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

5 ROR gamma was able to activate RORE-dependent transcript

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

7 ROR provides more prognostic information in endocrine-tr

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

9 ROR-gamma antagonists also markedly diminish genome-wide

10 ROR-gamma antagonists suppress the expression of both AR

11 ROR-gamma recruits nuclear receptor coactivator 1 and 3

12 RORs play a role in tissue development and circadian rhy

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

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

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

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

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

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

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

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

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

22 An ROR greater than 1 indicates larger treatment outcomes w

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

24 1, Bmal1, E4bp4, Rev-Erbalpha and Per2 in an ROR isotype- and tissue-selective manner without affecti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 n of the transcription factors RORgammat and ROR*.

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

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

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

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

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

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

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

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

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

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

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

57 l control of clock and metabolic networks by RORs.

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

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

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

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

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

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

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

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

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

67 containing large genomic fragments encoding ROR gamma.

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

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

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

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

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

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

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

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

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

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

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

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

80 Furthermore, ROR alpha and ROR gamma coexpression synergistically led

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

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

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

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

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

86 23R)(+), RAR-related orphan receptor gammat (ROR-gammat)(+)CD3(+)CD4(-)CD8(-), stem cell antigen 1 (S

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

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

89 longer able to induce apoptosis or generate ROR.

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

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

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

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

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

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

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

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

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

99 -6-phosphatase in HepG2 cells by T0901317 is ROR-dependent and is not due to the compound's LXR activ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Overexpression of ROR alpha promoted Th17 differentiation, possibly throug

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 ough generation of reactive oxygen radicals (ROR).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 3, or retinoic acid-related orphan receptor (ROR)gammat, and retroviral GATA-3 and RORgammat could no

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 e elements are equally important to suppress ROR transcription.

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

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

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

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

195 riptional coactivators of the circadian TFs, RORs.

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

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

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

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

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

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

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

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

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

205 The ROR score added clinically meaningful prognostic informa

206 The ROR score was significantly prognostic by itself in year

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 Without ROR silencing, TESC knockdown presents consistent and si