ライフサイエンスコーパス: GR

1 GR and KLF15 cooperate to stimulate bICP0 E promoter act

2 GR and KLF15 cooperatively stimulated bICP0 activity les

3 GR and KLF15, but not KLF4, occupied the bICP0 E promote

4 GR and KLF4, both pioneer transcription factors, coopera

5 GR antagonist mifepristone partially prevented CYP2R1 re

6 GR inhibition resensitized TLE3(KO) cells to enzalutamid

7 GR phases have high As uptake capacities at circum-neutr

8 GR seems to occupy a central position in the pathophysio

9 GR signaling transactivated the expression of multiple c

10 GR was also linked to extracellular superoxide productio

11 GR+ but not GR- HSCs and MkPs respond to GABA in patch c

12 GR, KLF4, and KLF15 occupied bICP0 E promoter sequences

13 GR-DBD adopts a discrete RNA-bound state, as assessed by

14 GR-DBD binds to a diverse range of RNA hairpin motifs, b

15 GR-MD-02 (belapectin) is an inhibitor of galectin 3 that

16 GRs typically consist of three subunits referred to as A

17 , PPD Reduction -0.397 mm (-0.810 to 0.015), GR Change 0.059 mm (-0.300 to 0.418), DBL Gain -0.250 mm

18 types IC-2489-88, M-633, MCP-632, HUJM 1080, GR-325 and DJ-65 recorded high NUE at low N.

19 in of such superior performance of Ni(OH)(2)-GR is attributed to its appropriate synergy on the enhan

20 (OH)(2) nanosheet arrays-graphene (Ni(OH)(2)-GR) composites exhibit superior photoactivity and select

21 A subunit of the Bacillus megaterium GerK(3) GR, revealing two distinct globular subdomains bisected

22 ly completed questionnaires (2,803 LR; 1,308 GR).

23 fects of Ppid upregulation were blocked by a GR antagonist.

24 they were incubated with medium containing a GR-specific antagonist (CORT-108297) or stripped fetal b

25 Treatment with dexamethasone, a GR activator, also induces changes in the pattern of alt

26 larvae is more like that of larvae lacking a GR than that of larvae with a GR, suggesting that the co

27 rvae lacking a GR than that of larvae with a GR, suggesting that the cortisol-treated larvae develop

28 The activated GR stimulates expression of, and interacts with, KLF15;

29 ne expression is stimulated by the activated GR.

30 -0.24 cm/y), and tumors with MET activation (GR, 0.15 cm/y; IQR, 0.053-0.32 cm/y; P < .001).

31 zed cellular and behavioral hallmarks of AD, GR signaling pathways, processing of amyloid precursor p

32 o account in the further design of adipocyte GR-selective modulators.

33 ogether, our results indicate that adipocyte GR is a key factor of adipose tissue expansion and gluco

34 otif on YJH08 is essential for high-affinity GR binding in vitro, high tissue uptake in vivo, and eff

35 anti-oxidative defence system (SOD, CAT, and GR) and Ver-1 gene of aflatoxin B(1) biosynthesis.

36 fasting, suggesting that glucocorticoids and GR contribute to the CYP2R1 repression during fasting.

37 ce, alpha-GA(1) reduced GA as well as GP and GR proteins, improved behavioral deficits, decreased neu

38 nvolved both in Tau hyperphosphorylation and GR activation.

39 1-4 (AtGRP7/2/4/8) RNA recognition motif and GR domains.

40 ly than GR and KL4: however, KLF6, PLZF, and GR had little effect on the bICP0 E promoter.

41 nistic and antagonistic effects on PPARG and GR, and mainly antagonistic, except for PCB153, effects

42 Depletion of PAF1C reduces RNA and GR dipeptide production from (G4C2)(30+) transgenes.

43 e stress by increasing GT, CAT, POD, SOD and GR activities and reducing GSSG.

