ライフサイエンスコーパス: ROR

1 ROR added significant prognostic information beyond CTS

2 ROR alpha 1 and ROR gamma inhibit the transactivation in

3 ROR alpha deficiency resulted in reduced IL-17 expressio

4 ROR distills disease-associated DR sequences and identif

5 ROR gamma is expressed as two mRNAs, 2.3 and 3.0 kb in s

6 ROR gamma was able to activate RORE-dependent transcript

7 ROR proteins, a class of Wnt-binding receptor tyrosine k

8 ROR provides more prognostic information in endocrine-tr

9 ROR(alpha) (NR1F1) and Reverb(alpha) (NR1D1) are two mem

10 ROR-gamma antagonists also markedly diminish genome-wide

11 ROR-gamma antagonists suppress the expression of both AR

12 ROR-gamma recruits nuclear receptor coactivator 1 and 3

13 RORs play a role in tissue development and circadian rhy

14 RORs were combined by random-effects meta-analysis model

15 ize multiple Wnts, suggesting that the CAM-1/ROR ECD sequesters Wnts.

16 PRR = 3.04, 95% CI: 1.73-5.31; chi2 = 16.13; ROR = 3.15, 95% CI: 1.74-5.70; IC = 1.46; IC025 = 0.48),

17 -based transition structures [(TMS(2)NLi)(2)(ROR')(ketone)].

18 the control of IL-6 stimulation of the IL-21/ROR/IL-17 pathway and to the Th17/Treg counterbalance.

19 (PPR = 1.27, 95% CI: 1.05-1.53; chi2 = 6.38; ROR = 1.28, 95% CI: 1.06-1.56; IC = 0.29, IC025 = -0.00)

20 PPR = 2.20, 95% CI: 1.79-2.71; chi2 = 56.55; ROR = 2.31, 95% CI: 1.84-2.88; IC = 1.03; IC025 = 0.68),

21 th birth weights (BWs) <2,500 g (DD = -11.8, ROR: 0.29, 95% CI: 0.10-0.82, p = 0.020).

22 also found on women's knowledge (DD = +14.8, ROR: 1.86, 95% CI: 1.32-2.62, p < 0.001) and physical IP

23 PRR = 3.72, 95% CI: 1.87-7.43; chi2 = 15.99; ROR = 3.75, 95% CI: 1.87-7.51; IC = 1.53, IC025 = 0.45),

24 RORalpha or RORgamma expression vector and a ROR-responsive element (RORE)-LUC reporter, and a mammal

25 e receptor, an acetylcholine receptor, and a ROR-type receptor tyrosine kinase in the interneuron RIA

26 er using luciferase reporter constructs of a ROR promoter deletion series.

27 RBalpha, two nuclear receptors that target a ROR-response element in the promoter of the BMAL1 gene.

28 the small molecule Nobiletin (NOB) activates ROR (retinoid acid receptor-related orphan receptor) nuc

29 ate sites, where it competes with activating ROR TFs.

30 AhR-ROR-gammat complex is a therapeutic target for MAP4K3/GL

31 , that inhibited GLK kinase activity and AhR-ROR-gammat interaction.

32 Collectively, the GLK-induced AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex i

33 ere, we investigated whether GLK-induced AhR-ROR-gammat complex in T cells is a therapeutic target fo

34 on of ROR-gammat phosphorylation and the AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex.

35 An ROR greater than 1 indicates larger treatment outcomes w

36 An ROR<1 indicated that the experimental intervention is mo

37 1, Bmal1, E4bp4, Rev-Erbalpha and Per2 in an ROR isotype- and tissue-selective manner without affecti

38 and phosphoenolpyruvate carboxykinase, in an ROR-dependent manner.

39 ignificant signal detection for anaphylaxis (ROR, 20.50 [95% CI, 20.37-20.63]; IC, 3.77 [IC(025), 3.7

40 ROR alpha 1 and ROR gamma inhibit the transactivation induced by GAL4(DB

41 this superfamily, such as NGFI-B, SF-1, and ROR, could also recognize unique geometric features in t

42 T-bet dominance over GATA-3 and ROR-gammat decreases with the disarmament of effector cy

43 Rather, GATA-3 and ROR-gammat levels are elevated when compared with cells

44 s NKp44, CD161, CCR6, IL1 receptor, AHR, and ROR-gammatau.

