ライフサイエンスコーパス: TRH

1 TRH and six TRH-like peptide levels in STR fell by 0.5h

2 TRH caused extensive receptor endocytosis in the presenc

3 TRH excited LH GABA neurons, and this was also reduced b

4 TRH had no effect on baseline glutamate/aspartate releas

5 TRH has anti-epileptic effects and regulates arousal, sl

6 TRH has been found to be efficacious in treating certain

7 TRH increased spontaneous IPSC frequency without affecti

8 TRH increased the action potential firing frequency reco

9 TRH inhibited seizure activity induced by Mg2+ deprivati

10 TRH inhibition of MCH neurons was attenuated by Na(+)-Ca

11 TRH-induced excitation persisted under conditions of syn

12 TRH-induced inward current had a reversal potential clos

13 TRH-like peptide levels, in general, were highly correla

14 membrane helices of the TRH receptor type 1 (TRH-R1) has been identified based on experimental eviden

15 ng hormone (TRH) receptors, subtypes 2 and 1(TRH-R2 and TRH-R1), can signal persistently in HEK-EM293

16 yrotropin-releasing hormone receptor type 2 (TRH-R2), not TRH-R1, has been proposed to mediate the CN

17 When D71A- and 4Ala-TRH receptors were expressed alone, neither underwent TR

18 a phosphorylation-defective receptor, the 6Q-TRH receptor did not recruit arrestin, undergo the typic

19 The 6Q-TRH receptor was not phosphorylated effectively in cells

20 Here we identify a TRH-like neuropeptide precursor in Caenorhabditis elegan

21 Dimerization of a TRH receptor-FK506-binding protein (FKBP) fusion protein

22 n afforded a novel lead for centrally acting TRH analogues.

23 ursor (proTRH) into five biologically active TRH peptides and several non-TRH peptides where two of t

24 ze receptor but still promoted high affinity TRH binding, acid/salt resistance, and desensitization.

25 a-arrestins and almost complete 20 min after TRH withdrawal.

26 Although TRH did not significantly alter either the frequency or

27 otostomian animals remains unknown, although TRH receptors are conserved in proto- and deuterostomian

28 easing hormone (TRH, pGlu-His-Pro-NH(2)) and TRH-like peptides (pGlu-X-Pro-NH(2), where "X" can be an

29 e leptin alone did not evoke any change, and TRH alone caused only approximately 1 degrees C increase

30 creasing the gene expression of both CRH and TRH in hypophysiotropic neurons, and CART-containing axo

31 relationships with hypophysiotropic CRH and TRH neurons, we propose that CART may signal to the nucl

32 the locus in the hindbrain where leptin and TRH act synergistically to increase thermogenesis will b

33 Specifically, exposure to both leptin and TRH elicited a 3.5 degrees C increase in brown adipose t

34 transduction interaction between leptin and TRH occurs within neurons of the solitary nucleus [NST],

35 e a basis for the synergy between leptin and TRH to increase thermogenesis.

36 We tested the hypothesis that leptin and TRH, acting in the hindbrain, co-regulate thermogenesis.

37 Co-application of leptin (5 mug) and TRH (0.1 microg) to the dorsal medulla produces an incre

38 aphe nuclei, (2) serotonin, substance P, and TRH activate RTN chemoreceptors, and (3) excitatory effe

39 ere activated by serotonin, substance P, and TRH.

40 opin-releasing hormone receptors (TRH-R1 and TRH-R2).

41 (TRH) receptors, subtypes 2 and 1(TRH-R2 and TRH-R1), can signal persistently in HEK-EM293 cells unde

42 ollicular heat production, whereas T3/T4 and TRH stimulated ATP production in cultured HF keratinocyt

43 Although TDH and TRH homologs can be encoded on extrachromosomal elements

44 share amino acid similarities to the TDH and TRH proteins of Vibrio parahaemolyticus, where they have

45 ttributed to the V. parahaemolyticus TDH and TRH proteins.

