Ralph Telgmann

TL;DR: It is demonstrated in a variety of cell types, including lymphocytes and endometrial stroma, that Pit-1 is not involved in the regulation of dPRL promoter/reporter gene constructs carrying 3 kb 5'-flanking DNA, and experiments show that activated PR does not confer direct transcriptional control on the d PRL promoter.

TL;DR: It is demonstrated that decidual PRL gene transcription is driven by an alternative upstream promoter (dPRL), approximately 6 kb upstream of the pituitary transcription start site, and this action was probably indirect as its kinetics differed from classic CRE-mediated responses.

TL;DR: It is shown that relaxin not only acutely but permanently elevates cellular cAMP levels and leads to induction of PRL secretion after 6 days and in decidualized ES cells, exposed to relaxin for more than 6 days, a significant reduction of RIα protein level occurs, whereas levels of all other forms remain unchanged.

TL;DR: Using validated monotypic antibodies recognizing different epitopes of the L GR7 receptor, and from different immunized animals, and in different primate species, a consistent pattern of LGR7 expression was observed in the stromal cells of the endometrium and breast, consistent also with the known physiology of the relaxin hormone.

TL;DR: It appears paradoxical that in vivo, in response to a permanent cAMP stimulus, ICER is up-regulated without displaying negative autoregulation of its own gene or suppression of the dPRL promoter.