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1 ERG binds to chromatin regions occupied by TEAD/YAP1 and
2 ERG controls the Wnt/beta-catenin pathway by promoting b
3 ERG currents have been previously studied primarily in t
4 ERG fusions retaining interstitial sequences occurred mo
5 ERG inhibitory peptides (EIPs) and derived peptidomimeti
6 ERG is not expressed in normal prostate epithelia, but w
7 ERG recruits PRMT5 to AR-target genes, where PRMT5 methy
8 ERG results are consistent with the structural analyses
9 ERG's oncogenic potential is well known because of its i
10 ERGs recorded after mice Kir7.1 suppression by shRNA, or
14 channels contribute directly to the abnormal ERG associated with blindness via alterations in sub-ret
15 the heart; relatively little is known about ERG function in the brain, although mutations in ERG cha
16 ne responses (the a-wave of the dark-adapted ERG protocol of 12.0 cd/s/m2) was longer (mean differenc
17 muV]; P=.003; the a-wave of the dark-adapted ERG protocol of 12.0 cd/s/m2: mean difference, -55.7 muV
18 ne responses (the a-wave of the dark-adapted ERG protocol of 3.0 cd/s/m2: mean difference, -48.9 muV
22 VEGF-responsive and ERG-dependent genes, and ERG chromatin immunoprecipitation (ChIP)-seq revealed th
25 identified a network of VEGF-responsive and ERG-dependent genes, and ERG chromatin immunoprecipitati
27 on of interstitial genes between TMPRSS2 and ERG has been reported to influence tumor progression in
28 the interstitial regions between TMPRSS2 and ERG Identifying these patients at biopsy might improve p
30 ring triggering stimuli appears to attenuate ERG currents, leading to membrane potential depolarizati
34 r toxicity, peak-to-peak comparisons between ERG studies before and after OAC treatment and CTCAE 4.0
36 competition model, ERF overexpression blocks ERG-dependent tumour growth, and ERF loss rescues TMPRSS
37 des (EIPs) and derived peptidomimetics bound ERG with high affinity and specificity, leading to prote
42 peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K(+) channels in carbon monoxide-induced pr
44 in human luminal-type prostate cancer cells, ERG binds to the promoter of YAP1 and is necessary for Y
49 Cone morphology of the dogs lacking cone ERG are truncated with shortened outer and inner segment
52 proaches demonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (which encode
53 ChIP)-seq revealed the presence of conserved ERG-bound putative enhancer elements near these target g
58 ween the number of injections and diminished ERG responses, such that on average each intravitreous m
63 Transcription of DLL4 coincides with dynamic ERG-dependent recruitment of the transcriptional co-acti
64 that prostate-specific activation of either ERG or YAP1 in mice induces similar transcriptional chan
66 inal inflammation, and an electroretinogram (ERG) illustrated decreased amplitude of the b wave in bo
68 B1 patients have a normal electroretinogram (ERG) a-wave, indicative of photoreceptor function, but l
73 n the eye as assessed by electroretinograms (ERG), corneal and retinal tomography, and histology.
75 ther variability in cone electroretinograms (ERGs) ranging from normal to absent in an extended RPGRI
76 ing DTL electrodes and electroretinographic (ERG) protocols with flash strengths of 0.009, 0.17, 3.0,
77 scotopic and photopic electroretinographic (ERG) responses to single-flash stimuli also show no diff
79 y clinical findings and electroretinography (ERG) on 244 evaluable injections in 63 patients using 30
80 n microscopy (TEM), and electroretinography (ERG) were used to analyze 6 genotypes including WT at th
81 ation, full-field flash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-
82 re performed, including electroretinography (ERG), multifocal ERG (mfERG), perimetry, optical coheren
85 neration using scotopic electroretinography (ERG), optical coherence tomography (OCT), and immunohist
86 ckness were found using electroretinography (ERG), fundus photography (FP), fundus fluorescein angiog
87 Visual acuity (VA), electroretinography (ERG), and spectral-domain optical coherence tomography (
88 otype was assessed with electroretinography (ERG), optical coherence tomography, psychophysics, and p
89 man leukemias according to Evi1/EVI1 and Erg/ERG expression, reflecting aggressiveness and cell of or
94 the degradation of the transcription factor ERG and that translocations of ERG or mutations in SPOP
95 e overexpression of the transcription factor ERG are present in approximately 50% of all prostate can
96 Here we identify the transcription factor ERG as a key regulator of endothelial Notch signalling.
99 MT in liver disease.The transcription factor ERG is key to endothelial lineage specification and vasc
100 , the gene encoding the transcription factor ERG is recurrently rearranged and plays a critical role
103 o overexpression of the transcription factor ERG, while a mutually exclusive 10% of prostate cancers
104 We recover seven transcription factors (ERG, HOXA5, HOXA9, HOXA10, LCOR, RUNX1 and SPI1) that ar
105 electrode types allow successful full-field ERG recording, although separate normative data for both
108 etic transcription factors (TFs) PU.1, FLI1, ERG, C/EBPalpha, C/EBPbeta, and MYB at nucleosome-deplet
109 of the isolated cone response (30-Hz flicker ERG: mean difference, -12.1 muV [95% CI, -22.5 to -1.6 m
110 e the isolated cone responses (30-Hz flicker ERG: mean difference, 1.2 milliseconds [95% CI, 0.5-1.8
112 est that SPOP acts as a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic
113 rs were ERG-positive, and being negative for ERG staining was associated with higher Gleason score.