46 Significant changes in TRH and TRH-like peptide levels for other brain regions were: CB

47 The rapid modulation of TRH and TRH-like peptide release combined with their similarity

48 Levels of TRH and TRH-like peptides were measured at 3.0 h, 10.5 h, 13.5 h

49 ies in raphe-derived neuromodulators such as TRH.

50 rmone (TRH) are more efficacious agonists at TRH receptors R1 and R2 than TRH itself.

51 f leptin to the food-deprived animal, before TRH injection, yields a substantial increase in BAT; whi

52 hemistry, we found close appositions between TRH-immunoreactive nerve terminals and orexin-A-immunore

53 hemistry revealed little interaction between TRH axons and MCH neurons, but showed TRH axons terminat

54 fferent fibers in the hindbrain possess both TRH type 1 receptor and long-form leptin receptor [TRHR1

55 M293 cells under appropriate conditions, but TRH-R2 exhibits higher persistent signaling activity.

56 are mediated primarily if not exclusively by TRH-R1 in mice.

57 that the CNS effects of TAL are mediated by TRH-R2, these effects are mediated primarily if not excl

58 knockdown decreased persistent signaling by TRH-R2 by 82%, and overexpression of Galpha(q/11) induce

59 of inositolmonophosphate (IP1) signaling by TRH-Rs.

60 c axis may play a regulatory role in cardiac TRH production.

61 receptor TRHR-1, promote growth in Celegans TRH-like peptides from pharyngeal motor neurons are requ

62 t with a more minor role for the V. cholerae TRH in T3SS-positive strains compared to the functions a

63 nopositive cells, was restored after chronic TRH treatment.

64 e of the four residues that directly contact TRH and other residues that restrain TRH-R1 in an inacti

65 ound that two residues that directly contact TRH, Asn-110 in transmembrane helix 3 (3.37) and Arg-306

66 l administration of nanoparticles containing TRH (TRH-NPs) could inhibit kindling development.

67 of d,l polylactide nanoparticles containing TRH was assessed against glutamate toxicity in cultured

68 in uptake/retention of pyridinium-containing TRH analogues (measured by in vivo microdialysis samplin

69 In contrast, TRH significantly reduced the frequency, but not amplitu

70 Furthermore, two phosphorylation-defective TRH receptors functionally complemented one another and

71 xis, we have generated mice that lack either TRH, the beta isoforms of TH receptors (TRbeta KO), or b

72 No binding to the endocrine TRH receptor was measured for the TRH analogues reported

73 ies suggest that exogenous and/or endogenous TRH may function, in part, to modulate excess glutamate

74 As expected, TRH (0.1 microg), alone, produces a small increase (+0.7

75 for receptor dephosphorylation, we expressed TRH receptors in fibroblasts from mice lacking beta-arre

76 ced persistent signaling in cells expressing TRH-R1.

77 In histamine-ir fibers TRH and galanin immunoreactivities were also detected in

78 Finally, TRH attenuated the excitation of MCH neurons by hypocret

79 athway of neuroendocrine cells yielding five TRH peptides and seven to nine other unique peptides.

80 Mutants deficient for TRH signaling have no defects in pharyngeal pumping or i

81 then exogenous leptin was not necessary for TRH to yield a large increase in BAT temperature.

82 zing TRH-R1 in an inactive state but not for TRH binding, was critical for midazolam binding.

83 stance and the affinity of 4Ala receptor for TRH.

84 These data suggest a novel role for TRH in the brain as an intrinsic regulator of thalamocor

85 her suggest an important functional role for TRH signalling in the mammalian CO2 chemoreflex.

86 was noted to have a 13-fold selectivity for TRH-R1 over TRH-R2.

