ライフサイエンスコーパス: GR

1 GR and MR genetic variation predicted unique cognitive f

2 GR deletion specifically in glutamatergic, but not in GA

3 GR expression in group 1 ILCs is required to limit their

4 GR expression is silenced in prostate cancer by a combin

5 GR genetic variation was implicated in attention and wor

6 GR utilizes multiple DNA-binding-dependent and -independ

7 GR-depleted preadipocytes show adipogenesis defects 1 we

8 GR-interacting protein-1 (GRIP1) is a GR corepressor in

9 ggesting a non-redundant GRIP1 function as a GR coactivator.

10 GR-interacting protein-1 (GRIP1) is a GR corepressor in macrophages, however, whether GRIP1 me

11 to TREs via sequence-specific contacts to a GR-binding sequence (GBS) half-site found embedded withi

12 versely, the ketogenic module operates via a GR-induced TF cascade, whereby PPARA levels are increase

13 Here, we demonstrate that adipocyte GR deficiency in mice significantly impacts systemic met

14 The adipocyte GR is indispensable for the feeding-fasting transition b

15 ological anxiety likely results from altered GR signaling in glutamatergic circuits of several forebr

16 ogether, our results uncovered that although GR preferentially binds accessible chromatin, its bindin

17 thasone induces the recruitment of ACTN4 and GR to putative GREs in dexamethasone-transactivated prom

18 trations, as well as the detection of AR and GR activity for which there were limited or no correspon

19 at the dual targeting action of ES on AR and GR can be further translated to PCa therapy.

20 ed the intrinsic specificities of the AR and GR DNA-binding domains using a refined version of SELEX-

21 ng models help explain differences in AR and GR genomic binding and provide a biophysical rationale f

22 d that the DNA-binding preferences of AR and GR homodimers differ significantly, both within and outs

23 Py-Im polyamide interfered with both AR- and GR-driven gene expression, whereas enzalutamide interfer

24 eptor as assessed with synthetic ligands and GR mutants with impaired transcriptional abilities.

25 odified SPCEs, such as GR/SPCE, CMF/SPCE and GR-CMF/SPCE.

26 ZNF764- and GR-binding sites demonstrated similar distribution in va

27 ur results demonstrate the utility of IS and GRs in discriminating closely related Wolbachia strains.

28 icity of (GR)50, suggesting that (PR)50 and (GR)50 exert their toxicity through partially distinct me

29 Both (PR)50- and (GR)50-green fluorescent protein tagged dipeptides were p

30 verified that GCGR was the target of aptamer GR-3.

31 immunogenicity, and easy synthesis, aptamer GR-3 against GCGR can be a promising tool with the poten

32 kinase IKK2 inhibitors, including TPCA-1, as GR enhancers that improve the anti-inflammatory effect o

33 mmobilized different modified SPCEs, such as GR/SPCE, CMF/SPCE and GR-CMF/SPCE.

34 hromatin remodeling and robust GR binding at GR-binding sites associated with blocked genes.

35 , phospho-GRIP1 and CDK9 are not detected at GR transrepression sites near pro-inflammatory genes.

36 a median cumulative activity of 14.8 GBq at GR and 24.2 GBq at MSKCC (P < 0.0001).

37 ons associated with blocked genes but not at GR-binding regions associated with other GC-regulated ge

38 for GR occupancy and chromatin remodeling at GR-binding regions associated with blocked genes but not

39 was 86.8% and 78.8% for patients treated at GR and at MSKCC, respectively (P < 0.01).

40 der patients with micrometastases treated at GR and MSKCC, respectively (P = not significant).

41 f Dex in NF-kappaB repression by attenuating GR down-regulation.

42 Using a cell-based GR activity assay that measures Dexamethasone (Dex)-medi

43 an podocytes, we demonstrated that the basic GR-signalling mechanism is intact and that Gc induced an

44 ion of GR antagonists is problematic because GR is essential for life.

45 be analysed to uncover relationships between GR and its interactants.

46 cific effects and specifically how it blocks GR binding to some genes but not others is unclear.

47 We show that DEX-bound GR accelerates adipogenesis by directly promoting the ex

48 e wild-type cells, indicating that DEX-bound GR accelerates, but is dispensable for, adipogenesis.