45 Furthermore, ROR alpha and ROR gamma coexpression synergistically led to greater Th

46 Double deficiencies in ROR alpha and ROR gamma globally impaired Th17 generation and complete

47 lated orphan nuclear receptors ROR alpha and ROR gamma t work together to regulate T helper (Th)17 ce

48 ge-specific nuclear receptors, ROR alpha and ROR gamma.

49 The nuclear receptors NGFI-B and ROR utilize a carboxyl-terminal extension (CTE) of the z

50 the expression of VDR, CYP27B1, CYP24A1, and ROR in relation to melanin levels, clinical stage and pr

51 Although Rev-Erb and ROR antagonize each other to control once-daily transcri

52 However, Rev-ErbA and ROR bind weakly to naturally occurring PPREs relative to

53 nomers of the nuclear receptors Rev-ErbA and ROR suggesting that the latter could bind to PPREs and a

54 direct competition between Rev-erbalpha and ROR TFs provides a universal mechanism for self-sustaine

55 ta to IL-23 further augmented ROR-gammat and ROR-alpha expression and suppressed Eomes expression, th

56 with increased expression of ROR-gammat and ROR-alpha.

57 y preferential expression of Tbet, Gata3 and ROR-gammat and production of IFN-gamma, IL-4 and IL-17,

58 I counts vary with background, location, and ROR by less than 3.2%, 3%, and 5.3%, respectively.

59 RORalpha and ROR gamma are expressed in human skin and serve as recep

60 downregulation, whereas STAT3, RORgamma, and ROR* were required for IL-17 expression in Treg cells.

61 n of the transcription factors RORgammat and ROR*.

62 lopment is absolutely dependent on Runx1 and ROR(gamma)t, transcription factors that influence, but a

63 GReX predicted lower proliferation score and ROR-P.

64 s Foxp3 expression, which requires STAT3 and ROR-gamma, which is encoded by Rorc.

65 OA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcr

66 01; IC(025): 1.46), ventricular arrhythmias (ROR: 4.7; 95% confidence interval: 3.7 to 5.9; p < 0.000

67 ome 1 (Cry1), as part of the same complex as RORs.

68 IL-6 and TGF-beta to IL-23 further augmented ROR-gammat and ROR-alpha expression and suppressed Eomes

69 Among females, brinzolamide (ROR = 409.63, 95% CI = 196.78-852.73) and salbutamol (RO

70 similar prognostic information was added by ROR and IHC4 in all patients but more by ROR in the HER2

71 node negative; more information was added by ROR than by RS.

72 by ROR and IHC4 in all patients but more by ROR in the HER2-negative/node-negative group.

73 the transactivation of the IL-10 promoter by ROR-alpha.

74 high risk and fewer as intermediate risk by ROR than by RS.

75 This transcriptional activation by RORs was associated with changes in histone acetylation

76 l control of clock and metabolic networks by RORs.

77 A canonical ROR response element was identified in the proximal prom

78 The combined ROR for all-cause mortality was 0.83 (95% confidence int

79 The combined ROR for subjective and objective outcomes was, respectiv

80 For subjective outcomes, the combined ROR was 1.07 (0.87-1.33).

81 n in the single most precise trial (combined ROR, 1.13 [95% CI, 1.07-1.19]) for subjective outcomes a

82 The case-control ROR may be preferred for single-disease/syndrome analyti

83 bit the transactivation induced by GAL4(DBD)-ROR gamma in fibroblast D1 cells suggesting that these r

84 was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolis

85 .0001; IC(025): 0.96), conduction disorders (ROR: 3.5; 95% confidence interval: 2.7 to 4.6; p < 0.000

86 ionship between Wnts and the sole C. elegans ROR homolog, cam-1, during C. elegans vulval development

87 containing large genomic fragments encoding ROR gamma.

88 Temporal deletion of Rorc (encoding ROR-gammat) in mature ILCs also did not impair cytokine

89 r coactivator-2 by RORalpha at an endogenous ROR target gene (G6Pase).