87 ot caused by slower dissociation of TRH from TRH-R2 (t(1/2)=77 +/- 8.1 min) compared with TRH-R1 (t(1

88 ibers immunoreactive (ir) for galanin, GABA, TRH, or methionine-enkephalin (mENK) were dense in the v

89 Prolonged exposure to 10 microM 3Me-H TRH was not toxic to the cells, whereas neurons exposed

90 analog of TRH, 3-Methyl-Histidine TRH (3Me-H TRH), given concurrently with Glu would protect such neu

91 treated with: control media, 10 microM 3Me-H TRH, 500 microM Glu or 500 microM Glu with either 10, 1,

92 Notably, 10, 1 and 0.1 microM 3Me-H TRH, when co-treated with 500 microM Glu, protected feta

93 ither 10, 1, 0.1, 0.01 or 0.001 microM 3Me-H TRH.

94 molysin (TDH) and the TDH-related hemolysin (TRH), which share amino acid similarities to the TDH and

95 ot reversed by long incubation times or high TRH concentrations.

96 o]propyl)pyridinium (1a) showed the highest (TRH-equivalent) potency and longest, dose-dependent dura

97 is that an analog of TRH, 3-Methyl-Histidine TRH (3Me-H TRH), given concurrently with Glu would prote

98 trally acting thyrotropin-releasing hormone (TRH) analogues were designed by replacing the central hi

99 ophysiotropic thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) neurons t

100 ns expressing thyrotropin-releasing hormone (TRH) and pituitary adenylate cyclase-activating polypept

101 s inputs from thyrotropin-releasing hormone (TRH) and substance P-expressing neurons.

102 rmones, i.e., thyrotropin-releasing hormone (TRH) and thyrotropin (TSH), are expressed in human hair

103 al analogs of thyrotropin-releasing hormone (TRH) are more efficacious agonists at TRH receptors R1 a

104 creased while thyrotropin-releasing hormone (TRH) expression is elevated.

105 Thyrotropin-releasing hormone (TRH) has previously been shown to promote wakefulness an

106 en leptin and thyrotropin releasing hormone (TRH) in the hindbrain to generate thermogenic responses.

107 reduction of Thyrotropin Releasing Hormone (TRH) in the hypothalamus of hypothyroid rats.

108 production of thyrotropin-releasing hormone (TRH) in the mediobasal hypothalamus (MBH) and thyroid-st

109 Thyrotropin-releasing hormone (TRH) increases activity and decreases food intake, body

110 enesis of rat thyrotropin releasing hormone (TRH) involves the processing of its precursor (proTRH) i

111 n vertebrates thyrotropin-releasing hormone (TRH) is a highly conserved neuropeptide that exerts the

112 Thyrotropin-releasing hormone (TRH) is a tripeptide that is widely distributed in the b

113 neuropeptide thyrotropin-releasing hormone (TRH) is recognized to play an important role in controll

114 Thyrotropin-releasing hormone (TRH) is reported to have anticonvulsant effects in anima

115 neuropeptide thyrotropin-releasing hormone (TRH) on the spontaneously active ferret geniculate slice

116 in (5-HT) and thyrotropin-releasing hormone (TRH) play important roles in fundamental, homeostatic co

117 xpression for thyrotropin-releasing hormone (TRH) precursor was increased in rats with heart failure

118 coupled thyrotropin (TSH)-releasing hormone (TRH) receptor forms homodimers.

119 otein-coupled thyrotropin-releasing hormone (TRH) receptor is phosphorylated and binds to beta-arrest

120 and TMH6) of thyrotropin-releasing hormone (TRH) receptor type I (TRH-R1) during activation were ana

121 The thyrotropin-releasing hormone (TRH) receptor undergoes rapid and extensive agonist-depe

122 ested whether thyrotropin-releasing hormone (TRH) receptors lacking phosphosites in the C-terminal ta

123 ow that mouse thyrotropin-releasing hormone (TRH) receptors, subtypes 2 and 1(TRH-R2 and TRH-R1), can

124 Hypothalamic thyrotropin-releasing hormone (TRH) stimulates thyroid-stimulating hormone (TSH) secret

125 cin (OXT) and thyrotropin releasing hormone (TRH) was reduced by about 50%.

