08 Jan 2013
Fleming et al. are the first to demonstrate a direct effect of the prolactin binding protein, delta 7/11, on prolactin-stimulated cell behaviours including inhibition of prolactin-induced cell proliferation as well as alteration of prolactin-induced rescue of cell cycle arrest/early senescence events in breast epithelial cells. Biochemical analyses demonstrated that delta 7/11 was heavily glycosylated, and that glycosylation regulated the cellular localization and secretion of delta 7/11. Further, low levels of delta 7/11 were detected in serum samples of healthy volunteers, but were undetectable in human milk samples. Collectively, these data demonstrate that delta 7/11 is a novel regulatory mechanism of prolactin bioavailability and signalling. Fleming et al. (2013) Journal of Molecular Endocrinology 50, 79-90.
Read the full article at DOI: 10.1530/JME-12-0201.
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