ライフサイエンスコーパス: ERG

1 ERG abnormalities appear to be associated with the sever

2 ERG abnormalities were related to demographics and uveit

3 ERG cone and rod luminance response functions were recor

4 ERG inhibitory peptides (EIPs) and derived peptidomimeti

5 ERG results are consistent with the structural analyses

6 ERG results are frequently affected in cases of noninfec

7 ERG's homeostatic function is lineage-specific, because

8 ERGs can be performed in vivo or alternatively using an

9 ERGs of the total 355 uveitis eyes were measured accordi

10 ERGs recorded after mice Kir7.1 suppression by shRNA, or

11 ERGs showed abnormalities in 235 eyes (66.2%).

12 13.12 (near PCIF1/MMP9/ZNF335), and 21q22.2 (ERG).

13 r TMPRSS2 (transmembrane protease, serine-2):ERG fusion-positive human prostate epithelial cancer cel

14 nction is lineage-specific, because aberrant ERG expression in cancer is oncogenic.

15 Specifically, delays in dark-adapted ERG oscillatory potential (OP) implicit times in respons

16 lternatively aid in generating a stand-alone ERG set-up without a patch-rig.

17 Transretinal signaling was recorded as an ERG from the superfused murine retina isolated from wild

18 Further, we discuss how to configure an ERG system without a patch-clamp rig.

19 rachloride (CCL4)-induced fibrogenesis in an ERG-dependent manner in mice.

20 age, but the resting retinal blood flow and ERG parameters remained unchanged.

21 Comparison of SPOP-mutant and ERG-fusion organoid models showed evidence of divergent,

22 on of the oncogenic driver genes AR, MYC and ERG.

23 OCT and ERG parameters, as well as AO-SLO cone densities, were s

24 the interstitial regions between TMPRSS2 and ERG Identifying these patients at biopsy might improve p

25 cancer associated genes such as TMPRSS2 and ERG show similar expression patterns.

26 tral domain optical coherence tomography and ERG.

27 Taken together, our results revealed an AR-ERG-centric higher-order chromatin structure that drives

28 single nucleotide polymorphisms (SNPs) at AR-ERG co-binding sites participating in chromatin interact

29 d functional data analysis, we found that AR-ERG interaction hub regions are characterized by distinc

30 nnected near protein-coding genes through AR-ERG looping.

31 ardiovascular disease and other diseases, at ERG endothelial enhancers and super-enhancers.

32 ssociated single nucleotide polymorphisms at ERG super-enhancers suggests that ERG-dependent transcri

33 ring triggering stimuli appears to attenuate ERG currents, leading to membrane potential depolarizati

34 The EIPs attenuated ERG-mediated transcription, chromatin recruitment, prote

35 In neuronal ensembles, attenuating ERG enhanced signal-to-noise ratios and reduced signal c

36 Np73/TAp73 expression ratio; and ID1, BAALC, ERG, and KMT2E gene expression levels, we modeled ISAPL

37 up B and no significant associations between ERG abnormalities and anatomical classification or speci

38 des (EIPs) and derived peptidomimetics bound ERG with high affinity and specificity, leading to prote

39 Pten loss that yields oncogenic activity by ERG.

40 l cells, this enhancer was normally bound by ERG, which was also required for arterial HEY2 expressio

41 cGMP synthesis was significantly elevated by ERG in PCa cells, leading to increased PKG activity and

42 peared less severe than the other mutants by ERG at adult ages.

43 ) was directly and specifically regulated by ERG in vitro and in vivo and was significantly associate

44 e in the process of prostate carcinogenesis, ERG knockout in established prostate cancer organoids di

45 peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K(+) channels in carbon monoxide-induced pr

46 arsenal with an interchangeable patch-clamp/ERG system.

47 aviour is comparable between normal and cone ERG(absent) RPGRIP1 (ins/ins) littermates.

48 Immunohistochemically, cone ERG(absent) RPGRIP1 (ins/ins) retinas have extensive L/M

49 Despite marked changes in cone ERG and retinal morphology, photopic vision-guided behav

50 Cone morphology of the dogs lacking cone ERG are truncated with shortened outer and inner segment

51 proaches demonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (which encode

52 ustains ERG+85-positive cells by controlling ERG ubiquitination.

