Searchable abstracts of presentations at key conferences in endocrinology
Previous issue | Volume 41 | ECE2016 | Next issue

18th European Congress of Endocrinology

Oral Communications

Receptors & Signalling

ea0041oc2.1 | Receptors & Signalling | ECE2016

3-T1AM signaling in the rat thyrocyte cell line PCCL3

Schanze Nancy , Khajavi Noushafarin , Mergler Stefan , Biebermann Heike , Kohrle Josef

The endogenous decarboxylated thyroid hormone (TH) metabolite 3-Iodothyronamine (3-T1AM) exerts partially TH antagonistic effects in rodents and was shown to suppress the hypothalamic pituitary thyroid axis in rats after single dose application. Therefore, it might play a role in maintaining TH homoeostasis. Among the molecular targets of 3-T1AM are G protein-coupled receptors like the trace amine associated receptor 1 (TAAR1) and adrenergic receptors. Furthermore, 3-T1AM was ...

ea0041oc2.2 | Receptors & Signalling | ECE2016

Expression levels of thyroglobulin processing proteases are reduced upon trace amine-associated receptor 1 deficiency in mice

Szumska Joanna , Batool Zaina , Qatato Maria , Gavilanes Emily Melisa Ullrich , Skripnik Vladislav , Shillova Nita , Grandy David K. , Brix Klaudia

The function of the thyroid gland is to maintain thyroid hormone (TH) levels in the blood circulation. Thyroid epithelial cells liberate TH from the precursor molecule thyroglobulin (Tg) by the combined proteolytic action of the cathepsin B, K, L, and S. Cathepsin L-deficiency in mice results in impaired processing of Tg and remnants of dead cells in the follicle lumen. Recently, we have shown that Trace amine-associated receptor 1 (Taar1) is localized on the primary cilia of ...

ea0041oc2.3 | Receptors & Signalling | ECE2016

PRKACA mutations in adrenal Cushing impair association with the PKA regulatory subunit

Bathon Kerstin , Weigand Isabel , Ronchi Cristina L. , Di Dalmazi Guido , Beuschlein Felix , Sbiera Silviu , Fassnacht Martin , Calebiro Davide

In a previous study we found mutations in the main catalytic subunit of protein kinase A (PKA Cα) to be responsible for cortisol-secreting adrenocortical adenomas (ACAs). These mutations interfere with the formation of a stable holoenzyme, thus causing constitutive PKA activation. More recently, we identified additional mutations affecting PKA Cα in ACAs associated with overt Cushing syndrome: Ser213Arg_Leu212_Lys214insIle-Ile-Leu-Arg, Cys200_Gly201insVal, Trp197Arg,...

ea0041oc2.4 | Receptors & Signalling | ECE2016

Link between cell cycle, steroidogenesis and PKA in adrenocortical tumors cells

Rizk-Rabin Marthe , Ragazzon Bruno , Bertherat Jerome

The cyclic AMP/PKA signalling cascade and PKA subunits are involved in the pathogenesis of a subset of cortisol-secreting adrenocortical tumors (ACT). In addition, steroid excess causes morbidity of all types of ACT.The PKA regulatory subunits PRKARIA, PRKARIIb control proliferation/apoptosis in the H295R adrenocortical cell line. Their inactivation enhances the accumulation of cells in the G2 phase, increases steroidogenesis and activa...

ea0041oc2.5 | Receptors & Signalling | ECE2016

11β-HSD1 is a regulator of brown adipose tissue function and mediates stress adaptation in glucocorticoid excess

Doig Craig , Morgan Stuart , Philp Andrew , Tomlinson Jeremy , Stewart Paul , Lavery Gareth

Glucocorticoids (GC) are critical to stress adaptation but in excess (Cushing’s syndrome) drive metabolic dysfunction. 11β-hydroxysteroid dehydrogenase type 1(11β-HSD1) amplifies intracellular GC signaling with 11β-HSD1KO mice protected from the side-effects of GC excess. Brown adipose tissue (BAT) function is impaired by GC’s, which repress UCP1 and beta-adrenergic stimulated thermogenesis. Identifying mechanisms regulating BAT function is important a...