ライフサイエンスコーパス: TSH

1 TSH at baseline was not significantly associated with in

2 TSH concentrations decreased during hypoglycemia (P<0.01

3 TSH level was positively associated with QRS interval in

4 TSH levels significantly affected the maximal keratometr

5 TSH levels were positively associated with Base of suppo

6 TSH levels were similarly elevated in PV mice regardless

7 TSH stimulated translocation of beta-arrestin-1 and -2 t

8 er MBq of (131)I administered, between the 2 TSH stimulation methods.

9 AM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-media

10 Further, we identified a TSH-like factor that may confer osteoprotection.

11 -70, a TSH-receptor antagonist, suggesting a TSH receptor-mediated action.

12 We predict that a TSH-induced, fast-forward short loop in bone marrow perm

13 only one newborn had a transiently abnormal TSH level at birth, which normalized at day 6 of life.

14 n California's Salinas Valley and abstracted TSH levels from their children's medical records.

15 ormation, and hyperresorption that accompany TSH deficiency.

16 However, even in the absence of added TSH, (125)I-TSH dissociated much more rapidly from the T

17 oinositide signaling, 60 min or longer after TSH removal.

18 Moreover, Alexa546-TSH-activated TSHR internalization was not accompanied b

19 01), T4t (p < .001), T3t/T4t (P = .001), and TSH (p = .001) plasma levels.

20 which includes early involvement of ACTH and TSH and a relatively rapid development of hypopituitaris

21 TAS2R agonists also inhibited basal and TSH-dependent iodide efflux.

22 was surprising because both the TSHR ECD and TSH holoreceptor contain the entire TSH-binding site, an

23 the manufacturers' methods for both FT4 and TSH has shown that the variability among immunoassays ca

24 As for FT4 and TSH levels, no significant distribution trend of myocard

25 es of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 production (EC(50)=50 mU/ml) were ind

26 rum total T4 was measured by immunoassay and TSH was measured by chemiluminescent assay.

27 hormone (TSH)-dependent Ca(2+) increases and TSH-dependent iodide efflux in thyrocytes.

28 could be contained via p53-dependent OIS and TSH is a major disruptor of this balance.

29 hormone (TSH) in women during pregnancy, and TSH in neonates.

30 sent with combined deficiency of GH, PRL and TSH.

31 Notably, as measured by calorimetry, T3 and TSH increased follicular heat production, whereas T3/T4

32 T4 and TSH concentrations were unchanged.

33 We categorized T4 and TSH into 7 groups with cut-offs at the 5(th), 20(th), 40

34 /DeltaID) Src-1(-/-) mice have normal TH and TSH levels and are triiodothryonine (T(3)) sensitive at

35 eam of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TSH/TSHR-me

36 ccording to the currently most reliable anti-TSH receptor antibody-ELISA used to diagnose Graves dise

37 Euthyroidism was defined as TSH of 0.45 to 4.49 mIU/L, subclinical hypothyroidism as

38 .9 mIU/L, and subclinical hyperthyroidism as TSH <0.45 mIU/L, the last two with normal free thyroxine

39 .49 mIU/L, and subclinical hypothyroidism as TSH 4.5 to 19.9 mIU/L with free thyroxine (fT4) levels w

40 to 4.49 mIU/L, subclinical hypothyroidism as TSH of 4.5 to 19.9 mIU/L, and subclinical hyperthyroidis

41 ions were not modified by infant sex, age at TSH measurement, maternal serum polychlorinated biphenyl

42 Cross-sectionally, AT TSH-beta (TSHB) mRNA was evaluated in 4 independent coho

43 in men, while a U-shape association between TSH and QRS was observed in women.

44 ans pointing to a strong association between TSH levels and thyroid cancer incidence.

45 imed to investigate the relationship between TSH mRNA and cholesterol metabolism in human adipose tis

46 -effectiveness acceptability curves for both TSH stimulation methods and (131)I activities.