53 Decreased ERG expression also correlates with EndMT in tissues fro

54 ina, we found early functional deficiencies (ERG) without photoreceptor cell (PRC) death and identifi

55 terations including iAMP21, IKZF1 deletions, ERG deletions, PAX5(AMP), which have clinical significan

56 Mechanistic studies of deregulated ERG in prostate cancer and other cancers continue to enh

57 ween the number of injections and diminished ERG responses, such that on average each intravitreous m

58 These tumors also frequently displayed ERG gene fusions involving alternative 5'-partners to TM

59 Three chemically diverse ERG channel blockers (terfenadine, ErgToxin-1, and E-403

60 An electronegative ERG was present in 4 patients (50%), but with additional

61 Electroretinogram (ERG) and optical coherence tomography of Erdj5-/- and P2

62 inal inflammation, and an electroretinogram (ERG) illustrated decreased amplitude of the b wave in bo

63 of 25 pmol MTX increased electroretinogram (ERG) response and rhodopsin level in the retinae of Rho(

64 - and b-wave responses of electroretinogram (ERG) are abolished.

65 Recordings of electroretinogram (ERG) oscillatory potentials and scotopic threshold respo

66 e opsin, loss of photopic electroretinogram (ERG) responses and loss of cone cells.

67 elective reduction of the electroretinogram (ERG) b-wave.

68 The electroretinogram (ERG) has proved to be a valuable tool to investigate psy

69 rkedly reduced or absent electroretinograms (ERG).

70 Electroretinograms (ERGs) can detect the associated light-induced extracellu

71 ther variability in cone electroretinograms (ERGs) ranging from normal to absent in an extended RPGRI

72 ce have severely reduced electroretinograms (ERGs) and progressive photoreceptor degeneration, which

73 ular contributions using electroretinograms (ERGs).

74 emonstrated by a lack of electroretinograph (ERG) response.

75 yperoxia; and on day 3, electroretinography (ERG) was performed.

76 y clinical findings and electroretinography (ERG) on 244 evaluable injections in 63 patients using 30

77 n microscopy (TEM), and electroretinography (ERG) were used to analyze 6 genotypes including WT at th

78 impaired as assessed by electroretinography (ERG).

79 By conducting electroretinography (ERG) recordings in live ndufs4 (-/-) mice, we now demons

80 tis by using full-field electroretinography (ERG) and correlate the ERG to disease duration and sever

81 assessed by full-field electroretinography (ERG) and fundus-controlled perimetry, and genotype.

82 Full-field electroretinography (ERG) and spectral-domain OCT were performed in all the s

83 ation, full-field flash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-

84 However, electroretinography (ERG) studies in humans and rodents have revealed that re

85 D optical cryo-imaging, electroretinography (ERG), spectral-domain optical coherence tomography (SD-O

86 oth were appreciated in electroretinography (ERG).

87 tofluorescence and OCT, electroretinography (ERG), and both microscopy and molecular genetic testing.

88 d scotopic and photopic electroretinography (ERG) responses in mice at 3 months of age, with nearly c

89 Scotopic electroretinography (ERG) showed a diminished c-wave amplitude in the CLN5 de

90 neration using scotopic electroretinography (ERG), optical coherence tomography (OCT), and immunohist

91 n of these mice through electroretinography (ERG).

92 ckness were found using electroretinography (ERG), fundus photography (FP), fundus fluorescein angiog

93 Here, we show that inducible endothelial ERG deletion (Erg(iEC-KO)) in mice is associated with sp

94 Boosting the immune response enhances ERG proliferation, but not addition of TH(+) neurons.

95 irm that this network of genes requires ERK, ERG and p300 activity.

96 ic transcripts-such as those involving ETV4, ERG, RSPO3, and PIK3CA-can be generated by gene-intergen

97 of human SPOP-mutant cancers do not express ERG.

98 ransformation-specific) transcription factor ERG (ETS-related gene) is essential for endothelial home

99 Here we identify the transcription factor ERG as a key regulator of endothelial Notch signalling.

100 ormation-specific (ETS) transcription factor ERG in prostate cells.