90 sites for AP-1, C/EBP beta, GATA, c-Rel, ER, ROR alpha, SREBP, and CREB.

91 Taken together, these results establish ROR-gamma as a key player in CRPC by acting upstream of

92 These findings thus establish ROR/INSIG2/SREBP as a molecular pathway by which circadi

93 (2)NLi) solvated by hindered dialkyl ethers (ROR') are described.

94 1.47-1.81) and psychological adverse events (ROR, 4.33; 95% CI, 4.17-4.49) in finasteride was identif

95 ral nervous system (CNS) hemorrhagic events (ROR: 3.7; 95% confidence interval: 3.4 to 4.1; p < 0.000

96 0.0001; IC(025): 0.76), CNS ischemic events (ROR: 2.2; 95% confidence interval: 2.0 to 2.5; p < 0.000

97 ally, Itch bound to the transcription factor ROR-gammat and targeted ROR-gammat for ubiquitination.

98 y T (Treg) cells of the transcription factor ROR-gammat in a MyD88-dependent manner, which was defici

99 The transcription factor ROR-gammat, which controls IL-23R expression, has a func

100 ; p < 0.0001; IC(025): 1.63), heart failure (ROR: 3.5; 95% confidence interval: 3.1 to 3.8; p < 0.000

101 Finally, ROR-gamma antagonists suppressed tumor growth in multipl

102 ed events, including anterior chamber flare (ROR = 1410.5), vitritis (853.3), retinal vasculitis (352

103 tamoxifen in the ATAC trial was assessed for ROR using the NanoString nCounter.

104 ify Reverb(alpha) as a novel target gene for ROR(alpha).

105 results reveal differential requirements for ROR-gammat in the maintenance of TH17 cell and ILC3 resp

106 Further ROR analysis of DR associations with autoantibodies find

107 Furthermore, ROR alpha and ROR gamma coexpression synergistically led

108 TAZ signaling axis" that consists of Wnt-FZD/ROR-Galpha12/13-Rho GTPases-Lats1/2 to promote YAP/TAZ a

109 acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; R

110 acid receptor-related orphan receptor gamma (ROR gamma)0/0 thymi, which accumulate immature single-po

111 ding retinoid-related orphan receptor gamma (ROR-gamma) and IL-23 receptor (IL-23R) produced abundant

112 acid receptor-related orphan receptor gamma (ROR-gamma) is overexpressed and amplified in metastatic

113 23R)(+), RAR-related orphan receptor gammat (ROR-gammat)(+)CD3(+)CD4(-)CD8(-), stem cell antigen 1 (S

114 cid receptor-related orphan receptor-gammaT (ROR-gammaT) and IL-17F.

115 ptor-related orphan nuclear receptor-gammat (ROR-gammat) complex formation.

116 RAR-related orphan receptor-gammat (ROR-gammat) directs differentiation of proinflammatory T

117 longer able to induce apoptosis or generate ROR.

118 as a comparator, semaglutide showed a higher ROR for ION (ROR = 9.84, 95% CI = 4.25-22.81, P < .0001,

119 These results demonstrate how ROR proteins help to refine the spatial pattern of Wnt a

120 To clarify how RORs inhibit the Wnt pathway, we examined the relationsh

121 However, ROR-gammat-dependent group 3 innate lymphoid cells ILC3s

122 calization of both mouse ROR gamma and human ROR gamma (HGMW-approved symbol RORC).

123 gamma) is highly homologous to that of human ROR gamma, with an overall identity of 88%.

124 The human ROR gamma was mapped to chromosome region 1q21.

125 < 0.0001; IC(025): 0.73), and hypertension (ROR: 1.7; 95% confidence interval: 1.5 to 1.9; p < 0.000

126 Double deficiencies in ROR alpha and ROR gamma globally impaired Th17 generatio

127 rsus control exposures, while the changes in RORs for irbesartan and losartan were only 20-30% higher

128 arranged V alpha 14J alpha 18 transgene into ROR gamma(0/0) mice results in functional iNKT cells.

129 , introgression of a Bcl-x(L) transgene into ROR gamma(0/0) mice, which promotes survival and permits

130 plementary positive feedback loop (involving ROR).