47 n primary cultures of human thyrocytes, both TSH and the agonists increase mRNA levels for thyroglobu

48 TSHR activation by TSH phosphorylates protein kinases AKT1, p38alpha, and E

49 on of B-Raf also inhibited ERK activation by TSH, forskolin, and 6MB-cAMP, but not that stimulated by

50 ant-negative Ras inhibited ERK activation by TSH, forskolin, and N(6)-monobutyryl (6MB)-cAMP, a selec

51 signal-regulated kinase (ERK) activation by TSH.

52 l, peripheral target organ for regulation by TSH.

53 tested whether persistent cAMP signaling by TSH receptor (TSHR) is dependent on internalization.

54 ssion analyses comparing fold stimulation by TSH of IP1 vs. cAMP production were 0.044 +/- 0.0047, 0.

55 In U2OS-TSHR cells, TSH up-regulated pAKT1 (7.1+/-0.5-fold), p38alpha (2.9+/

56 Negatively charged TSH-hydrazone ions furthermore show a simple and predict

57 Although circadian TSH secretion has been well documented, the mechanism of

58 enes during chronic elevation of circulating TSH.

59 ced total T4 in pregnant women and decreased TSH in male neonates.

60 dies now indicate that immune system-derived TSH, in particular, a splice variant of TSHbeta that is

61 ssary postoperatively to achieve the desired TSH goal.

62 iquid formulation with the same L-T4 dosage, TSH circulating levels were normalized.

63 ive L-T4 in tablets, maintaining the dosage, TSH levels worsened again reaching levels in the hypothy

64 the possible anabolic effects shown earlier, TSH both prevents bone loss and restores the lost bone a

65 Golgi/TGN organization all impair efficient TSH-dependent cAMP response element binding protein (CRE

66 Hypothyroid R429Q KI mice displayed elevated TSH subunit mRNA levels, and T(3) treatment failed to no

67 It is unclear to what extent the elevated TSH contributes to tumor progression.

68 internalization in thyroid cells, endogenous TSH receptors traffic retrogradely to the trans-Golgi ne

69 n was reduced in Mct8-KO in which endogenous TSH and T4 were suppressed by administration of triiodot

70 ECD and TSH holoreceptor contain the entire TSH-binding site, and the TSH binding affinities for bot

71 function by maternal melatonin and establish TSH signal transduction as a key substrate for the encod

72 For TSH, we identify a novel variant in SYN2 (MAF=23.5%, P=6

73 .65 (95% confidence interval, 0.84-3.23) for TSH of 7.0 to 9.9 mIU/L, 1.86 (95% confidence interval,

74 .01 (95% confidence interval, 0.81-1.26) for TSH of 4.5 to 6.9 mIU/L, 1.65 (95% confidence interval,

75 .94 (95% confidence interval, 1.01-3.72) for TSH <0.10 mIU/L (P for trend=0.047).

76 .86 (95% confidence interval, 1.27-2.72) for TSH of 10.0 to 19.9 mIU/L (P for trend <0.01) and 1.31 (

77 .31 (95% confidence interval, 0.88-1.95) for TSH of 0.10 to 0.44 mIU/L and 1.94 (95% confidence inter

78 (odds ratio (OR) per standard deviation for TSH 1.05, 95% confidence interval (CI) 0.97 to 1.12; for

79 TSH receptor (TSHR) and is indispensable for TSH/TSHR-mediated proliferation of thyroid follicular ce

80 igher and lower TSH levels, particularly for TSH >/=10 and <0.10 mIU/L.

81 after it was reported that the receptor for TSH (TSH-R) is transcribed and translated by selected cu

82 Dose responses for TSH-stimulated dissociation of prebound (125)I-TSH (nega

83 an approach to harmonization of results for TSH.

84 We found TSH-induced phosphorylation of these kinases in 2 cell l

85 L-, inhibited ACTH- and did not alter LH/FSH/TSH-release; and 3) resistin increased ACTH-release and

86 ed ACTH-release and did not alter PRL/LH/FSH/TSH-secretion.