126 d (GABA), and thyrotropin-releasing hormone (TRH) were colocalized with histamine in some but not all

127 ng pocket for thyrotropin-releasing hormone (TRH) within the transmembrane helices of the TRH recepto

128 modulated by thyrotropin-releasing hormone (TRH), an endogenous stimulant of wakefulness and locomot

129 ormone (MCH), thyrotropin-releasing hormone (TRH), gonadotropin-releasing hormone (GnRH), and kisspep

130 population of thyrotropin-releasing hormone (TRH)-expressing neurons in the PVN (5.93% +/- 1.20% SEM)

131 stimulating hormone (TSH)-releasing hormone (TRH)-positive neurons in the paraventricular nucleus are

132 tin 2 reduced thyrotropin-releasing hormone (TRH)-stimulated inositol phosphate production and accele

133 nesis such as thyrotropin-releasing hormone (TRH).

134 es, including thyrotropin-releasing hormone (TRH).

135 reported that thyrotropin-releasing hormone (TRH, pGlu-His-Pro-NH(2)) and TRH-like peptides (pGlu-X-P

136 Thyrotropin-releasing hormone (TRH; protirelin), a brain-derived tripeptide, has shown

137 en leptin and thyrotropin-releasing hormone [TRH] to activate hindbrain generated thermogenic respons

138 en leptin and thyrotropin-releasing hormone [TRH] to activate hindbrain-generated thermogenic respons

139 milar in vitro expression patterns, however, TRH is not required for AM-19226 to colonize the infant

140 the CART-IR innervation of hypophysiotropic TRH neurons.

141 pin-releasing hormone (TRH) receptor type I (TRH-R1) during activation were analyzed by cysteine-scan

142 Significant changes in TRH and TRH-like peptide levels for other brain regions

143 eral, were highly correlated with changes in TRH concentration, within and between brain regions, and

144 Highly significant changes in TRH-like peptide levels were observed in the striatum, p

145 ith the protease PC1, an important enzyme in TRH biosynthesis.

146 anently kindled was significantly greater in TRH-NP-treated subjects.

147 tricted to the heart, because no increase in TRH mRNA abundance was observed in the hypothalamus, kid

148 hemical dimerizer caused a large increase in TRH-dependent phosphorylation within 1 min, whereas a mo

149 endent of the nature of the modifications in TRH structure.

150 reduced indicating a less severe seizure in TRH-NP-treated subjects.

151 Anti-HA IgG strongly increased TRH-induced phosphorylation, whereas monomeric Fab fragm

152 Regulated receptor dimerization increases TRH-induced receptor endocytosis.

153 2ko mice and 0% for R1/R2ko mice, indicating TRH-R1 is the predominant receptor expressed in the brai

154 on with high potassium KRB (50 mM [K(+)] +/- TRH).

155 The present study shows that the leptin-TRH synergy in controlling brown adipose [BAT] thermogen

156 The leptin-TRH synergy was uncoupled by pretreatment with the phosp

157 When injected into the LHA, TRH increased locomotor activity in wild-type mice but n

158 rol), or KRB containing 0.1, 1, or 10 microM TRH respectively, prior to and during 5 min depolarizati

159 ding affinity and signaling potency at mouse TRH-R2 than TRH-R1 in a model cell system.

160 l model, whereby the excitatory neuropeptide TRH depolarizes gap-junction-coupled dopamine neurons, l

161 ked within seconds and was maximal at 100 nm TRH.

162 TRH-R1 mRNA in R1ko and R1/R2ko mice and no TRH-R2 mRNA in R2ko and R1/R2ko mice.

163 There was no TRH-R1 mRNA in R1ko and R1/R2ko mice and no TRH-R2 mRNA

164 ogically active TRH peptides and several non-TRH peptides where two of them had been attributed poten

165 f CART to phosphorylate CREB in CRH, but not TRH neurons in the PVN.