131 or, semaglutide showed a higher ROR for ION (ROR = 9.84, 95% CI = 4.25-22.81, P < .0001, IC(025) = 0.

132 -6-phosphatase in HepG2 cells by T0901317 is ROR-dependent and is not due to the compound's LXR activ

133 Here, we show that the lncRNA ROR occupies and activates the TESC promoter by repellin

134 y stem cells, we demonstrate that the lncRNA ROR, a regulator of embryonic stem cell pluripotency, is

135 However, in other regions, the matched ROR was noticeably different than the PMR.

136 Reverb(alpha) transcription via a monomeric ROR response element located in the Reverb(alpha) gene p

137 d the chromosomal localization of both mouse ROR gamma and human ROR gamma (HGMW-approved symbol RORC

138 The amino acid sequence of mouse ROR gamma (mROR gamma) is highly homologous to that of h

139 we determined the genomic structure of mouse ROR gamma and the chromosomal localization of both mouse

140 escence in situ hybridization that the mouse ROR gamma gene is located on chromosome 3, in a region t

141 The genomic structure of the mouse ROR gamma gene was derived from the analysis of P1 vecto

142 Thus, commensals activate a MyD88/ROR-gammat pathway in nascent Treg cells to protect agai

143 the Th1 mixture expressed T-bet, whereas no ROR-gamma t was detected in Th1 incubated with Th17 mixt

144 In HF skeletal muscle, the NOB-ROR axis broadly activates genes for mitochondrial respi

145 a process that is dependent on STAT3 but not ROR-gamma.

146 ssion of Rev-Erbalpha or addition of a novel ROR antagonist repressed this activation.

147 RS's proliferation module explained 72.5% of ROR's variance, while the estrogen module explained only

148 ellent starting point for the development of ROR selective modulators.

149 ecies, which promotes the differentiation of ROR-gammat(+) regulatory T cells to suppress FA.

150 be partially due to the inhibitory effect of ROR gamma t on c-Rel transcription.

151 The discovered negative effect of ROR-gamma on the degradation of the toxic Abeta peptides

152 Furthermore, ectopic expression of ROR gamma t inhibits the proliferation of mature and imm

153 that 7alpha-OHC modulates the expression of ROR target genes, including Glc-6-Pase and phosphoenolpy

154 Ectopic expression of ROR(alpha)1 in L6 cells significantly induces Reverb(alp

155 was associated with increased expression of ROR-gammat and ROR-alpha.

156 rt acute toxic effects via the generation of ROR in macrophages.

157 tor Runx1 is essential for the generation of ROR-gammat expressing iNKT17 cells.

158 Inhibition or genetic inactivation of ROR-gammat attenuated IL-17 expression and reduced spont

159 rom patients with SLE displayed induction of ROR-gammat phosphorylation and the AhR-ROR-gammat (and A

160 strate that transient chemical inhibition of ROR-gammat in mice selectively reduces cytokine producti

161 ses and suggest that transient inhibition of ROR-gammat is a safe and effective therapeutic approach

162 Finally, pharmacologic inhibition of ROR-gammat provided therapeutic benefit in mouse models

163 Overexpression of ROR alpha promoted Th17 differentiation, possibly throug

164 SiRNAs targeting other regions of ROR-gamma not only confirmed the observed reporter activ

165 Our data suggest that down-regulation of ROR gamma t expression in thymocytes is essential for th

166 of Prox1 are critical for its repression of ROR transcriptional activity.

167 Suppression of ROR in tumors results in silencing of TESC expression, a

168 RORalpha/gamma-dependent transactivation of ROR-responsive reporter genes and in HepG2 cells reduced

169 new therapeutic targets for the treatment of ROR-related diseases.

170 models to determine the prognostic value of ROR for distant recurrence beyond 5 years in the combine

171 The AF2 domain of RORs is essential for the interaction, whereas Prox1 int

172 We observed that NRF2 knockdown or ROR overexpression leads to increased stem cell self-ren

173 (OR) for each study design, the ratio of OR (ROR) between the designs and the summary ROR across clin

174 oci, we applied a novel recursive organizer (ROR) to discover disease-associated amino acid residues.

