Searchable abstracts of presentations at key conferences in endocrinology

ea0084op-11-56 | Oral Session 11: Young Investigators / Basic | ETA2022

Focusing on the role of the enigmatic TRα2 isoform in modulation of thyroid hormone action

Harting Nina , Eckhold Juliane , Sebastian Hones G. , Mittag Jens , J. Kaiser Frank

Thyroid hormones (TH) are important regulators of human metabolism and development, which modulate expression of target genes via nuclear thyroid hormone receptors (TRs). Different isoforms of these classical TRs including TRβ isoforms TRβ1 and TRβ2 as well as TRα1 were shown to be functional TH-responsive transcription factors and have been extensively studied. In contrast, the cellular function of TRα2, an alternative splice variant of TRα1, is ...

ea0092op-07-04 | Oral Session 7: Thyroid hormone receptors | ETA2023

Characterizing cell-type specific activities of tralpha2 in the modulation of thyroid hormone action

Harting Nina , Sebastian Hones G. , Eckhold Juliane , Kilpert Fabian , Gemoll Timo , Mittag Jens , Kaiser Frank J.

Objectives: The canonical function of thyroid hormone receptors (TRs) as mediators of thyroid hormone action on target gene expression is well known. However, the physiological function of the thyroid hormone receptor α splice variant TRα2, that does not bind thyroid hormones, remains elusive. Initial studies addressing the function of TRα2 indicated that it might act as a TRα1 antagonist, but the mechanisms underlying the dominant-negative activity of TR&#...

ea0092op-01-05 | Oral Session 1: Highlights in Thyroidology: in Memory of Jacques Dumont | ETA2023

RNA guanine-quadruplexes as novel regulators of translation and alternative splicing of tr alpha isoforms

Jayethevan Girththana , Harting Nina , Beuck Christine , Fuhrer-Sakel Dagmar , Christian Moller Lars , Kaiser Frank J. , Sebastian Hones G.

Objectives: The thyroid hormone receptor α (TRα) is crucial for organ development, regulation of growth, heart rate and energy homeostasis. In humans, THRA encodes for the two major TRα isoforms, TRα1 and TRα2. TRα2 is generated by alternative splicing and is unable to bind T3 and thus antagonizes TRα1 signaling. Therefore, the physiological effects of TRα require strictly controlled spatiotemporal expression of TRα isoform...