101 The transcription factor ERG is essential to maintain endothelial homeostasis.

102 MT in liver disease.The transcription factor ERG is key to endothelial lineage specification and vasc

103 , the gene encoding the transcription factor ERG is recurrently rearranged and plays a critical role

104 The transcription factor ERG promotes endothelial homeostasis via regulation of l

105 d activation of the ETS transcription factor ERG, a prerequisite for DLL4 induction.

106 o overexpression of the transcription factor ERG, while a mutually exclusive 10% of prostate cancers

107 erimetry results, and with normal full-field ERG recordings.

108 into P23H-3 rats, analysis of the full-field ERG suggested that overexpression of ERdj5 reduced visua

109 We find ERG mediates the late phase of spike-frequency adaptatio

110 In accordance with this finding, ERG-positive human prostate cancers had a repressed AKT

111 ), fundus autofluorescence and OCT findings, ERG phenotype, and microscopy/molecular genetics.

112 Full-field flash ERG findings were normal in both eyes.

113 ies that did not generate measurable flicker-ERG and alter the PERG response.

114 r-enhancers that remained constant following ERG inhibition.

115 The molecular basis for ERG lineage-specific activity is unknown.

116 est that SPOP acts as a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic

117 rs were ERG-positive, and being negative for ERG staining was associated with higher Gleason score.

118 iated phosphorylation of ERG is required for ERG functions in prostate cells, but the reason for this

119 to reconfigure a typical patch-clamp rig for ERG recordings.

120 Epithelial cells derived from ERG transgenic mouse prostates have increased prostasphe

121 Furthermore, ERG traces from regenerated retinas displayed waveforms

122 ator genes, including well-established (e.g. ERG) and underexplored (e.g. PPARGC1A, encodes PGC1alpha

123 TS) transcription factors, ETS-related gene (ERG) and Friend leukemia integration 1 (FLI1), prior to

124 rent mediated by Ether-a-go-go-Related Gene (ERG) channels.

125 ally mediated by Ether-a-go-go-Related Gene (ERG) K(+) channels contributes to persistent firing in n

126 lity by reducing Ether-a-go-go Related Gene (ERG) K(+) current.

127 elial transcription factor ETS-related gene (ERG) promotes liver homoeostasis by controlling canonica

128 oblast transformation-specific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.

129 oblast transformation-specific related gene (ERG), using chromatin interaction analysis by paired-end

130 specific antigen (PSA) and ETS-related gene (ERG).

131 S mutant form of ether-a-go-go-related gene (ERG; Kv11.1).

132 roblast transformation-specific related gene(ERG) exerts an important role in maintaining normal aort

133 terns of expression of early response genes (ERGs) are regulated by class IIa HDACs 4 and 5, transcri

134 specific diencephalic ependymo-radial glial (ERG) progenitor cells give rise to new dopaminergic [tyr

135 th Organization (WHO) Evidence Review Group (ERG) on the Cardiotoxicity of Antimalarials.

136 -stimulated OP delays using a novel handheld ERG system (RETeval) at baseline and 2 and 4 weeks.

137 However, ERG is dispensable for TM expression in high SS conditio

138 We identified ERG-associated long-range chromatin interactions as a co

139 Furthermore, we identify ERG as a cofactor that activates AR's ability to bind DN

140 ts (36%) had a greater than 20% asymmetry in ERG values between the 2 eyes.

141 on was associated with a 5.3-muV decrease in ERG amplitude (P < 0.001).

142 nstream effectors Grp78/BiP and eIF2alpha in ERG transgenic mouse prostate glands indicate the presen

143 be exploited for therapeutic intervention in ERG-positive prostate cancers.

144 s, and over 90% of these fusions occurred in ERG exons 3 or 4.

145 significantly associated with a reduction in ERG (P = 0.045).

146 se (PI3K)/Akt-dependent manner, resulting in ERG enrichment at Dll4 promoter and multiple enhancers.

147 mice showed significant increased b-wave in ERG, compared to WT mice.