49 Mechanistically, DEX-bound GR recruits histone H3K27 acetyltransferase CBP to promo

50 utamatergic or GABAergic neurons by breeding GR(flox/flox) mice to Nex-Cre or Dlx5/6-Cre mice, respec

51 This effect was not affected by GR ligand exposure, and occurred without significant GR

52 cal rationale for how promiscuous binding by GR allows functional substitution for AR in some castrat

53 r-proximal GR binding for genes regulated by GR across cell types than for cell type-specific target

54 ort of genes was differentially regulated by GR depending on the presence or absence of MDFIC.

55 ropose that cell type-specific regulation by GR preferentially occurs via distal enhancers, whose chr

56 expression, but not anxiety, is regulated by GRs in glutamatergic neurons of the BLA.

57 oward specific biologic pathways by changing GR binding and transcriptional activity on the glucocort

58 Identification of chemical GR modulators may provide insights into the regulatory m

59 ely transformed into chloride-green rust (Cl-GR) within 5 min and persisted over 18 days.

60 ting in increased Fe(III) contents in the Cl-GR.

61 Conversely, GR deficiency attenuated aging-/diet-associated obesity,

62 Pax8-Cre/GR(fl/fl) mice did not exhibit an overt spontaneous phen

63 ly in kidney epithelial cells using Pax8-Cre/GR(fl/fl) mice.

64 In culture, GR-deficient primary or immortalized white and brown pre

65 entify a new binding partner for cytoplasmic GR that modulates the receptor transcriptome and contrib

66 ion, siRNA-mediated IKK2 knockdown decreased GR down-regulation and increased GR expression.

67 s compromised in mice expressing a defective GR in the nonhematopoietic compartment or selectively la

68 equired for adipogenesis in vivo By deleting GR in precursors of brown adipocytes, we found unexpecte

69 Thus, ZNF764 is a cofactor directing GR transcriptional activity toward specific biologic pat

70 hroughput screening platform for discovering GR-modulating compounds that may be repurposed to improv

71 iding enzymatic protection against excessive GR activation in obesity.

72 the current model is insufficient to explain GR action at these sites.

73 in organisms where GR is natively expressed, GR likely contributes to stress responses through non-tr

74 explained partially by the presence of fewer GR recognition sequences, arguing for the existence of a

75 This work also represents the first GR structure in complex with SHP, which has been suggest

76 whereby PPARA levels are increased following GR activation, facilitating gradual enhancer maturation

77 FIC) was identified as a binding partner for GR.

78 Furthermore, CHD9 and BRM were required for GR occupancy and chromatin remodeling at GR-binding regi

79 n, suggesting a nontranscriptional route for GR to activate HIF signaling.

80 is highly effective, lack of selectivity for GR leads to unwanted side effects in some patients.

81 eralocorticoid receptor; MR) that encode for GRs and MRs, predicted cognitive performance.

82 ad a similar gene-expression profile as from GR pre-activation, while ameliorating the disruption of

83 d cadaverine contents discriminated PRs from GRs and HVs (Wilks' lambda = 0.499, P <0.012).

84 e under gastric conditions caused no further GR hydrolysis.

85 ces of the androgen (AR) and glucocorticoid (GR) receptors are virtually identical, yet these transcr

86 h source of the glucosinolate glucoraphanin (GR).

87 sequent year, therapeutic response was good (GR, n = 9) or poor (PR, n = 7; including five cigarette

88 end of carbon nanotubes (CNTs) and graphene (GR) was employed to enhance the surface area of the work

89 tolerance with evidence for enhanced hepatic GR signaling.

90 ggested to play a role in modulating hepatic GR function.

91 Interestingly, high GR expression or activation correlates with poor therape

92 radoxical findings can be reconciled and how GR ultimately shifts the balance to a net anti-inflammat

93 stance in yeast ectopically expressing human GR, which required expression of both the N-terminal tra

94 ty patients presenting Miller Class I and II GRs were previously treated by CTG (control group; n = 2

95 TG in the treatment of Miller Class I and II GRs.

96 t participants with single Miller Class I/II GRs were treated with CAF (n = 17), CAF + CM (n = 17), C

97 patients presenting one Miller Class I or II GRs were randomly assigned to receive either CAF (n = 17

98 Compared with laccase immobilized GR and CMF modified SPCEs, a well-defined redox couple o

99 laccase was observed at laccase immobilized GR-CMF composite modified SPCE.

100 functionally active ordered conformation in GR's ID AF1 domain.

101 and revealed an unexpected role for IKK2 in GR down-regulation.

102 This is the first report of PMGF in GR common waterhemp and the results are critical in expl

103 <0.01) and with CAL change after therapy in GR (R(2) = 0.49, P <0.05).