44 nd that combination treatment with STAT3 and GR inhibitors could provide synergistic therapeutic effi

45 er through rational combination of STAT3 and GR inhibitors.

46 Treatment of these cells with the anti-GR agent mifepristone showed that they were more sensiti

47 at proteins (R-DPRs), poly-glycine arginine (GR) and poly-proline arginine (PR), and are protective i

48 glucocorticoid receptor NR3C1 (also known as GR) forms tetramers on enhancers, owing to an allosteric

49 More importantly, these new insights into As-GR interaction mechanisms highlight the impact of GR pha

50 ption sites of both As(III) and As(V) are at GR crystal edges.

51 ditional targeting of TFs that include ATF3, GR, and PREP1.

52 imary repression through cooperation between GR and NF-kB at a subset of regulatory regions.

53 ing from transcriptional cooperation between GR and NF-kB.

54 so occurs through local interactions between GR and inflammatory gene regulatory elements has been co

55 e bonding and interaction mechanisms between GR sulfate and As species [As(III) and As(V)] under anox

56 nd phenotypic evidences that a single bitter GR is a major factor affecting the insect feeding prefer

57 of GR (cardioGRKO), MR (cardioMRKO), or both GR and MR (cardioGRMRdKO).

58 s blocked by the GR antagonist RU-486 and by GR siRNA transfection and that DPP4 enzyme activity is r

59 from those under transcriptional control by GR, suggesting an additional mechanism of glucocorticoid

60 n of hepatic glucose and lipid metabolism by GR, and that loss of E47 prevents the development of hyp

61 ary study outcomes were changes in PPD, CAL, GR, and bone fill.

62 transcriptional induction through canonical GR binding sites is associated with reciprocal repressio

63 terials such as polymer/GR, activated carbon/GR, metal oxide/GR, metal/graphene and carbon fibre/GR h

64 er lymphoid tissues is independent of B cell GRs.

65 Whether and how concurrent GR and neurotrophin signaling integrate to modulate syna

66 PR/Cas9 gene editing to create a conditional GR knockdown in Sprague Dawley rats.

67 ses are likely caused, in part, by decreased GR and cytokine induction of C/EBP and NF-kappaB transcr

68 morphism Val66Met disrupt the BDNF-dependent GR-PO(4) pathway necessary for preserving training-induc

69 ing that the cortisol-treated larvae develop GR resistance.

70 paired Dexamethasone (Dex)-stimulated direct GR-dependent gene up- and down-regulation.

71 The enhanced GR turnover observed in beta-arrestin-1-deficient cells

72 Epithelial GR-null mice had elevated expression of proinflammatory

73 in vitro bioactivities (e.g., agonism of ER, GR, and PPARgamma) and BC concentrations; fathead minnow

74 Following the WWTP replacement, ER, GR, and PPARgamma bioactivities were reduced by approxim

75 omoter by two pioneer transcription factors (GR and KLF4) correlates with stimulating lytic cycle vir

76 Two pioneer transcription factors, GR and Kruppel-like transcription factor 4 (KLF4), coope

77 al oxide/GR, metal/graphene and carbon fibre/GR have been investigated in more detail.

78 R)- and (S)-enantiomers are equally avid for GR by occupying discrete binding modes.

79 contains enhancer-like domains necessary for GR- and KLF4-mediated transactivation that are distinct

80 sactivation that are distinct from those for GR and KLF15.

81 Furthermore, GR and dexamethasone stimulate productive infection and

82 Furthermore, GR and KLF4 stimulated productive infection.

83 Furthermore, GR binding was observed proximal to TLE3/AR-shared genes

84 ent GT was found to inversely predict future GR.

85 Mutating both half GR binding sites did not significantly reduce GR- and KL

86 age was independently associated with higher GR (P = .005).