175 with 75-fold selectivity for RORc over other ROR family members and >200-fold selectivity over 25 add

176 Comparing the C-index of DGM-CM6 and PAM50-ROR scores, the former performed better than the latter

177 However, the EP, BCI, and particularly ROR scores are determined largely by proliferative featu

178 duced AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex is a therapeutic target for the GLK(

179 d the AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex.

180 and 0.78 for CTS, CTS plus RS, and CTS plus ROR, respectively.

181 analysis suggests that Prox1 is a potential ROR target gene in liver, which is supported by the regu

182 of GRIP-1/TIF-2, but not SRC-1, potentiates ROR(alpha)-stimulated Reverb(alpha) promoter activity in

183 % CI: 1.09-4.61, p = 0.029 and DD = +9.1 pp, ROR: 2.65, 95% CI: 1.01-6.98, p = 0.048) and household f

184 healthcare for sick children (DD = -26.4 pp, ROR: 0.23, 95% CI: 0.08-0.66, p = 0.006).

185 dity 2 week's prior to report (DD = -3.5 pp, ROR: 0.80, 95% CI: 0.56-1.14, p = 0.214) but reduced the

186 ce foods (ASFs) (respectively, DD = +4.5 pp, ROR: 2.24, 95% CI: 1.09-4.61, p = 0.029 and DD = +9.1 pp

187 ivering in a health facility (DD = +10.6 pp, ROR: 1.53, 95% CI: 1.10-2.13, p = 0.012) and lower odds

188 nd household food insecurity (DD = -10.7 pp, ROR: 0.63, 95% CI: 0.43-0.91, p = 0.016).

189 , p < 0.001) and physical IPV (DD = -7.9 pp, ROR: 0.60, 95% CI: 0.36-0.99, p = 0.048).

190 b and Nlrp3 genes revealed multiple putative ROR response elements (ROREs) that were occupied by RORg

191 ough generation of reactive oxygen radicals (ROR).

192 Moreover, reporting odds ratio (ROR) and P value were calculated to quantify the signals

193 ld of IC(0.25) and the reporting odds ratio (ROR) with 95% confidence intervals (CI).

194 visit, to calculate a reporting odds ratio (ROR).

195 percentage points [pp], relative odds ratio [ROR]: 0.74, 95% CI: 0.51-1.06, p = 0.097).

196 nality analysis using reporting odds ratios (ROR) and information component (IC) to determine whether

197 nd by calculating the reporting odds ratios (ROR) with 95% confidence intervals.

198 rategy, expressed as a ratio of odds ratios (ROR), was assessed considering the dependency between st

199 The reported odds ratios (RORs) for alendronate, ibandronate, and risedronate were

200 ty was assessed using reporting odds ratios (RORs, 95% confidence interval).

201 ic expression of the orphan nuclear receptor ROR gamma t in mature T cells down-regulates their surfa

202 ation, including the orphan nuclear receptor ROR gamma t, the IL-1 receptor, and the IL-23 receptor.

203 cells downregulated orphan nuclear receptor ROR-gammat but increased Fas ligand expression and died

204 at produce retinoid-related orphan receptor (ROR) agonists that activate RORgammat.

205 ck of retinoic acid-related orphan receptor (ROR) gamma or alpha expression in mice significantly red

206 ulate retinoic acid-related orphan receptor (ROR) gammat during positive selection, similar to the bl

207 ctor, retinoic acid-related orphan receptor (ROR) gammat, IFN-gamma, IL-17A, and IL-22, all hallmarks

208 inoic acid receptor-related orphan receptor (ROR) gammat; and 3) alveolar bone loss (ABL) in experime

209 , a homolog of the retinoid orphan receptor (ROR), is a transcription factor in the nuclear hormone r

210 ors (TFs), retinoid-related orphan receptor (ROR)-alpha and -gamma, in the hepatic circadian clock.

211 inoic acid receptor-related orphan receptor (ROR)-gamma mediate the lineage specification.