166 easing hormone receptor type 2 (TRH-R2), not TRH-R1, has been proposed to mediate the CNS effects of

167 logs originated from the enhanced ability of TRH-R complexed to the low affinity agonists to directly

168 aps leptin "gates" the thermogenic action of TRH in the hindbrain by invoking this same mechanism.

169 ntribute to the arousal-enhancing actions of TRH.

170 o explain some of the hippocampal actions of TRH.

171 Acute intravenous administration of TRH to rats with ischemic cardiomyopathy caused a signif

172 ons to test the hypothesis that an analog of TRH, 3-Methyl-Histidine TRH (3Me-H TRH), given concurren

173 ical studies showed that bath application of TRH caused concentration-dependent membrane depolarizati

174 Furthermore, application of TRH prominently enhanced the afterdepolarization that fo

175 Bath application of TRH resulted in a transient cessation of both spindle wa

176 Intranasal application of TRH-NPs resulted in a significant reduction in seizure A

177 ulation of PCs in the PVN, concentrations of TRH in the PVN and ME were substantially reduced in the

178 tabilization of the inactive conformation of TRH-R1.

179 ion of dynamin slowed the desensitization of TRH responses.

180 We conclude that the efficacy differences of TRH analogs originated from the enhanced ability of TRH-

181 ing was not caused by slower dissociation of TRH from TRH-R2 (t(1/2)=77 +/- 8.1 min) compared with TR

182 stand the mechanism of this potent effect of TRH and its implication in various CNS disorders.

183 a potent and prolonged inhibitory effect of TRH on evoked glutamate/aspartate release in vitro.

184 t for an important neuroprotective effect of TRH/analogs against glutamate toxicity in primary hippoc

185 been proposed to mediate the CNS effects of TRH and its more effective analog taltirelin (TAL).

186 To begin to understand the effects of TRH on CNS control of energy balance, we first mapped ne

187 We examined the effects of TRH on GABAergic transmission in the hippocampus and fou

188 Because the effects of TRH were mediated via Galphaq/11, but were independent o

189 Expression of TRH-R1 (TRH receptor 1) is enriched in the tuberal and l

190 egans that belongs to a bilaterian family of TRH precursors.

191 ies suggested that the thermogenic impact of TRH in the hindbrain is amplified by the action of lepti

192 To elucidate the relative importance of TRH and TH in regulating the hypothalamic-pituitary-thyr

193 Ajp, as well as the potential involvement of TRH neurons within this region in metabolic disease asso

194 Levels of TRH and TRH-like peptides were measured at 3.0 h, 10.5 h

195 s induced in cells expressing high levels of TRH-R1.

196 motility response to DMV microinjections of TRH were decreased significantly.

197 The rapid modulation of TRH and TRH-like peptide release combined with their sim

198 nt binding protein (CREB), in the nucleus of TRH and CRH neurons.

199 ainstem pathways reduced the total number of TRH neurons contacted by CART from 99.4 +/- 0.9% on the

200 ues that form the putative binding pocket of TRH receptors further verified the binding modality of t

201 A 5 min pulse of TRH (10 microM) had no affect on basal glutamate/asparta

202 d implicate a potentially beneficial role of TRH/analogs in neurodegenerative diseases.

203 ors were fully phosphorylated within 15 s of TRH addition.

204 nd norepinephrine, a natural secretagogue of TRH.

205 umber of CART varicosities on the surface of TRH neurons from 6.0 +/- 0.9 to 2.3 +/- 0.4 CART-IR vari

206 hanisms by which CART mediates its effect on TRH and CRH neurons, we determined whether the exogenous

207 Although opposing TRH and TH inputs regulate the hypothalamic-pituitary-th

208 aily treatments of either blank (control) or TRH-NPs for 7 days before initiation of kindling.

209 o have a 13-fold selectivity for TRH-R1 over TRH-R2.