87 y key transcription factors including HNF4A, GR, STAT3 and STAT5, which show specific binding at enha

88 Altogether, our results illustrate how GR and E47 regulate hepatic metabolism, and might provid

89 We show how GR partitions metabolic processes by time-dependent targ

90 Thirty-six patients with Miller Class I GR defects were randomly assigned to be treated by eithe

91 ocked rhythmic CXCL5 production, identifying GR as required to confer circadian control to CXCL5.

92 h contributing a single Miller Class I or II GR defect, were treated by CAF+CTG (control; n = 19) or

93 gest that many RNAs have potential to impact GR biology.

94 al that Akt1 and Ak2, but not Akt3, impaired GR- and dexamethasone-mediated transactivation of the Bo

95 was insufficient evidence of a difference in GR reduction between acellular dermal matrix grafts (ADM

96 nced by the lack of circadian rhythmicity in GR-deficient B cell counts normally associated with diur

97 refrontal cortex (PFC), particularly rich in GR, early altered in AD and involved in HPA axis control

98 al regulator that was both underexpressed in GR(369-) larvae and consistently overexpressed in cortis

99 There were significant differences in GRs when stratified by genetic alteration.

100 ta reveal four common glucocorticoid-induced GR binding sites (GBSs).

101 ER (24 ng 17beta-estradiol equivalents/L)-, GR (60 ng dexamethasone equivalents/L)-, and PPARgamma-m

102 criptional repression does not require local GR occupancy.

103 ary transcriptional repression without local GR occupancy and secondary anti-inflammatory effects res

104 Here we mapped GR's chromatin occupancy in mouse livers throughout the

105 results in the treatment of single maxillary GRs.

106 BAP1-deficient tumors had the fastest median GR (0.6 cm/y; interquartile range [IQR], 0.57-0.68 cm/y)

107 stress signaling in the heart to favor more GR and less MR activity may provide an improved approach

108 uninfected, TG contained significantly more GR-positive neurons following explant when treated with

109 may be used for treating single or multiple GR.

110 R-Cas9 to produce a new frameshift mutation, GR(369-), which eliminates all potential in-frame initia

111 GR+ but not GR- HSCs and MkPs respond to GABA in patch clamp studies

112 causes cardiac aging via impairing the Nrf2-GR pathway.

113 presence of putative homologs to T. oceanica GR in other representative marine phytoplankton and ocea

114 assigning 87.20% of AR binders and 96.81% of GR binders in a 25% test set using holdout cross-validat

115 Our study highlights that ablation of GR in the hindbrain results in excessive barbering, obse

116 tathione, the preferred electron acceptor of GR.

117 e focus in on the industrial applications of GR nanocomposite, including super capacitors, biosensors

118 gently needed to elaborate the complexity of GR signaling in normal physiology and human disorders, a

119 mice with cardiomyocyte-specific deletion of GR (cardioGRKO), MR (cardioMRKO), or both GR and MR (car

120 Deletion of GR in myeloid cells alone did not prevent circadian vari

121 However, deletion of GR in the bronchial epithelium blocked rhythmic CXCL5 pr

122 tagonist propranolol abolished the effect of GR agonist administration into the PrL on memory enhance

123 ndomized trial of the safety and efficacy of GR-MD-02 in patients with NASH, cirrhosis, and portal hy

124 In this pilot study, the expression of GR isoforms and MKP-1 corresponded with patients' clinic

125 teraction mechanisms highlight the impact of GR phases on As sequestration in anoxic subsurface envir

126 e, 15 demonstrated substantial inhibition of GR transcriptional activity in the GR positive HCC1806 t

127 migration, and siRNA-mediated knockdowns of GR and DPP4 blocked dexamethasone-induced THP1-MPhi migr

128 -YJH08 PET to make the first measurements of GR expression in human subjects.

129 entify the bHLH factor E47 as a modulator of GR target genes.