104 0.19 +/- 0.10 and 0.20 +/- 0.09 mumol/mg in GRs and HVs, but 0.07 +/- 0.03 mumol/mg in PRs (Kruskal-

105 n decreased GR down-regulation and increased GR expression.

106 urvival effect required Hsp104, and, indeed, GR expression increased Hsp104 expression.

107 9 (CDK9), which is recruited into GC-induced GR:GRIP1:CDK9 hetero-complexes, producing distinct GRE-s

108 regulation of a third gene set by inhibiting GR binding.

109 Hic-5 selectively inhibits GR interaction with CHD9 and BRM, thereby blocking chrom

110 Further, we found that an intact GR dimerization interface was a prerequisite for the sup

111 mutants lose their ability to bind liganded GR and support GRE-mediated transcriptional activity.

112 eport that, in breast cancer cells, liganded GR represses a large ERalpha-activated transcriptional p

113 Yet, when exposed to LPS, GR knockout podocytes demonstrated fewer stress fibers a

114 Mechanistically, GR and ACTN4 interact in the nucleus of HPCs.

115 nown which of these cell populations mediate GR actions that eventually regulate fear- and anxiety-re

116 Importantly, viral-mediated GR deletion additionally showed that fear expression, bu

117 macrophages, however, whether GRIP1 mediates GR-activated transcription, and what dictates its coacti

118 mobilized on graphene-cellulose microfibers (GR-CMF) composite modified screen printed carbon electro

119 ihydrocortisol is a novel pathway modulating GR activation and providing enzymatic protection against

120 d in both chGRKO mice and their Cre-negative GR(flox/flox) littermates [wild type (WT)].

121 ic GCs or a novel generation of nonsteroidal GR-targeting molecules, to meet the increasing clinical

122 emic glucose tolerance was improved in obese GR-deficient mice, which was associated with increased i

123 demonstrate that DEX-mediated activation of GR accelerates, but is dispensable for, adipogenesis.

124 The late activation of GR had a similar gene-expression profile as from GR pre-

125 to regulate the transcriptional activity of GR.

126 untering this mechanism by administration of GR antagonists is problematic because GR is essential fo

127 Here we show that site-specific blocking of GR binding is due to gene-specific requirements for ATP-

128 lated with a decreased lipolytic capacity of GR-deficient adipocytes under postabsorptive and fasting

129 The contents of GR, SF and SFN did not change after further digestion, a

130 How the conversion of GR and bioaccessibility of released breakdown products a

131 ng GC biology and the mechanistic details of GR-regulated transcription.

132 ritical in explaining the rapid dispersal of GR common waterhemp in Midwestern United States.

133 These findings parallel the distribution of GR and MR in primate brain and their putative roles in s

134 analyses revealed a marked global effect of GR deficiency on systemic metabolite abundance and, thus

135 or suppress the anti-inflammatory effect of GR function.

136 that improve the anti-inflammatory effect of GR.

137 (CT) dehalogenation by the chloride form of GR (GRCl) was tested in the presence of glycine (GLY) an

138 mechanisms of anti-inflammatory functions of GR and help improve GC-based therapy.

139 After hydrolysis of GR by the endogenous enzyme myrosinase, sulforaphane (SF

140 reduces dexamethasone-mediated induction of GR target genes and GRE-driven reporter activity without

141 Our findings point to the involvement of GR sensitivity as a potential key mechanism shaping resp

142 vealing an underlying molecular mechanism of GR-driven drug resistance, these data suggest that inhib

143 anism has served as the predominant model of GR-mediated transrepression of inflammatory genes.

144 ation via multiple mechanisms: modulation of GR ligands and induction of the long noncoding RNA Gas5,

145 ed chemical compounds as novel modulators of GR and revealed an unexpected role for IKK2 in GR down-r

146 Chromatin occupancy of GR was not predictive of Dex-regulated gene expression,

147 ell proliferation through down-regulation of GR and up-regulation of manganese superoxide dismutase a

148 adaptive and reversible due to regulation of GR expression by a tissue-specific enhancer.

149 These results clarify the role of GR in adipogenesis in vivo and demonstrate that DEX-medi

150 gated potential non-transcriptional roles of GR in cellular stress response using fission yeast as a

151 des both pro- and anti-inflammatory roles of GR, and a future challenge will be to understand how suc

152 erate a high-resolution crystal structure of GR in complex with the potent glucocorticoid triamcinolo

153 -independent mechanism involves tethering of GR to the pro-inflammatory transcription factor activato

154 xamethasone-induced nuclear translocation of GR.

