | Tumours, diabetes, bone | SFEBES2008

Obesity resulting from Gsα mutations in the maternal (but not paternal) allele is a consequence of Gsα imprinting in the central nervous system

Chen Min , Dickerson Kathryn , Wang Jie , Kelleher James , Gavrilova Oksana , Zhang Qing-Hong , Xie Tao , Weinstein Lee

Gsα is a ubiquitously expressed G protein α-subunit that couples receptors to adenylyl cyclase and cAMP generation. In patients with Albright hereditary osteodystrophy (AHO), heterozygous Gsα mutations only lead to obesity when present on the maternal allele. Similarly, mice with heterozygous germline Gsα mutations on the maternal allele develop severe obesity and insulin resistance with reduced energy expenditure relative t...

ea0049oc4.2 | Thyroid Disease 1 | ECE2017

Inducible thyrocyte-specific Gs alpha-deficient mice as a novel model for hypothyroidism

Patyra Konrad , Jaeschke Holger , Undeutsch Henriette , Lof Christoffer , Ruohonen Suvi , Jannari Meeri , Chen Min , Weinstein Lee S. , Paschke Ralf , Toppari Jorma , Kero Jukka

The thyroid gland produces thyroid hormones, which are essential regulators of growth, development and metabolism of the body and is mainly regulated by the thyroid stimulating hormone (TSH)/TSH receptor (TSHR) interplay. The TSHR couples to all four G protein families in vitro but only for the Gs and Gq signaling cascade a role has been identified in vivo. To gain further insights into the complex signaling networks mediated by G proteins in the thyroid, we generated...