130 ace between the two subdomains in the NTD of GR A subunits serves as the germinant binding site and p

131 oth reduced direct transcriptional output of GR whereas p300 overexpression and NFkappaB inhibition r

132 thermore, cardiac-specific overexpression of GR prevented excessive oxidative stress, apoptosis, and

133 GCs enhanced phosphorylation of GR at Ser211 and TGF-beta-induced ACTA2 expression.

134 7 is needed for the efficient recruitment of GR and coregulators such as Mediator to chromatin.

135 Thus, we find that the dual regulation of GR by PI3K and PTEN functions as a rheostat that can be

136 rn of 12 genes involved in the regulation of GR signaling in two African populations of heavily traum

137 portant for the gene regulatory responses of GR.

138 However, the precise role of GR in the pathophysiology of AD remains unclear.

139 f anxiety and depression, though the role of GR signalling in the hindbrain remains poorly characteri

140 oscillating genes are bound by and depend on GR.

141 ET that engages the ligand binding domain on GR.

142 determine the de facto As binding nature on GR surfaces.

143 e duration of the glucocorticoid response on GR target genes.

144 designs effectively improved RECH and VAL on GR defects.

145 One GR cofactor that interacted significantly less with the

146 polymer/GR, activated carbon/GR, metal oxide/GR, metal/graphene and carbon fibre/GR have been investi

147 he HPA axis and a feed-forward effect on PFC GR sensitivity could participate in the etiology of AD,

148 The two enriched in arginine, poly(GR) and poly(PR), infiltrate liquid-like nucleoli, co-lo

149 TD is dipeptide repeat proteins such as poly(GR), whose toxicity has been well documented in cellular

150 itochondrial protease YME1L in clearing poly(GR), revealing mitochondria as major sites of poly(GR) m

151 ginine-rich dipeptide repeats (R-DPRs), poly(GR) and poly(PR).

152 However, it is not known how poly(GR) toxicity can be alleviated, especially in patient ne

153 However, poly(GR) translation on mitochondrial surface is frequently s

154 , inducing ectopic Atp5a1 expression in poly(GR)-expressing neurons or reducing poly(GR) level in adu

155 Low-level poly(GR) expression induced FTD/ALS-associated synaptic dysfu

156 evealing mitochondria as major sites of poly(GR) metabolism.

157 established an inducible mouse model of poly(GR) toxicity in which (GR)(80) gradually accumulates in

158 tified a number of genetic modifiers of poly(GR) toxicity.

159 w that CAT-tailing-like modification of poly(GR), a dipeptide repeat derived from amyotrophic lateral

160 CTE promotes poly(GR) stabilization, aggregation, and toxicity.

161 poly(GR)-expressing neurons or reducing poly(GR) level in adult mice after disease onset rescued poly

162 adult mice after disease onset rescued poly(GR)-induced neurotoxicity.

163 pinges on the RQC machinery to restrain poly(GR) accumulation, at least in part through the AKT/VCP a

164 chondria-targeting signal, causing some poly(GR) to be cotranslationally imported into mitochondria.

165 ssential DNA repair protein, suppressed poly(GR)-induced retinal degeneration in flies.

166 an (Lilli) activity strongly suppresses poly(GR) toxicity by specifically downregulating the transcri

167 We find that poly(GR) can act as a mitochondria-targeting signal, causing

168 the cytoplasm, whereas for poly-PR and poly-GR, several toxicity pathways have been proposed.

169 city associated with two of these DPRs, poly-GR and poly-PR, has been associated with nucleocytoplasm

170 e measured nuclear import and export in poly-GR or poly-PR expressing Hela cells, neuronal-like SH-SY

171 To investigate the causal role of poly-GR or poly-PR on active nucleocytoplasmic transport, we

172 h three are known to be toxic: poly-PR, poly-GR, and poly-GA.