87 levels of free triiodothyronine (FT3), FT4, TSH, and TPOAb were measured.

88 Furthermore, TSH increased expression of osteoblast marker genes ALPL

89 a clinical laboratory-based third-generation TSH immunoassay.

90 Within the DTC group, TSH level was predictive for cardiovascular mortality; t

91 mone biosynthesis and consequently have high TSH levels.

92 E level was related to elevated odds of high TSH (>/=80th percentile), but associations were not stat

93 ently stimulate cAMP signaling and at higher TSH concentrations to acutely stimulate phosphoinositide

94 er longevity has been associated with higher TSH and lower TH levels, but mechanisms underlying TSH/T

95 was defined as thyroid-stimulating hormone (TSH) 0.45 to 4.49 mIU/L, and subclinical hypothyroidism

96 noassays, using thyroid stimulating hormone (TSH) and 17beta-estradiol (E2) as model analytes, respec

97 ating levels of thyroid stimulating hormone (TSH) and thyroid hormone (TH) in an inverse relationship

98 s downstream of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TS

99 ined as a serum thyroid-stimulating hormone (TSH) concentration greater than the pregnancy-specific r

100 Since thyroid-stimulating hormone (TSH) exerts an inductor effect on cholesterol biosynthes

101 with antihuman thyroid stimulating hormone (TSH) IgG molecules and the detection of TSH antigens wer

102 one (ACTH), and thyroid stimulating hormone (TSH) in both normal and tumor tissues can be assessed by

103 lamus (MBH) and thyroid-stimulating hormone (TSH) in the pituitary.

104 , total T4, and thyroid-stimulating hormone (TSH) in women during pregnancy, and TSH in neonates.

105 i-quantitative thyr oid stimulating hormone (TSH) lateral flow immunochromatographic assays (LFA) are

106 ined as a serum thyroid-stimulating hormone (TSH) level of 5.0 to 19.96 mIU/l with normal total thyro

107 uppressed serum thyroid-stimulating hormone (TSH) level, respectively.

108 ons between low thyroid-stimulating hormone (TSH) levels and high bone turnover markers, low bone min

109 onal control of thyroid-stimulating hormone (TSH) levels as well as neuromodulatory functions.

110 e have measured thyroid-stimulating hormone (TSH) levels in neonates.

111 e (TH) and high thyroid-stimulating hormone (TSH) levels in the serum, is strongly associated with no

112 xine (T(4)) and thyroid-stimulating hormone (TSH) levels were measured at birth.

113 priately normal thyroid-stimulating hormone (TSH) levels, consistent with hypothalamic-pituitary RTH.

114 d with maternal thyroid-stimulating hormone (TSH) levels.

115 ormone (TH) and thyroid-stimulating hormone (TSH) levels.

116 onal reserve of thyroid-stimulating hormone (TSH) production and the TSH set point later in life.

117 nt of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many pat

118 The thyroid-stimulating hormone (TSH) receptor signals via G(s) to produce cAMP and via G

119 ly regulated by thyroid-stimulating hormone (TSH) secretion within the hypothalamic-pituitary-thyroid

120 ent for the two thyroid-stimulating hormone (TSH) stimulation methods (thyroid hormone withdrawal [TH

121 ormed and serum thyroid stimulating hormone (TSH) was measured.

122 been known that thyroid stimulating hormone (TSH), a central component of the HPT axis, can be made b

123 y expression of thyroid-stimulating hormone (TSH), an increase in the blood concentration of thyroid

124 Plasma free T4, thyroid-stimulating hormone (TSH), and 8 am cortisol levels were normal.

125 ncentrations of thyroid-stimulating hormone (TSH), and autoantibodies to thyroperoxidase (ATPO) in re

126 hyroxine (FT4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) were obtai

127 uitary hormone, thyroid-stimulating hormone (TSH), can bypass the thyroid to exert a direct protectiv

