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Göteborgs universitets publikationer

TSH receptor signaling via cyclic AMP inhibits cell surface degradation and internalization of E-cadherin in pig thyroid epithelium.

Författare och institution:
Fredrik Larsson (Institutionen för anatomi och cellbiologi); Henrik Fagman (Institutionen för anatomi och cellbiologi); Mikael Nilsson (Institutionen för anatomi och cellbiologi)
Publicerad i:
Cellular and molecular life sciences : CMLS, 61 ( 14 ) s. 1834-42
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Incorporation of E-cadherin into the adherens junction is a highly regulated process required to establish firm cell-cell adhesion in most epithelia. Less is known about the mechanisms that govern the clearance of E-cadherin from the cell surface in both normal and pathological states. In this study, we found that the steady-state removal of E-cadherin in primary cultured pig thyroid cell monolayers is slow and involves intracellular degradation. Experimental abrogation of adhesion by a Ca2+ switch induces rapid cell surface proteolysis of E-cadherin. At the same time, endocytosed intact E-cadherin and newly synthesized E-cadherin accumulate in intracellular compartments that largely escape further degradation. Acute stimulation with thyroid-stimulating hormone (TSH) or forskolin prevents all signs of accelerated E-cadherin turnover. The findings indicate that TSH receptor signaling via cyclic AMP stabilizes the assembly and retention of E-cadherin at the cell surface. This suggests a new mechanism by which TSH supports maintenance of thyroid follicular integrity.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Animals, Cadherins, genetics, metabolism, Calcium, metabolism, Cyclic AMP, metabolism, Epithelium, metabolism, Forskolin, metabolism, Receptors, Thyrotropin, metabolism, Signal Transduction, physiology, Swine, Thyroid Gland, metabolism, Thyrotropin, metabolism
Postens nummer:
Posten skapad:
2007-11-01 14:03
Posten ändrad:
2011-01-20 09:59

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