212 A-1), retinoic-acid-related orphan receptor (ROR)-gammat and IL-23R, and these cells markedly accumul

213 inoic acid receptor-related orphan receptor (ROR)-gammat, IL-17, IL-17F, CCL20, and CCR6 expression,

214 Retinoic acid-related orphan receptor (ROR)-gammat, the master transcription factor of the Th17

215 ression of retinoid-related orphan receptor (ROR)-gammat, which is consistent with a crucial role for

216 ells, Retinoic acid-related orphan receptor (ROR)-gammat-dependent lymphocytes, (NK)1.1(+) cells, nat

217 inoic acid receptor-related orphan receptor (ROR)alpha, and that this interaction inhibits transcript

218 ptor, retinoid acid-related orphan receptor (ROR)alpha, is essential for the development of cerebella

219 e presence of retinoic acid orphan receptor (ROR)C2 and the surface expression of CD161 and CCR6.

220 In ontogeny, retinoic acid orphan receptor (ROR)gamma-dependent lymphoid tissue inducer (LTi) cells

221 press retinoic acid-related orphan receptor (ROR)gammat (TC17 cells) have been shown to promote proca

222 ptors retinoic acid-related orphan receptor (ROR)gammat and RORalpha, which in turn induce expression

223 ression of retinoid-related orphan receptor (ROR)gammat or RORalpha in committed Th17 cells.

224 xp3(+)retinoic acid-related orphan receptor (ROR)gammat(+) T cells have recently been characterized a

225 nhanced CCR6(+) RAR-related orphan receptor (ROR)gammat(+) Th17 cell differentiation in vitro and inc

226 3, or retinoic acid-related orphan receptor (ROR)gammat, and retroviral GATA-3 and RORgammat could no

227 actor retinoic acid-related orphan receptor (ROR)gammat.

228 expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta an

229 (high retinoic acid-related orphan receptor-(ROR)gammat, IL-17A, IL-17F; low T-bet and eomesodermin),

230 the closely related orphan nuclear receptors ROR alpha and ROR gamma t work together to regulate T he

231 the retinoic acid-related orphan receptors (ROR) alpha (RORalpha) and gamma (RORgamma) in these tiss

232 The retinoid-related orphan receptors (ROR) comprise a distinct subfamily of nuclear receptors

233 The retinoid-related orphan receptors (RORs) and liver X receptors (LXRs) were postulated to ha

234 s (LXRs), retinoid-related orphan receptors (RORs) and Rev-ERBs.

235 Retinoic acid-related orphan receptors (RORs) and the basic helix-loop-helix-PAS transcription f

236 noic acid receptor-related orphan receptors (RORs) regulate a variety of physiological processes incl

237 noic acid receptor-related orphan receptors (RORs), in several pathologies, including osteoporosis, s

238 d by two lineage-specific nuclear receptors, ROR alpha and ROR gamma.

239 own that the PAM50-based risk of recurrence (ROR) score is significantly correlated with distant recu

240 The PAM50 risk of recurrence (ROR) score provides an alternative approach, which also

241 of Microarray 50 (PAM50) Risk of Recurrence (ROR), EndoPredict (EP), and Breast Cancer Index (BCI) ar

242 A Robust Optimal Resolution (ROR) beamforming method is proposed to minimize the wors

243 ith background activity, radius of rotation (ROR), tumor location, and size.

244 t of a clinical treatment score (CTS) by RS, ROR, or IHC4, an index of DR risk derived from immunohis

245 Analyses for RS, ROR, EP, and BCI were conducted by the manufacturers in

246 mouse homologue of the orphan receptor, RZR/ROR gamma, a member of the nuclear receptor superfamily,

247 .63, 95% CI = 196.78-852.73) and salbutamol (ROR = 67.12, 95% CI = 28.37-158.80) were disproportionat

248 eased the expression of RORgamma and several ROR-target genes, along with increased histone acetylati

249 were selected for analysis, and significant RORs were most commonly observed in the skin, nail, gast

250 RORalpha directly bound to a specific ROR response element on the promoter of Sema3e and negat

251 nteracting LXXLL-peptide, were used to study ROR-antagonist activities.