155 Here, we use an ancestral variant of GR as a tool to generate a high-resolution crystal struc

156 mutations failed to modify the toxicity of (GR)50, suggesting that (PR)50 and (GR)50 exert their tox

157 the estrogen E2 program appears to depend on GR SUMOylation, which leads to stable trans-recruitment

158 well as the NF-kappaB (p65) binding sites on GR-transrepressed promoters such as IL-1beta, IL-6, and

159 rol epoxide and glucocorticoid metabolism or GR may be novel strategies to prevent and treat BC.

160 Expression of either (PR)50 or (GR)50 during development caused a highly penetrant devel

161 In vitro, prednisolone and the pharmacologic GR antagonist mifepristone each acted directly on primar

162 docytes isolated from wild type and podocyte GR knockout mice showed similar actin stress fiber stain

163 ither LPS or nephrotoxic serum, the podocyte GR knockout mice demonstrated worsened proteinuria compa

164 repeat proteins (DPR: poly GA, poly GP, poly GR, poly PA, and poly PR), which aggregate into neuronal

165 PA are sequestered by poly GA, whereas poly GR and poly PR are rarely co-localised with poly GA.

166 ents (less than 400 bp) containing potential GR and KLF binding sites were identified and examined fo

167 ind a higher percentage of promoter-proximal GR binding for genes regulated by GR across cell types t

168 Rather, GR activation resulted in genome-wide blockade of NF-kap

169 ite polymorphism and genomic rearrangements (GR).

170 our expectation, we found that GC receptor (GR) expression in immune cells was dispensable for succe

171 energy metabolism depend on the GC receptor (GR) in adipocytes remains unclear.

172 GCs work by activating the GC receptor (GR), a ligand-induced transcription factor, which in tur

173 Their target receptor, the GC receptor (GR), is a multi-tasking transcription factor, changing i

174 The glucocorticoid (GC) receptor (GR) suppresses inflammation by activating anti-inflammat

175 olecular effects of glucocorticoid receptor (GR) activation at a clinically relevant time point, afte

176 ined the effects of glucocorticoid receptor (GR) activation prior to inflammatory challenges.

177 androgen (AR), and glucocorticoid receptor (GR) activity, along with a broad suite of chemical analy

178 ption factors (TFs) glucocorticoid receptor (GR) and CREB within minutes and increases expression of

179 targeting of AR and glucocorticoid receptor (GR) and downstream pro-oxidant signaling.

180 The nonselective glucocorticoid receptor (GR) antagonist mifepristone has been approved in the U.S

181 ns of ZNF764 on the glucocorticoid receptor (GR) in HeLa cells as a model system.

182 y, interacting with glucocorticoid receptor (GR) in patients with chronic rhinosinusitis with nasal p

183 uous binding to the glucocorticoid receptor (GR) in T cells.

184 organization of the glucocorticoid receptor (GR) in the interphase nucleus of living cells.

185 interacts with the glucocorticoid receptor (GR) in the nucleus of human podocytes (HPCs), a key cell

186 The glucocorticoid receptor (GR) is a ligand-regulated transcription factor that cont

187 The glucocorticoid receptor (GR) is essential for the stress response in mammals.

188 The glucocorticoid receptor (GR) is the major receptor for the stress hormone cortiso

189 ta suggest that the glucocorticoid receptor (GR) is upregulated in this context, stimulating expressi

190 e podocyte-specific glucocorticoid receptor (GR) knockout mice had similar renal function and protein

191 d hormone-activated glucocorticoid receptor (GR) regulates cellular stress pathways by binding to gen

192 use it contains two glucocorticoid receptor (GR) response elements (GREs).

193 we inactivated the glucocorticoid receptor (GR) specifically in kidney epithelial cells using Pax8-C

194 ing ligands for the glucocorticoid receptor (GR) transcription factor.

195 c loci bound by the glucocorticoid receptor (GR), a hormone-activated transcription factor, show litt

196 e drugs bind to the glucocorticoid receptor (GR), a ligand-activated transcription factor and member

197 e fasting response: glucocorticoid receptor (GR), cAMP responsive element binding protein 1 (CREB1),

198 15 (KLF15) and the glucocorticoid receptor (GR), cooperate to stimulate productive infection and vir

199 ynthetic ligand for glucocorticoid receptor (GR), is routinely used to stimulate adipogenesis in cult

200 h by binding to the glucocorticoid receptor (GR), the nuclear receptor of endogenous cortisol.