128 cally predicted thyroid stimulating hormone (TSH), free thyroxine (FT4) and thyroid peroxidase antibo

129 ncentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and thyroglobulin, vary wide

130 rolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT

131 Serum levels of thyroid-stimulating hormone (TSH), total thyroxine (TT4), and PFAAs were measured dur

132 sensitivity to thyroid stimulating hormone (TSH), which is dramatically and persistently increased b

133 , however, that thyroid-stimulating hormone (TSH), which is low in most hyperthyroid states, directly

134 tively regulate thyroid-stimulating hormone (TSH)-dependent Ca(2+) increases and TSH-dependent iodide

135 Thyroid-stimulating hormone (TSH)-induced reduction in ligand binding affinity (negat

136 LXRs activated thyroid-stimulating hormone (TSH)-releasing hormone (TRH)-positive neurons in the par

137 in response to thyroid-stimulating hormone (TSH).

138 levels of serum thyroid-stimulating hormone (TSH).

139 3), free T4, or thyroid-stimulating hormone (TSH).

140 zation of serum thyroid-stimulating hormone (TSH).

141 he thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to acutely and persistent

142 at thyrotropin [thyroid-stimulating hormone (TSH)]-stimulated persistent cAMP signaling is dependent

143 elation between thyroid-stimulating hormone (TSH; also known as thyrotropin) level and these outcome

144 hormones, like thyroid-stimulating hormone (TSH; thyrotropin), have only recently been reported, and

145 ct of different thyroid-stimulation hormone (TSH) levels.

146 [TT3 and FT3], thyroid-stimulating hormone [TSH], and thyroglobulin [Tg]) and levels of Pb, Hg, and

147 vels of estradiol (E2) and thyroid hormones (TSH, T3t, T4t) were also determined.

148 rmone withdrawal [THW] and recombinant human TSH [rhTSH]) and the two iodine-131 ((131)I) activities

149 In addition, recombinant human TSH alpha/beta administration resulted in increased HMGC

150 f drugs to use in place of recombinant human TSH in patients with thyroid cancer.

151 H-stimulated dissociation of prebound (125)I-TSH (negative cooperativity; EC(50)=70 mU/ml), which req

152 er, even in the absence of added TSH, (125)I-TSH dissociated much more rapidly from the TSHR ECD-GPI

153 of dissociation (k(off)) of prebound (125)I-TSH from CHO cells expressing the TSH holoreceptor.

154 a-tagged TSH and binding assays using (125)I-TSH.

155 Depletion of B-Raf impaired TSH-induced DNA synthesis, indicating a functional role

156 or silencing the expression of Rap1 impaired TSH or forskolin-induced ERK activation in Wistar rat th

157 d in men, with no corresponding decreases in TSH.

158 evidence for a functional role for B-Raf in TSH signaling.

159 s, indicating a functional role for B-Raf in TSH-regulated proliferation.

160 respective roles of PKA versus Epac/Rap1 in TSH signaling remain unclear.

161 n variants explain >/=20% of the variance in TSH and FT4.

162 al testosterone and PRL levels and increased TSH levels.

163 east one nonagenarian sibling have increased TSH secretion but similar bioactivity of TSH and similar

164 d from cells previously exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulatin

165 the constitutively active ligand-independent TSH receptor (TSHR).

166 Knockdown of beta-arrestin-1 inhibited TSH-stimulated up-regulation of mRNAs for OPN by 87 +/-

167 e agonist and a neutral antagonist inhibited TSH-stimulated persistent IP1 production, whereas the in

168 lation of beta-arrestin-1 by siRNA inhibited TSH-stimulated phosphorylation of ERK1/2, p38alpha, and

169 ich is what has been observed upon injecting TSH.

170 e the old question of whether intracutaneous TSH-R stimulation by autoantibodies contributes to the s

171 ) Leptin stimulated PRL/ACTH/FSH- but not LH/TSH-release; 2) adiponectin stimulated PRL-, inhibited A

172 s initiated by binding of the hormone ligand TSH to the ECD.

