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Merck
  • Thyrotropin-releasing hormone receptor activation does not elevate intracellular cyclic adenosine 3',5'-monophosphate in cells expressing high levels of receptors.

Thyrotropin-releasing hormone receptor activation does not elevate intracellular cyclic adenosine 3',5'-monophosphate in cells expressing high levels of receptors.

The Journal of clinical endocrinology and metabolism (1994-08-01)
M Heinflink, D R Nussenzveig, A M Friedman, M C Gershengorn
摘要

Activation of TRH receptors (TRH-R) stimulates a signal transduction pathway that leads to the formation of two second messenger molecules, inositol 1,4,5-trisphosphate and 1,2-diacylglycerol. It has been suggested that TRH may also cause an elevation of another second messenger, cAMP. As adenovirus-mediated gene transfer allows expression of TRH-R to high levels in a number of cell types, we tested again whether TRH-R activation might elevate intracellular cAMP in these more sensitive cell systems. In five cell lines, including three human lines, infection with a replication defective adenovirus that encodes the mouse TRH-R complementary DNA (AdCMVmTRHR) induced the expression of 0.2-2 million TRH-R/cell. AdCMVmTRHR-infected cells were activated by a maximally effective dose of TRH, and the levels of inositol phosphates and cAMP were measured. TRH stimulated the production of inositol phosphates from 5- to 9-fold in all cell types, but did not elevate cAMP in any cell type. These data confirm that TRH-R activation does not lead to an elevation of intracellular cAMP.

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Sigma-Aldrich
促甲状腺素释放激素, ≥98% (HPLC), powder