201 r hormone receptor, glucocorticoid receptor (GR), which has similar DNA-binding specificity to the an

202 GCs)-ligands of the glucocorticoid receptor (GR)-are widely used to treat inflammatory diseases, but

203 nally, we show that glucocorticoid receptor (GR)-regulated genes are significantly enriched in this c

204 gonist of the human glucocorticoid receptor (GR).

205 ol, ligands for the glucocorticoid receptor (GR).

206 nancies through the glucocorticoid receptor (GR).

207 AR) blockade by the glucocorticoid receptor (GR).

208 on in genes, NR3C1 (glucocorticoid receptor; GR) and NR3C2 (mineralocorticoid receptor; MR) that enco

209 osing functions of glucocorticoid receptors (GRs) and estrogen receptor alpha (ERalpha) in breast can

210 uitously expressed glucocorticoid receptors (GRs), this steroid hormone has pleiotropic effects on ma

211 gingiva associated with gingival recession (GR) at baseline were treated with FGGs in a private prac

212 r treatment of localized gingival recession (GR) by a coronally advanced flap (CAF) combined with CM

213 LLLT in the treatment of gingival recession (GR) defects.

214 Gingival recession (GR) might be associated with patient discomfort due to c

215 exEq L(-1)); however, none of the recognized GR-active compounds on the target-chemical analyte list

216 This was paralleled by reduced GR-dependent electrophysiological responses in the basol

217 ng motif present in ACTN4 results in reduced GR interaction and dexamethasone-mediated transactivatio

218 appear to be required for ZNF764 to regulate GR transcriptional activity.

219 Thus, Hic-5 regulates GR binding site selection by a novel mechanism, exploiti

220 gene flow (PMGF) from glyphosate-resistant (GR) to -susceptible (GS) common waterhemp using a concen

221 gene flow (PMGF) from glyphosate-resistant (GR) to glyphosate-susceptible (GS) giant ragweed under s

222 we show that fasting or glucose restriction (GR) regulate PKA and AMP-activated protein kinase (AMPK)

223 teorhodopsin (PR) and Gloeobacter rhodopsin (GR) are retinal-based light-driven proton pumps that abs

224 eby blocking chromatin remodeling and robust GR binding at GR-binding sites associated with blocked g

225 fixed activity of 3.7 GBq at Gustave Roussy (GR, n = 231) or by personalized activity (2.7-18.6 GBq)

226 ered Fe(II)-Fe(III) hydroxides (green rusts, GRs) are promising reactants for reductive dechlorinatio

227 ated in the human glucocorticoid receptor's (GR's) ID AF1 domain.

228 wever, ChIP-seq data have consistently shown GR to occupy AP-1 response elements (TREs), even in the

229 morphisms of genes involved in GC signaling (GR, GLCCI1) and drug metabolism and transport (CYP3A5, A

230 d exposure, and occurred without significant GR nuclear accumulation.

231 Similarly, GR agonism was detected in 9/35 samples (range, 6.0-43 n

232 In vivo, T-cell-specific GR deletion in pregnant animals undergoing experimental

233 g tumor cortisol concentrations to stimulate GR and enzalutamide resistance.

234 PCa growth, suggesting that ES can suppress GR-induced resistant phenotype upon AR antagonism and th

235 identified several compounds that suppressed GR activity, including multiple GSK3beta inhibitors and

236 tion of drug candidates to minimize systemic GR activation.

237 inhalation combined with a moderate systemic GR-effect, assessed as thymic involution.

238 lated with more enthalpy-driven binding than GR.

239 h AR more sensitive to sequence changes than GR.

240 As such, there is consensus that GR deserves a second life as a drug target, with either

241 Given that GR almost exclusively binds accessible chromatin, we pro

242 They report that GR activation causes a global reduction in NF-kappaB bin

243 Single-molecule tracking revealed that GR increases the number and DNA residence time of a port

244 Binding analysis revealed that GR-3 could recognize other cells with different affinity

245 ogy and biochemical approaches, we show that GR binds directly to TREs via sequence-specific contacts

246 Finally, we show that GR directly represses the MDFIC gene, revealing a negati

247 Here, we show that GR regulates a subset of inflammatory genes in a DNA-bin

248 fixed genomic alterations, here we show that GR-mediated antiandrogen resistance is adaptive and reve

249 a paradigm shift in the field, showing that GR uses multiple mechanisms to suppress inflammatory gen

250 Hepatic tissue imaging suggested that GR-3 could bind the cell membrane of hepatic tissues.

251 brown adipocytes, we found unexpectedly that GR is dispensable for brown adipose tissue development i

252 The GR is widely recognized as a therapeutic target for its

253 onal studies demonstrated that KLF15 and the GR form a stable complex and that these stress-induced t

254 tion studies demonstrated that KLF15 and the GR were associated with each other in transfected cells.