210 expressing the TRH precursor peptide, prepro-TRH (ppTRH) in the paraventricular nucleus of the rat hy

211 g AtT20 cells stably transfected with prepro-TRH cDNA, we found that two specific N- and C-terminal p

212 We refined our previous TRH-R1 models by embedding them into a hydrated explicit

213 Pro-TRH gene expression was induced in cardiac interstitial

214 Rat prothyrotropin-releasing hormone (pro-TRH) is endoproteolyzed within the regulated secretory p

215 Prothyrotropin-releasing hormone (pro-TRH) is initially cleaved by the prohormone convertase-1

216 ion to catecholamine and angiotensin II, pro-TRH/TRH may be another important axis that affects hemod

217 Proteolysis of pro-TRH begins in the trans-Golgi network and forms two inte

218 Transcript abundance of pro-TRH can be increased in cultured cardiac fibroblasts by

219 we show that after MI, the expression of pro-TRH is induced in the heart coordinately with the protea

220 When a mutant form of pro-TRH, which has the dibasic sites of initial processing m

221 y be necessary for downstream sorting of pro-TRH-derived peptides as it occurs before Golgi exit and

222 sorting events that result in storage of pro-TRH-derived peptides in mature secretory granules.

223 that initial processing action of PC1 on pro-TRH in the trans-Golgi network, and not a cargo-receptor

224 ely secreted form of PC1 does not target pro-TRH peptides to the constitutive secretory pathway but r

225 Furthermore, the C-terminal pro-TRH-derived peptides were more efficiently released in r

226 In summary, our data show that pro-TRH-derived peptides are differentially sorted within th

227 We now report that when pro-TRH is transiently expressed in GH4C1 cells, a neuroendo

228 or amplitude of spontaneous excitatory PSCs, TRH (100 nm) increased the frequency of spontaneous inhi

229 Expression of TRH-R1 (TRH receptor 1) is enriched in the tuberal and lateral h

230 the thyrotropin-releasing hormone receptors (TRH-R1 and TRH-R2).

231 With intracellular recordings, TRH application to the GABAergic neurons of the perigeni

232 At 30 min, endogenous beta-arrestins reduced TRH-stimulated inositol phosphate production by 48% (bet

233 hat intranasal delivery of sustained-release TRH-NPs may be neuroprotective and can be utilized to su

234 Consistent with previous reports, TRH excited hypocretin/orexin neurons.

235 contact TRH and other residues that restrain TRH-R1 in an inactive conformation were screened by muta

236 etween TRH axons and MCH neurons, but showed TRH axons terminating on or near GABA neurons.

237 ter transgenic mouse brain slices that shows TRH modulates the activity of MCH neurons.

238 TRH and six TRH-like peptide levels in STR fell by 0.5h consistent w

239 h was reported to be critical in stabilizing TRH-R1 in an inactive state but not for TRH binding, was

240 ced in BN rats, and injections of the stable TRH analogue Taltirelin (TAL) stimulated breathing dose-

241 In the presence of tetrodotoxin, TRH induced inward currents that were associated with a

242 e thalamic network, yet the role of thalamic TRH remains obscure.

243 ntains these complexes more efficiently than TRH-R1.

244 core temperature more than 300% greater than TRH alone (+3.5 degrees C).

245 ous agonists at TRH receptors R1 and R2 than TRH itself.

246 y and signaling potency at mouse TRH-R2 than TRH-R1 in a model cell system.

247 exes are established and maintained and that TRH-R2 forms and maintains these complexes more efficien

248 We conclude that TRH-like peptides may be important components of chronob

249 -clamp recording, we unexpectedly found that TRH and its agonist, montrelin, dose-dependently inhibit

250 ansmission in the hippocampus and found that TRH increased the frequency of GABAA receptor-mediated s

251 e-cell patch-clamp recordings, we found that TRH robustly increased the action potential firing rate

252 campal slices, we tested the hypothesis that TRH could inhibit evoked glutamate/aspartate release in

253 ults are consistent with the hypothesis that TRH modulates behavioral arousal, in part, through the H

254 in sleep/wake control, we hypothesized that TRH provides modulatory input to the Hcrt cells.