173 anic and polymeric materials such as polymer/GR, activated carbon/GR, metal oxide/GR, metal/graphene

174 Tumor growth rates (GR) were calculated and patients were stratified by gene

175 In the As(III)-reacted GR sulfate, no secondary Fe-As phases were observed.

176 like morphology, formed in the As(V)-reacted GR sulfate and acts as an additional immobilization path

177 Furthermore, group cross-reactive (GR)-antibody-ablated homologous fusion peptide-mutated (

178 t in BMC from mice in which the GC receptor (GR) was deleted in stromal cells/osteoblasts.

179 ransrepression functions of the GC receptor (GR), whereas the activation of its GC-induced indirect t

180 The glucocorticoid receptor (GR) agonist RU 28362 administered into the PrL, but not

181 The glucocorticoid receptor (GR) and KLF15 form a feed-forward transcription loop tha

182 lear receptors, the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), both of which a

183 s hormone-activated glucocorticoid receptor (GR) and neurotrophic factor release.

184 hydroxylase (Th)], glucocorticoid receptor (GR) and plasma corticosterone, as well as brain-derived

185 Glucocorticoid receptor (GR) and STAT3 bind to the same genomic regulatory region

186 roids targeting the glucocorticoid receptor (GR) are the current standard of care but drive adverse s

187 n receptor (AR) and glucocorticoid receptor (GR) binding using ToxCast data.

188 The glucocorticoid receptor (GR) binds the noncoding RNA Gas5 via its DNA-binding dom

189 Activation of the glucocorticoid receptor (GR) by the synthetic corticosteroid dexamethasone (DEX)

190 Ligand-activated glucocorticoid receptor (GR) elicits variable glucocorticoid-modulated transcript

191 ls of expression of glucocorticoid receptor (GR) encoded by NR3C1.

192 dient of increasing glucocorticoid receptor (GR) expression and signaling from naive to dysfunctional

193 orter 1 (GLUT1) and glucocorticoid receptor (GR) expression in response to Delta9-THC exposure.

194 olocalized with the glucocorticoid receptor (GR) in BLA neurons and found that the extinction-facilit

195 ess the role of the Glucocorticoid Receptor (GR) in such programming, we used CRISPR-Cas9 to produce

196 The glucocorticoid receptor (GR) is a potent metabolic regulator and a major drug tar

197 PI3Ks act to reduce glucocorticoid receptor (GR) levels, which are rescued by loss of PTEN protein-ph

198 rticosterone to the glucocorticoid receptor (GR) ligand, corticosterone.

199 Bmal1 regulated glucocorticoid receptor (GR) recruitment to the neutrophil chemokine, CXC chemoki

200 ains two functional glucocorticoid receptor (GR) response elements (GREs) that have the potential to

201 s approximately 100 glucocorticoid receptor (GR) response elements (GREs).

202 ve methods to study glucocorticoid receptor (GR) signaling are urgently needed to elaborate the compl

203 e activation of the glucocorticoid receptor (GR) stimulates productive infection and promoters that d

204 arch has linked the glucocorticoid receptor (GR) to memory processes, and to risk and symptoms of pos

205 o activation of the glucocorticoid receptor (GR), a pioneer transcription factor.

206 2) Glucocorticoid receptor (GR), an immunity-modulating transcription factor (TF), i

207 ion function of the glucocorticoid receptor (GR), and could therefore be a selective glucocorticoid r

208 ptor gamma (PPARG), glucocorticoid receptor (GR), and thyroid hormone receptor beta (THRB), when expo

209 r cognate receptor, glucocorticoid receptor (GR), is expressed in nearly all immune cells.

210 ed on the adipocyte glucocorticoid receptor (GR), its precise role in the molecular mechanisms of the

211 d activation of the glucocorticoid receptor (GR), stimulates viral gene expression and productive inf

212 gen-receptor (ER)-, glucocorticoid receptor (GR)-, and peroxisome proliferator-activated receptor-gam

213 Glucocorticoid receptor (GR)-alpha phosphorylated at serine 226 was increased in

214 nflammatory pathway glucocorticoid receptor (GR)-annexin A1 (ANXA1) occurs.