252 The nuclear orphan receptor subfamily ROR/RZR is part of the steroid and thyroid hormone/retin

253 t disproportionality signal for suicidality (ROR, 1.63; 95% CI, 1.47-1.81) and psychological adverse

254 nonrandomized vs randomized studies (summary ROR, 0.95; 95% credible interval [CrI], 0.89-1.02).

255 OR (ROR) between the designs and the summary ROR across clinical questions.

256 e elements are equally important to suppress ROR transcription.

257 ting of supraventricular arrhythmias (SVAs) (ROR: 23.1; 95% confidence interval: 21.6 to 24.7; p < 0.

258 -response element using in vitro synthesized ROR gamma revealed that it binds as a monomer to respons

259 id receptor-related orphan receptor gamma t (ROR-gammat)(+) Treg cell differentiation.

260 and pointed to a potential receptor target, ROR-gamma.

261 transcription factor ROR-gammat and targeted ROR-gammat for ubiquitination.

262 in the intestine, suggesting that targeting ROR-gammat could also result in impaired host defense af

263 riptional coactivators of the circadian TFs, RORs.

264 mplified in metastatic CRPC tumors, and that ROR-gamma drives AR expression in the tumors.

265 the Reverb(alpha) promoter demonstrate that ROR(alpha) regulates the Reverb(alpha) gene at the trans

266 rmore, mutagenesis experiments indicate that ROR(alpha) regulates Reverb(alpha) transcription via a m

267 Here, we show that ROR(alpha) and Reverb(alpha) are expressed with a simila

268 ctrophoretic mobility shift assays show that ROR(alpha) binds strongly to this site in a specific-man

269 nt expression in DP thymocytes, suggest that ROR gamma t controls these distinct phenotypic features

270 with the wild-type mice, which suggests that ROR(alpha) is involved in the regulation of Reverb(alpha

271 The ROR gamma t transgene inhibits IL-2 production by mature

272 The ROR gamma-binding specificity was further defined by mut

273 The ROR score added clinically meaningful prognostic informa

274 The ROR score was significantly prognostic by itself in year

275 romatin modification and EZH2 binding at the ROR promoter that was dependent on NRF2 binding.

276 for late distant recurrence was added by the ROR score compared with the CTS.

277 These neurons express the ROR alpha (RORalpha) nuclear orphan receptor and are sel

278 specific NRF2 response elements flanking the ROR promoter and that these two NRF2 response elements a

279 mined predicted NRF2 binding elements in the ROR promoter using luciferase reporter constructs of a R

280 was considered when the lower limits of the ROR and IC were above 1 and 0, respectively.

281 here was consistency in the magnitude of the ROR and proportionate morbidity ratio (PMR) in regions s

282 rbalpha (Nr1d1), through coactivation of the ROR family of orphan nuclear receptors.

283 , the most recently identified member of the ROR family, has been shown to be important for the devel

284 Analysis of the ROR gamma-response element using in vitro synthesized RO

285 ression with Rev-Erbalpha or addition of the ROR inverse agonist T0901317.

286 Here, we focus on the ROR score for predicting distant recurrence after 5 year

287 The results demonstrate that the ROR gamma genes are located in chromosomal regions that

288 These results suggest that the ROR score may be helpful for separating patients into ri

289 ted that in liver, Prox1 is recruited to the ROR response element sites of the clock genes, brain and

290 izes the studies identifying ligands for the RORs and evaluates their role as targets for potential t

291 ecent studies have established roles for the RORs in physiological development and the advent of dise

292 he initial identification of ligands for the RORs when X-ray crystallographic studies identified seve

293 Identification of ligands for the RORs, both endogenous and synthetic, has established the

294 at small molecules can be used to target the RORs for therapeutic intervention in metabolic and immun

295 with increased histone acetylation at these ROR response element sites.

296 REV-ERBalpha binds to ROR response elements (RORE) in Th17 cells and inhibits

297 cores (rho = 0.63-0.74) except for RS versus ROR (rho = 0.32) and RS versus BCI (rho = 0.35).

298 ur results reveal a novel mechanism by which ROR may serve as a decoy oncoRNA that blocks binding sur

299 he interaction, whereas Prox1 interacts with RORs through either its 28 amino acids N-terminal region

300 Without ROR silencing, TESC knockdown presents consistent and si