173 aints within the ECD of the TSHR, its ligand TSH, and the hormone-receptor complex.

174 0.15 (95% CI: -0.28, -0.03) lower serum log(TSH)mIU/L with adjustment for covariates.

175 Thus, we have suggested that a low TSH level may contribute to the bone loss of hyperthyroi

176 peculate that TNFalpha elevations due to low TSH signaling in human hyperthyroidism contribute to the

177 In order to determine whether low TSH levels contribute to bone loss in hyperthyroidism, w

178 This phenomenon, suggesting a lower TSH affinity for the former, was surprising because both

179 A lower TSH level is associated with increased cardiovascular mo

180 ts were increased with both higher and lower TSH levels (P for quadratic pattern <0.01); the hazard r

181 ts were increased with both higher and lower TSH levels, particularly for TSH >/=10 and <0.10 mIU/L.

182 for each 10-fold decrease in geometric mean TSH level.

183 he LFA format, however, is unable to measure TSH in the normal range or detect suppressed levels of T

184 ghput screening to identify a small-molecule TSH receptor (TSHR) agonist that was modified to produce

185 general US population is related to neonatal TSH.

186 serum PBDE was not associated with neonatal TSH (beta = 0.00, 95% confidence interval: -0.06, 0.06).

187 nsignificant inverse relations with neonatal TSH.

188 ultured human scalp HFs whether TRH (30 nM), TSH (10 mU ml(-1)), thyroxine (T4) (100 nM), and triiodo

189 d NCoRDeltaID, have low TH levels and normal TSH.

190 af(V600E)-induced PTC (BVE-PTC) under normal TSH, we transplanted BVE-PTC tumors subcutaneously into

191 yroxinemia as fT4<5th percentile with normal TSH.

192 uals, higher circulating fT4 levels, but not TSH levels, are associated with increased risk of incide

193 e, thereby demonstrating that the absence of TSH signaling contributes to bone loss.

194 rofound and lasting antiresorptive action of TSH is mimicked in cells that genetically overexpress th

195 gical studies identifying a direct action of TSH on the skeleton.

196 Here we show that the skeletal actions of TSH deficiency are mediated, in part, through TNFalpha.

197 revealed an inverted U-shaped association of TSH (p < 0.001), but no association of FT4 concentration

198 The association of TSH levels in the euthyroid and subclinical hypothyroid

199 icular, we found evidence for association of TSH levels with SNPs in the THRB (rs1505287, p = 7.3 x 1

200 sed TSH secretion but similar bioactivity of TSH and similar TH levels compared to controls.

201 and enhances the synthesis and biopotency of TSH, the hormone secreted by thyrotropes.

202 transient exposure to high concentrations of TSH causes persistent phosphoinositide and cAMP signalin

203 one (TSH) IgG molecules and the detection of TSH antigens were employed to demonstrate high protein i

204 was associated only with the development of TSH deficiency; the 4-year cumulative incidence was 44%

205 However, the direct influence of TSH on the osteoblast has remained unclear.

206 ollicular cells was due to the inhibition of TSH-mediated activation of the mTOR complex 1/ribosomal

207 normal range or detect suppressed levels of TSH (<0.4 mIU L(-1); hyperthyroidism).

208 nerally confirm the expected binding mode of TSH to the ECD as well as the general fold of the domain

209 aling is dependent on binding 2 molecules of TSH to TSHR homodimer, causing a conformational change a

210 The potency of TSH for cAMP signaling is higher than for phosphoinositi

211 or rapid and point-of-care quantification of TSH using a cell phone.

212 Quantification of TSH was performed in an iOS application directly on the

213 T4-mediated negative feedback regulation of TSH expression.

214 first in vitro study of NCOR1 regulation of TSH in a physiologically relevant cell system, the Talph

215 study identifies GLIS3 as a key regulator of TSH/TSHR-mediated thyroid hormone biosynthesis and proli

216 These data demonstrate the key role of TSH signaling in Braf-induced papillary thyroid cancer i

217 ypothalamus and thus stimulated secretion of TSH from the pituitary.