148 We show that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K

149 molecular mechanisms involving ERK-mediated ERG activation that could be exploited for therapeutic i

150 Moreover, ERG represents a promising candidate biomarker for asses

151 However, most ERG set-ups require their own unique set of tools.

152 ed on light-adapted perimetry and multifocal ERG but with near-normal rod-mediated vision according t

153 ash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-color dark-adapted p

154 to investigate temporal trends in multifocal ERG (mfERG) parameters and analyze their relationships w

155 Notably ERG, a transcriptional factor downstream from MEK/ERK, b

156 ied the ubiquitin hydrolase USP9X as a novel ERG transcriptional target that sustains ERG+85-positive

157 xpression of ERG channels and the ability of ERG blocks to abolish persistent firing evoked by both s

158 Ablation of ERG expression results in endothelial-to-mesenchymal tra

159 hosphorylation of MEK1/ERK and activation of ERG leading to expression of VE-cadherin, which is requi

160 plex 2 (PRC2), transcriptional activation of ERG target genes, and increased cell migration.

161 Focal copy number alterations of ERG, IKZF1, PAX5, ETV6, RB1, BTG1, EBF1, CDKN2A/2B, and

162 The potential association of ERG and PTEN alterations with worse outcomes warrants ad

163 Attenuation of ERG during coincident depolarization and ACh release lea

164 des a selection pressure in the continuum of ERG dependent neoplastic process.

165 In this model, deletion of ERG significantly dampened AR-dependent gene expression.

166 specifically with the DNA binding domain of ERG.

167 te organoid system to explore the effects of ERG on tumorigenesis and determined the mechanism underl

168 ements leading to the aberrant expression of ERG are the most common early events in prostate cancer

169 The broad expression of ERG channels and the ability of ERG blocks to abolish pe

170 the morphological and phenotypic features of ERG gain in normal mouse prostate cells, including expan

171 serine 2) gene to the open reading frame of ERG, encoding an ETS family transcription factor.

172 nderstanding of the mechanistic functions of ERG in prostate tumor biology and towards development of

173 c reticulum stress in the prostate glands of ERG transgenic mice.

174 otif (AIM) in the ETS domain, independent of ERG's own DNA binding ability.

175 lence ratios and 95% confidence intervals of ERG expression in relation to patient characteristics.

176 in the two arms showed comparable levels of ERG, PTEN, androgen receptor PSA, and glucocorticoid rec

177 dentify a pathogenic mechanism where loss of ERG causes endothelial-dependent liver fibrogenesis via

178 Loss of ERG expression is associated with diseases including ath

179 nhancers (including DLL4 and CLDN5), loss of ERG results in significant reduction in gene expression

180 ther, these data reveal a novel mechanism of ERG oncogene addiction in prostate cancer, whereby ERG f

181 organoid models to uncover the mechanism of ERG-mediated tumorigenesis and subsequent oncogenic depe

182 knowledge about the molecular mechanisms of ERG function in prostate cells has hampered efforts to t

183 ular step stimuli suggest that modulation of ERG channels may underlie many forms of persistent activ

184 ta provide evidence that the oncogenicity of ERG is mediated, in part, by competition with ERF and th

185 nism whereby ERK-mediated phosphorylation of ERG at one serine residue causes a conformational change

186 ERK-mediated phosphorylation of ERG is required for ERG functions in prostate cells, but

187 during chronic ER stress due to presence of ERG in prostate epithelium induces survival pathways and

188 immune response, increased proliferation of ERG progenitor cells, and increased addition of new TH(+

189 elial cells and highlight the unique role of ERG in controlling a core subset of super-enhancers.

190 In the more common scenario of ERG upregulation, chromatin immunoprecipitation followed

191 the ERG gene as the established surrogate of ERG fusion genes among 262 prostate cancer biopsies from

192 ing are essential for effective targeting of ERG protein by genotoxic therapeutics in fusion-positive

193 lly broad experience-dependent expression of ERGs, altered synaptic architecture and function, elevat

194 ism underlying prostate cancer dependence on ERG.

195 Amplitudes and implicit times on ERG, mean deviation on VF, central subfield mean thickne

196 Here, we show that oncogenic ERG repressed PI3K signaling through direct transcriptio

197 2, PIK3CA, or MSH2, or expression of SOX2 or ERG and ARSi resistance.

198 te organoids lacking PTEN and overexpressing ERG (Pten(-/-) R26-ERG) faithfully recapitulated distinc

199 al, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz photopic flicker sti

200 Photopic ERG, visual evoked potentials, IHC and cell counting ind

201 Better VA, greater photopic ERG 30-Hz flicker amplitudes, higher mean microperimetry

202 MS, and normal controls) but not in photopic ERGs.

203 control of the endothelial-specific promoter ERG [3, 4].