215 is from single-copy glucocorticoid receptor (GR)-regulated transcription sites (TSs) under pulsed (ul

216 levels activate the glucocorticoid receptor (GR).

217 ive effects via the glucocorticoid receptor (GR).

218 d repressors of the glucocorticoid receptor (GR).

219 protein (CREB), and glucocorticoid receptor (GR).

220 their receptor, the glucocorticoid receptor (GR).

221 ich act through the glucocorticoid receptor (GR).

222 udies investigating Glucocorticoid Receptor (GR/NR3C1) in the brain have primarily focused on the for

223 sphorylation of the glucocorticoid receptor (GR:NR3C1) and activation of NR4A1 was analyzed by wester

224 ncodes a putative bitter gustatory receptor (GR) that is responsible for the mulberry-specific feedin

225 Glucocorticoid receptors (GR) have diverse functions relevant to maintenance of ho

226 orticoids (GC) and glucocorticoid receptors (GR) signaling impairment.

227 in of mice lacking glucocorticoid receptors (GRs) specifically in B cells, we show that reduced CXCR4

228 ant Receptors (ORs) and Gustatory Receptors (GRs) together represent one of the largest families of l

229 ment of single maxillary gingival recession (GR) defects.

230 periodontal support and gingival recession (GR).

231 attachment level [CAL], gingival recession [GR]) and radiographic (defect Bone level [(DBL)] paramet

232 coverage (3,539 treated gingival recessions [GRs]), and 10 for non-root coverage procedures (699 tota

233 R binding sites did not significantly reduce GR- and KLF4-mediated transactivation of the bICP0 E pro

234 nd Akt2, but not Akt3, significantly reduced GR-mediated transactivation of the BoHV-1 immediate earl

235 ic network by vamorolone selectively reduces GR-driven transactivation while leaving transrepression

236 e dismutase (SOD) and glutathione reductase (GR) activities, which led to a marked reduction in fluor

237 equence similarity to glutathione reductase (GR) was implicated in this process.

238 line with this, inhibition of GSH reductase (GR), the enzyme responsible for GSH recycling, promoted

239 results in terms of CAL gain, PPD reduction, GR increase and DBL gain in comparison with the EMD+ABG

240 pulsars are affected by general relativity (GR), causing the spin axis of each pulsar to precess.

241 containing pine sawdust (PS), grape residue (GR), cotton cake (CC) and jatropha seed cake (JC).

242 aire for Labrador (LR) and Golden retriever (GR) owners to evaluate canine skin health with respect t

243 of AGO2 is enriched with arginine-glycine RG/GR repeats, which are methylated by protein arginine met

244 ly ten times higher compared to L. rhamnosus GR-1.

245 In Arabidopsis, AtSRBP1 is a glycine-rich (GR) RNA-binding protein, also known as AtGRP7, which we

246 Highlighting the dominant role GR plays in synchronizing circadian amplitudes, we find

247 "Green rust" (GR), a redox-active Fe(II)-Fe(III) layered double hydrox

248 Treatment with a selective GR modulator (sGRm) normalized plasma GC levels and all

249 ture design of partial agonists as selective GR modulators with an improved therapeutic index.

250 disorders, as well as to identify selective GR modulators to treat diseases.

251 erapies, the beneficial effects of selective GR modulators are now being explored.

252 These new data show GR is required to confer circadian control to some infla

253 Tumors from the same patient had similar GRs.

254 test the impact of cell- and region-specific GR knockdown on physiology and behavior, we targeted GR

255 erstanding the importance of tissue-specific GR function in physiology and behavior has been hampered

256 echanistically, Klotho deficiency suppressed GR (glutathione reductase) expression and activity in th

257 ors and genetic risk of type 2 diabetes (T2D-GR), captured by genetic risk score (GRS) and family his

258 s with the healthiest lifestyle and high T2D-GR was 2.24 (95% confidence interval (CI): 1.76, 2.86);

259 ith the least healthy lifestyle and high T2D-GR, it was 8.72 (95% CI: 7.46, 10.19).