218 in mice with wild-type TshR, suppression of TSH did not revert the phenotype.

219 dies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in pe

220 PRL (P<0.01) were lower while the values of TSH (P = 0.02), fT3 (P = 0.08), and fT4 (P = 0.04) were

221 m the Rotterdam Study with data available on TSH (thyroid-stimulating hormone), FT4 (free thyroxine)

222 r TSHR/C41S heterodimers could only bind one TSH, TSH-stimulated IP1 production was decreased relativ

223 t adjuvant enhanced the levels of pathogenic TSH-binding inhibition and thyroid-stimulating Abs, as w

224 The increased amount of pituitary TSH was caused by reduced expression of type 2 iodothyro

225 This locally produced TSH suppresses osteoclast formation in a negative feedba

226 gold nanoparticles on an LFA for quantifying TSH levels.

227 s able to provide point-of-care quantitative TSH results with a high level of sensitivity and reprodu

228 Obtaining quantitative TSH results, especially in the low concentration range,

229 In fact, it does not provide quantitative TSH values at all.

230 nists for thyrocyte-expressed TAS2Rs reduced TSH-dependent Ca(2+) release in Nthy-Ori 3-1 cells, but

231 ngenital central hypothyroidism with reduced TSH biopotency, over-secretion of FSH at neonatal minipu

232 A concentrations was associated with reduced TSH in boys (-9.9% per log2 unit; 95% CI: -15.9%, -3.5%)

233 ssor, NCOR1, has been postulated to regulate TSH expression, presumably by interacting with thyroid h

234 g affinity (negative cooperativity) requires TSH receptor (TSHR) homodimerization, the latter involvi

235 perativity; EC(50)=70 mU/ml), which requires TSH binding to both sites of the TSH receptor (TSHR) hom

236 The resulting TSH-hydrazones are separated by ultrahigh-performance li

237 Our findings reveal TSH as a circannual output of the PT, which in turn regu

238 efined subclinical hypothyroidism as a serum TSH between 5 and 10 mIU/L, and overt hypothyroidism as

239 0 mIU/L, and overt hypothyroidism as a serum TSH greater than 10 mIU/L, but this is not the commonly

240 Euthyroidism was defined as a serum TSH level of 0.47 to 4.9 mIU/l.

241 thyroxine should be started to achieve serum TSH concentrations within the reference ranges for pregn

242 subclinical and antibody-negative) and serum TSH concentration.

243 range for each laboratory value, or by serum TSH concentrations greater than 2.5 mIU/L in the first t

244 ic assays (LFA) are used to screen for serum TSH concentration >5 mIUL(-1) (hypothyroidism).

245 d an approximately 3-fold elevation in serum TSH levels and a 40% reduction in biological activity.

246 to liquid oral formulation normalised serum TSH levels, and that switching back to tablets caused th

247 the importance of rigorous control of serum TSH in PTC patients.

248 However, normalization of serum TSH with L-T4 monotherapy results in relatively low seru

249 monotherapy at doses to normalize the serum TSH became the standard of care.

250 hyroidism despite normalization of the serum TSH has been identified.

251 s in XPA/FOXE1 (TTF-2) associated with serum TSH (p = 5.5E-08 to 1.0E-09); a nonsynonymous SNP (p = 1

252 xpression in FRTL5 cells modify the specific TSH response.

253 firmed the increased affinity of stimulating TSH receptor antibodies for the shed A subunit rather th

254 e system; however, the role of immune system TSH remains enigmatic and most studies have viewed it as

255 y fluorescence microscopy using Alexa-tagged TSH and binding assays using (125)I-TSH.