204 The most frequent and pronounced ERG abnormality was a prolonged implicit time of the con

205 factor-D (VEGF-D), ETS-related gene protein (ERG), and insulin-like growth factor-1 (IGF-1) were meas

206 biomarker proteins ETS-related gene protein (ERG), insulin-like growth factor-1 (IGF-1), pigment epit

207 g PTEN and overexpressing ERG (Pten(-/-) R26-ERG) faithfully recapitulated distinct stages of prostat

208 phenotype characterized by severely reduced ERG responses as early as 4 weeks of age.

209 osphorylation, which correlated with reduced ERG function and decreased photoreceptor survival at bot

210 tanding gating mechanisms of EAG and related ERG and ELK K(+) channels and places the PAS domain as a

211 ression and interaction with the ETS-related ERG protein at enhancer elements.

212 effect on the ex-vivo isolated mouse retina ERG where the RPE is not attached to the isolated retina

213 Scotopic ERG responses over a range of flash intensities were sig

214 in patients with AQP4-IgG+ NMOSD in scotopic ERGs (compared with AQP4-IgG- subjects, patients with MS

215 Ocular survival, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz ph

216 vel ERG transcriptional target that sustains ERG+85-positive cells by controlling ERG ubiquitination.

217 Interventions/Urinary PCA3 and T2:ERG RNA measurement before prostate biopsy.

218 ined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal examination w

219 Combined urinary testing for T2:ERG and PCA3 can avert unnecessary biopsy while retainin

220 33-85 years) combining testing of urinary T2:ERG and PCA3 at thresholds that preserved 95% sensitivit

221 s hampered efforts to therapeutically target ERG.

222 nal heterogeneity and suggest that targeting ERG via USP9X inhibition may be a potential treatment st

223 Finally, we demonstrate that ERG directly interacts with Notch intracellular domain (

224 of DNA-bound AR complexes demonstrated that ERG deletion causes a loss of recruitment of critical AR

225 In summary, we found no evidence that ERG is an effector of SPOP mutation in human prostate ca

226 We find that ERG drives transcription of the anticoagulant thrombomod

227 We find that ERG mediates Ang1-dependent regulation of Notch ligands

228 tation followed by sequencing indicates that ERG inhibits the ability of ERF to bind DNA at consensus

229 a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic effector of SPOP muta

230 etically engineered mouse models reveal that ERG overexpression alone is not sufficient to induce tum

231 Here the authors show that ERG balances TGFbeta signalling through the SMAD1 and SM

232 We show that ERG controls the balance between Notch ligands by drivin

233 Here, we show that ERG, through its physical interaction with androgen rece

234 In C. elegans, we show that ERG-28, an endoplasmic reticulum (ER) membrane protein,

235 umbilical vein endothelial cells showed that ERG binds 93% of super-enhancers ranked according to H3K

236 Molecular analysis shows that ERG binds to SMAD3, restricting its access to DNA.

237 rphisms at ERG super-enhancers suggests that ERG-dependent transcription modulates disease risk.

238 The ERG a-wave is the light-induced hyperpolarization of ret

239 The ERG phenotype is associated with a defect in the recycli

240 The ERG waveform parameters used in this study provided a ve

241 There were no differences between the ERG abnormalities in group A and those in group B and no

242 emistry to assess oncoprotein encoded by the ERG gene as the established surrogate of ERG fusion gene

243 easure of photoreceptor-BP connectivity, the ERG, was restored to a normal waveform.

244 electroretinography (ERG) and correlate the ERG to disease duration and severity of inflammation.

245 lished adenocarcinoma, it is unknown how the ERG oncogene promotes a cancerous phenotype and maintain

246 d intraretinal schisis and reductions in the ERG that were greater for the b-wave than the a-wave.

247 The aberrant activation of the ERG oncogenic pathway due to the TMPRSS2-ERG gene fusion

248 y, leading to proteolytic degradation of the ERG protein.

249 We observed heterogeneous activity of the ERG+85 enhancer-based fluorescent reporter in human leuk

250 USP9X led to preferential inhibition of the ERG-dependent leukemias.

251 hermore, the immediately effect of KA on the ERG b-wave modulation was assessed.