255 Taken together, these results indicate that TRH is specifically induced in the heart after MI and th

256 PSC frequency or amplitude, indicating that TRH also reduces the probability of glutamate release on

257 Cas9 and RNAi reverse genetics, we show that TRH-like neuropeptides, through the activation of their

258 Our findings suggest that TRH binding induces a separation of the cytoplasmic ends

259 Together, our data suggest that TRH inhibits MCH neurons by increasing synaptic inhibiti

260 uced membrane depolarization suggesting that TRH increases the excitability of interneurons to facili

261 to the K+ reversal potential suggesting that TRH inhibits resting K+ channels.

262 assical K+ channel blockers, suggesting that TRH inhibits the two-pore domain K+ channels.

263 hat generated by picrotoxin, suggesting that TRH-mediated increase in GABA release contributes to its

264 Our study suggests that TRH is an evolutionarily ancient neuropeptide, having it

265 The TRH inhibition of MCH neurons was eliminated by bicucull

266 The TRH receptor signals through the PLC complex.

267 The TRH transduction mechanism utilizes phospholipase C [PLC

268 In thalamocortical cells, the TRH-induced depolarization was of sufficient amplitude t

269 ance, we first mapped neurons expressing the TRH precursor peptide, prepro-TRH (ppTRH) in the paraven

270 endocrine TRH receptor was measured for the TRH analogues reported here; therefore, our design affor

271 Like many GPCRs, the TRH receptor is predicted to form an amphipathic helix,

272 etween these two CNS-mediated actions of the TRH analogues was obtained in subject animals.

273 the brainstem to the CART innervation of the TRH neurons in the PVN, the major ascending brainstem ax

274 TRH) within the transmembrane helices of the TRH receptor type 1 (TRH-R1) has been identified based o

275 unoccupied TRH-R1 to generate a model of the TRH-R1/midazolam complex.

276 iquitination are an inherent property of the TRH/TSH feedback mechanism and indicate that only consta

277 e helical pocket that partially overlaps the TRH binding pocket.

278 crease in BAT temperature by sensitizing the TRH-PLC-IP3-calcium release mechanism.

279 Our results show that the TRH receptor can rapidly cycle between a phosphorylated

280 These results suggest that the TRH receptor is phosphorylated preferentially when it is

281 substitution experiments suggested that the TRH-induced inward current was mediated in part by Ca(2+

282 ibition of MCH neurons may contribute to the TRH-mediated reduction in food intake and sleep.

283 sal glutamate/aspartate release, whereas the TRH pre-pulsed slices failed to release glutamate/aspart

284 glutamate/aspartate release, while all three TRH doses significantly (P < 0.05) inhibited peak 50 mM

285 Thus, TRH is absolutely required for both TSH and TH synthesis

286 d to be important in its binding affinity to TRH receptors; the most potent stereoisomer was noted to

287 the complex suggest that midazolam binds to TRH-R1 within a transmembrane helical pocket that partia

288 tein-coupled receptor kinases in response to TRH.

289 nted receptor phosphorylation in response to TRH.

290 ntly augments NST neurons' responsiveness to TRH.

291 sulfide bond formation that was sensitive to TRH occupancy.

292 inistration of nanoparticles containing TRH (TRH-NPs) could inhibit kindling development.

293 tors were expressed alone, neither underwent TRH-dependent phosphorylation.

294 We used our previous model of the unoccupied TRH-R1 to generate a model of the TRH-R1/midazolam compl

295 We used TRH-R1 knockout (R1ko), R2ko and R1/R2ko mice to determi

296 in the brain including the hippocampus where TRH receptors are also expressed.

297 ed in organ-cultured human scalp HFs whether TRH (30 nM), TSH (10 mU ml(-1)), thyroxine (T4) (100 nM)

298 but there was no ER-beta colocalization with TRH.

299 TRH-R2 (t(1/2)=77 +/- 8.1 min) compared with TRH-R1 (t(1/2)=82 +/- 12 min) and was independent of int

300 tronger in tissue from animals injected with TRH.