256 Thyroid Association guidelines of tempering TSH suppression in patients with low risk of cancer recu

257 We conclude that TSH enhances osteoblast differentiation in U2OS cells th

258 ligand dilution approach, we confirmed that TSH increased the rate of dissociation (k(off)) of prebo

259 nical studies together have established that TSH inhibits osteoclastic bone resorption.

260 novel study provides little indication that TSH, FT4 or TPOAb positivity affects IHD, despite potent

261 ture mineralizing osteoblasts, and show that TSH stimulates osteoblast differentiation primarily thro

262 x vivo bone marrow cell cultures showed that TSH inhibits and stimulates TNFalpha production from mac

263 We present data suggesting that TSH-stimulated TG phosphorylation contributes to enhance

264 The TSH effects on MTCO1, TFAM, and porin could be abolished

265 contain the entire TSH-binding site, and the TSH binding affinities for both receptor forms should, t

266 stimulating hormone (TSH) production and the TSH set point later in life.

267 Mutations in the genes encoding the TSH receptor (TSHR) or the Gs protein alpha subunit (GNA

268 und (125)I-TSH from CHO cells expressing the TSH holoreceptor.

269 ifference in ligand binding kinetics for the TSH holoreceptor and TSHR ECD-GPI was obtained upon comp

270 PI was significantly lower than that for the TSH holoreceptor.

271 rapidly from the TSHR ECD-GPI than from the TSH holoreceptor.

272 ECD-GPI was obtained upon comparison of the TSH K(d) values for these two receptor forms at 4 degree

273 ch requires TSH binding to both sites of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 pr

274 Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmembrane-spanning receptor

275 nd competition studies, we observed that the TSH binding affinity for the TSHR ECD-GPI was significan

276 ociated hinge region that contributes to the TSH-binding site.

277 Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmem

278 Thyrotropin (TSH) regulates thyroid cell proliferation and function t

279 icularly thyroid peroxidase and thyrotropin (TSH) receptor] and of high affinity monoclonal antibodie

280 onine (T3), thyroxine (T4), and thyrotropin (TSH) were measured in plasma for 4 mo before supplementa

281 pin-releasing hormone (TRH) and thyrotropin (TSH), are expressed in human hair follicles (HFs) and re

282 ols thyroid hormone production, thyrotropin (TSH), caught the attention of skin researchers only afte

283 astritis, who showed high serum thyrotropin (TSH) levels (in the hypothyroid range) while in therapy

284 athogenic autoantibodies to the thyrotropin (TSH) receptor (TSHR), can be treated but not cured.

285 or the heritable thyroid traits thyrotropin (TSH) and free thyroxine (FT4), we analyse whole-genome s

286 l thyroid function tests (serum thyrotropin [TSH], free thyroxine [fT4], and thyroid peroxidase [TPO]

287 th thyroid hormone receptors (THRs) bound to TSH subunit genes.

288 ivatization with p-toluenesulfonylhydrazine (TSH).

289 tination are an inherent property of the TRH/TSH feedback mechanism and indicate that only constant d

290 r it was reported that the receptor for TSH (TSH-R) is transcribed and translated by selected culture

291 R/C41S heterodimers could only bind one TSH, TSH-stimulated IP1 production was decreased relative to

292 in after washing the cells to remove unbound TSH, and TSHR internalization by fluorescence microscopy

293 d lower TH levels, but mechanisms underlying TSH/TH differences and longevity remain unknown.

294 rnalized by 30 min incubation with unlabeled TSH; however, expression of beta-arrestin-2 promoted TSH

295 IP1 production increased progressively when TSH exposure was increased from 1 to 30 min, whereas the

296 To determine whether TSH signaling cooperates with oncogenic Braf in this pro

297 r common variants (MAF>/=1%) associated with TSH and FT4 (N=16,335).

298 shift in serum PFOA was not associated with TSH or TT4 levels in all children combined.

299 sing human embryonic kidney-EM293 cells with TSH and measuring cAMP or inositol monophosphate (IP1) p

300 uman thyrocyte cultures hyperstimulated with TSH also showed an increased intrinsic ability to form T