260 ute risk reduction among those with high T2D-GR.

261 with the least healthy lifestyle and low T2D-GR, it was 4.05 (95% CI: 3.56, 4.62); and for participan

262 ts with the healthiest lifestyle and low T2D-GR, the relative risk of T2D for participants with the h

263 We defined 2 categories of T2D-GR: high GRS (upper one-third) with FH and low GRS or wi

264 down on physiology and behavior, we targeted GR knockdown to output neurons of the prelimbic cortex.

265 mulated bICP0 activity less efficiently than GR and KL4: however, KLF6, PLZF, and GR had little effec

266 romoter activity but significantly less than GR and KLF4.

267 te whales, polar bears, and humans, and that GR-LBD is identical in killer whales and minke whales an

268 This study demonstrates that GR and STAT3 cooperate to activate the canonical gene ex

269 This study demonstrates that GR and STAT3 cooperate to regulate the basal-like breast

270 binding study where we have determined that GR-DBD is a robust structure-specific RNA-binding domain

271 ith chronic cortisol treatment, we find that GR mediates most of the effects of the treatment, and pa

272 We found that GR directly induces DPP4 gene expression by binding to t

273 (E) promoter, we tested the hypothesis that GR and KLF family members transactivate the bICP0 E prom

274 ith several recent reports that suggest that GR expression is an alternative signaling mechanism that

275 ally binds to UBR1, strongly suggesting that GR is a physiological substrate of the Arg/N-degron path

276 The GR-ANXA1 pathway is a pathological player and a candidat

277 The GR/beta-arrestin-1 interaction uncovered here may help u

278 erated form CpdX-D3 selectively activate the GR indirect transrepression function and are as effectiv

279 Although the GR had little effect on ICP0 promoter activity alone, th

280 nsequently, these data suggest KLF15 and the GR form a feed-forward loop that activates viral gene ex

281 the exact interaction mechanism between the GR phases and As species is still poorly understood.

282 id-induced DPP4 expression is blocked by the GR antagonist RU-486 and by GR siRNA transfection and th

283 In transfected or infected cells, the GR and KLF15 occupied ICP0 sequences important for trans

284 High levels of methylation in the GR gene (nuclear receptor subfamily 3, group C, member 1

285 bition of GR transcriptional activity in the GR positive HCC1806 triple negative breast cancer xenogr

286 Conditional deletion of the GR in CD8(+) TILs improved effector differentiation, red

287 lvement of the C-terminal alpha-helix of the GR-DBD in RNA-binding.

288 Cav1) as a direct interaction partner of the GR.

289 and through this mechanism, they repress the GR transcriptional network both in cultured cells and in

290 Cellular-based studies revealed the GR domain as being necessary and sufficient for SRBP1 ce

291 -mapping (BioID), however, revealed that the GR interactome was strongly modulated by TNF.

292 iption factor 15 (KLF15) cooperated with the GR to stimulate promoter activity in transfected cells.

293 IQR, 0.25-0.57 cm/y), FLCN-deficient tumors (GR, 0.10 cm/y; IQR, 0.04-0.24 cm/y), and tumors with MET

294 .68 cm/y), followed by VHL-deficient tumors (GR, 0.37 cm/y; IQR, 0.25-0.57 cm/y), FLCN-deficient tumo

295 observed that beta-arrestin-1 and unliganded GR interact in the cytoplasm and that, following glucoco

296 to study AR-null cells that have upregulated GR to sustain growth.

297 e mouse model of poly(GR) toxicity in which (GR)(80) gradually accumulates in cortical excitatory neu

298 While GR is known to play integral roles in circadian biology,

299 promoter sequences lack a consensus "whole" GR response element (GRE) but contain putative half-GREs

300 hat reduced CXCR4 expression associated with GR deficiency results in impaired homing of mature B cel