255 hort region were stimulated by KLF15 and the GR.

256 binding and EZH2-mediated repression at the GR locus, but is restored in advanced prostate cancers u

257 l role for transcriptional regulation by the GR in this cell type.

258 the BoHV-1 genome are transactivated by the GR or stress-induced transcription factors.

259 Defining the GR-cistrome identified Gc regulation of motility genes.

260 c mouse model in which the gene encoding the GR is selectively deleted in NKp46(+) innate lymphoid ce

261 t tumors to Enz by selectively impairing the GR signaling axis via this enhancer.

262 utant line harboring a point mutation in the GR DNA-binding domain, suggesting a nontranscriptional r

263 ietic compartment or selectively lacking the GR in airway epithelial cells.

264 Mechanistically, the GR survival effect required Hsp104, and, indeed, GR expr

265 The ability of the GR and KLF15 to synergistically stimulate viral gene exp

266 However, genetic inactivation of the GR in kidney epithelial cells did not induce the immunos

267 essive GN), this genetic inactivation of the GR in kidney epithelial cells exerted renal benefits, in

268 of Tregs via differential engagement of the GR in T cells.

269 also reversed FPP-mediated induction of the GR target, the transcription factor c-Myc (a biomarker o

270 rticoids resulted in the dissociation of the GR-MDFIC complex.

271 To investigate the function of the GR-MDFIC interaction, we performed a genome-wide microar

272 ich leads to stable trans-recruitment of the GR-N-CoR/SMRT-HDAC3 corepressor complex on these enhance

273 omain, but not the DNA-binding domain of the GR.

274 Since the GR stimulates KLF15 expression, we suggest that these tw

275 mmunoprecipitation studies revealed that the GR and KLF15 interacted with sequences within IEtu1 GREs

276 In this study, we demonstrate that the GR and KLF15 were frequently expressed in the same trige

277 We conclude that the GR in adipocytes exerts central but diverging roles in t

278 -type mice, pharmacologic treatment with the GR antagonist mifepristone also attenuated disease as ef

279 re conducted in a concentric design with the GR giant ragweed pollen source planted in the center and

280 Importantly, this GR-assisted CREB1 binding was enhancer-selective and did

281 Thus, GR restricts actions of its own coregulator via CDK9-med

282 -related behavior can largely be ascribed to GR signaling in glutamatergic neurons of the BLA.

283 domain, and both its physical interaction to GR and zinc finger domain appear to be required for ZNF7

284 nt macrophages globally directs GRIP1 toward GR binding sites dominated by palindromic GC response el

285 vant timing highlights mechanisms underlying GR actions for modulating the "inflamed epigenome."

286 vestigated the complex mechanisms underlying GR functions.

287 hen differentiation was extended to 3 weeks, GR-deficient preadipocytes showed levels of adipogenesis

288 This suggests that in organisms where GR is natively expressed, GR likely contributes to stres

289 f chromatin and sequence in specifying where GR binds, we used Bayesian modeling within the universe

290 e operates through assisted loading, whereby GR doubles the number of sites occupied by CREB1 as well

291 However, it has remained unclear whether GR is required for adipogenesis in vivo By deleting GR i

292 Which GR-regulated genes are required for GC cytotoxicity, whi

293 MDFIC associated with GR in the cytoplasm of cells, and treatment with glucoco

294 with the strongest negative association with GR binding, but found that this correlation does not ref

295 To discover new proteins that interact with GR and modulate its function, we performed a yeast two-h

296 ZNF764 physically interacted with GR at ligand-binding domain through its KRAB domain, and

297 of additional mechanisms that interfere with GR binding at promoters.

298 lecular level, the interaction of MDFIC with GR altered the phosphorylation status of the receptor.

299 potential towards CC than SPCE modified with GR-CMF composite.

300 ed quality of life (OHRQoL) of patients with GR.