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1 ells stably expressing the G protein-coupled TRH receptor.
5 bited a 650-fold lower affinity than TRH for TRH receptor and was 430-fold less potent than TRH in st
6 ituitary lactotrophs, which normally express TRH receptors, and in AtT20 pituitary corticotrophs, TRH
8 otostomian animals remains unknown, although TRH receptors are conserved in proto- and deuterostomian
11 rm of the rat thyrotropin-releasing hormone (TRH) receptor (clone E2) were further transfected with a
12 In transiently transfected COS7 cells, the TRH receptor colocalized with endoplasmic reticulum and
15 injected with thyrotropin-releasing hormone (TRH) receptor cRNA 48 h postinjection, larger Galpha16 a
16 ate that the subcellular localization of the TRH receptor depends on the cell context in which it is
17 a phosphorylation-defective receptor, the 6Q-TRH receptor did not recruit arrestin, undergo the typic
18 ncreased phosphorylation and dimerization of TRH receptors expressed in GHFT pre-lactotroph cells.
21 Furthermore, two phosphorylation-defective TRH receptors functionally complemented one another and
22 ues that form the putative binding pocket of TRH receptors further verified the binding modality of t
23 tudies of the thyrotropin-releasing hormone (TRH) receptor identified several residues in its binding
25 ptors, and in AtT20 pituitary corticotrophs, TRH receptor immunoreactivity was primarily confined to
26 for receptor dephosphorylation, we expressed TRH receptors in fibroblasts from mice lacking beta-arre
27 sults suggest that activation of presynaptic TRH receptors initiates an intracellular signalling casc
30 otein-coupled thyrotropin-releasing hormone (TRH) receptor is phosphorylated and binds to beta-arrest
32 ested whether thyrotropin-releasing hormone (TRH) receptors lacking phosphosites in the C-terminal ta
33 suggesting that cell-specific differences in TRH receptor localization were not simply the result of
34 the agonist-occupied long isoform of the rat TRH receptor may be able to partially differentiate betw
36 In HEK 293 cells expressing the transfected TRH receptor, protein synthesis inhibitors caused transl
38 results prove that calcium signaling by the TRH receptor requires coupling to a G protein in the Gq
40 ow that mouse thyrotropin-releasing hormone (TRH) receptors, subtypes 2 and 1(TRH-R2 and TRH-R1), can
43 d to be important in its binding affinity to TRH receptors; the most potent stereoisomer was noted to
45 sidues of the thyrotropin-releasing hormone (TRH) receptor (TRH-R) that are predicted by computer mod
46 loops of the thyrotropin-releasing hormone (TRH) receptor (TRHR) was constructed, and molecular dyna
47 TRH) within the transmembrane helices of the TRH receptor type 1 (TRH-R1) has been identified based o
48 and TMH6) of thyrotropin-releasing hormone (TRH) receptor type I (TRH-R1) during activation were ana
53 horylation of thyrotropin-releasing hormone (TRH) receptors was characterized using HEK293 and pituit
56 xpressing the thyrotropin-releasing hormone (TRH) receptor were transfected with cameleon Ca(2+) indi
57 ately 48 h after injection, co-expression of TRH receptor with Galpha16 results in enhanced responses
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