252 This supports the ERG as a tool that could aid the clinician in the differ

253 us carbidopa) for 2 weeks and compared their ERG findings with those of control subjects (no diabetes

254 , 0.011, 0.22]) and not associated with this ERG abnormality.

255 wed gliosis and degenerative changes, though ERG responses were minimally affected.

256 type ERG and TMPRSS2-ERG oncoprotein through ERG threonine-187 and tyrosine-190 phosphorylation media

257 TMPRSS2-ERG gene fusion occurs in approximately 50% of cases of

258 TMPRSS2-ERG gene fusions occur in over 50% of prostate cancers,

259 TMPRSS2-ERG gene fusions were observed in 44% of cases, and over

260 everage cellular signaling to ablate TMPRSS2-ERG oncoprotein for PCa treatment remains elusive.

261 mal degradation of wild-type ERG and TMPRSS2-ERG oncoprotein through ERG threonine-187 and tyrosine-1

262 Lastly, tumors displaying TMPRSS2-ERG fusions that retained interstitial genes were less l

263 treatment repressed tumor growth in TMPRSS2-ERG-positive PCa xenograft models and can act in synergy

264 DNA damage-induced TMPRSS2-ERG degradation was abolished by cancer-associated PTEN

265 Blockade of DNA damage-induced TMPRSS2-ERG oncoprotein degradation causes chemotherapy-resistan

266 his study, we analyzed the status of TMPRSS2-ERG fusion genes and interstitial genes in tumors from a

267 The TMPRSS2-ERG fusion is the most common genomic rearrangement in h

268 s in prostate cancer, especially the TMPRSS2-ERG fusion.

269 the ERG oncogenic pathway due to the TMPRSS2-ERG gene fusion is the major event that contributes to p

270 l prostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expres

271 e of the oncogenic fusion transcript TMPRSS2-ERG.

272 gs uncover a previously unrecognized TMPRSS2-ERG protein destruction mechanism and demonstrate that i

273 nd was significantly associated with TMPRSS2-ERG fusion in clinical PCa cohorts.

274 py for prostate cancer patients with TMPRSS2-ERG fusions and mutations in DNA repair genes, PARG inhi

275 erapeutic strategy to treat PCa with TMPRSS2-ERG gene fusion.

276 y genes, which retained interstitial TMPRSS2/ERG sequences.

277 Additionally, TMPRSS2:ERG variants are detectable in urine to provide non-inva

278 hat combined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal exami

279 The lower prevalence of TMPRSS2:ERG fusions in men of African descent implies that alter

280 ta-analysis showed the prevalence of TMPRSS2:ERG fusions in prostate cancer to be highest in men of E

281 stematic review and meta-analysis of TMPRSS2:ERG fusions in relation to race, Gleason score, and tumo

282 tion-specific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.

283 increased tumoral expression of the TMPRSS2:ERG fusion-oncogene in The Cancer Genome Atlas, suggesti

284 ays for identifying multiple urinary TMPRSS2:ERG variants are potentially useful to aid in early canc

285 The dual phosphorylation triggers ERG recognition and degradation by the E3 ubiquitin liga

286 Tumor ERG positivity and PTEN loss were associated with more e

287 induces proteasomal degradation of wild-type ERG and TMPRSS2-ERG oncoprotein through ERG threonine-18

288 a-wave reduction, there was an undetectable ERG in the remaining 4 patients.

289 In vitro, ERG regulates TM expression under low SS conditions, by

290 eceptor function was not observed in ex vivo ERG recordings from isolated retinas, indicating that ph

291 ir responses obtained by ex vivo and in vivo ERG recordings.

292 for performing high signal-to-noise ex vivo ERGs.

293 Compared to in vivo ERGs, these are superior when measuring small responses,

294 d that 47 of 262 (18%) prostate cancers were ERG-positive, and being negative for ERG staining was as

295 cogene addiction in prostate cancer, whereby ERG facilitates AR signaling by maintaining coregulator

296 While ERG was able to reprogram the AR cistrome in the process

297 proach further revealed that NR2F2 acts with ERG (ETS-related gene) at many of these sites to drive v

298 tipsychotic dosages were not correlated with ERG parameters.

299 opy-number alterations that co-occurred with ERG genomic rearrangements.

300 NR2F2 was bound to this site, together with ERG, and prevented its activation.