114 iated phosphorylation of ERG is required for ERG functions in prostate cells, but the reason for this
120 e DUX4 and the ETS transcription factor gene ERG is a hallmark of a subtype of B-progenitor ALL that
123 ally mediated by Ether-a-go-go-Related Gene (ERG) K(+) channels contributes to persistent firing in n
124 elial transcription factor ETS-related gene (ERG) promotes liver homoeostasis by controlling canonica
125 oblast transformation-specific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.
127 entification of early redox-regulated genes (ERGs) in the nucleus of the model organism Arabidopsis t
135 nstream effectors Grp78/BiP and eIF2alpha in ERG transgenic mouse prostate glands indicate the presen
137 function in the brain, although mutations in ERG channels have recently been linked to schizophrenia.
141 se (PI3K)/Akt-dependent manner, resulting in ERG enrichment at Dll4 promoter and multiple enhancers.
145 el was associated with a reduction in mature ERG expression and an increase in the expression of seve
146 molecular mechanisms involving ERK-mediated ERG activation that could be exploited for therapeutic i
149 ed on light-adapted perimetry and multifocal ERG but with near-normal rod-mediated vision according t
150 ash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-color dark-adapted p
151 luding electroretinography (ERG), multifocal ERG (mfERG), perimetry, optical coherence tomography (OC
153 xpression of ERG channels and the ability of ERG blocks to abolish persistent firing evoked by both s
158 expression and the clinicopathologic data of ERG and IL-6 using immunohistochemical double staining a
160 ow that constitutive endothelial deletion of ERG (Erg(cEC-KO)) in mice causes embryonic lethality wit
162 companied by transcriptional deregulation of ERG, expression of a novel ERG isoform, ERGalt, and freq
164 e DNA-binding and transactivation domains of ERG, but it inhibits wild-type ERG transcriptional activ
165 suggesting that the proliferative effects of ERG and PRMT5 are mediated through attenuating AR's abil
168 vely, our study shows that the expression of ERG in prostate cancer is linked to the expression of IL
170 e cancer did not result in the expression of ERG protein in histologically normal prostate glands, hi
171 the morphological and phenotypic features of ERG gain in normal mouse prostate cells, including expan
173 deregulation results in loss of function of ERG, either by deletion or induced expression of an isof
174 nderstanding of the mechanistic functions of ERG in prostate tumor biology and towards development of
176 lence ratios and 95% confidence intervals of ERG expression in relation to patient characteristics.
177 dentify a pathogenic mechanism where loss of ERG causes endothelial-dependent liver fibrogenesis via
179 s the ERG-cistrome and a genome-wide loss of ERG-mediated transcriptional activation and cell migrati
181 knowledge about the molecular mechanisms of ERG function in prostate cells has hampered efforts to t
182 ular step stimuli suggest that modulation of ERG channels may underlie many forms of persistent activ
183 ta provide evidence that the oncogenicity of ERG is mediated, in part, by competition with ERF and th
184 nism whereby ERK-mediated phosphorylation of ERG at one serine residue causes a conformational change
186 during chronic ER stress due to presence of ERG in prostate epithelium induces survival pathways and
188 to calculate HRs and 95% CIs for the risk of ERG-positive and, separately, ERG-negative disease.
189 take was associated with a decreased risk of ERG-positive disease (HR: 0.54; 95% CI: 0.37, 0.81; P-tr
191 the ERG gene as the established surrogate of ERG fusion genes among 262 prostate cancer biopsies from
192 on in a transgenic mouse model with those of ERG knockdown in a TMPRSS2:ERG-positive PC cell line.
193 iption factor ERG and that translocations of ERG or mutations in SPOP prevent CRL3(SPOP)-dependent de
198 al, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz photopic flicker sti
202 osphorylation, which correlated with reduced ERG function and decreased photoreceptor survival at bot
204 From a screen for functionally relevant ERG interactors, we identify the arginine methyltransfer
205 effect on the ex-vivo isolated mouse retina ERG where the RPE is not attached to the isolated retina
209 Ocular survival, disease-free survival, ERG: peak-to-peak ERG amplitudes in response to 30-Hz ph
211 ined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal examination w
213 33-85 years) combining testing of urinary T2:ERG and PCA3 at thresholds that preserved 95% sensitivit
216 uorescence and electrophysiological testing (ERG and EOG) may indicate initial stages or more widespr
222 tation followed by sequencing indicates that ERG inhibits the ability of ERF to bind DNA at consensus
224 a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic effector of SPOP muta
233 y-resistant cell population, suggesting that ERG may have a direct role in preventing resistance to a
236 6 resulted in recruitment of EZH2 across the ERG-cistrome and a genome-wide loss of ERG-mediated tran
237 etween the TMPRSS2 promoter sequence and the ERG coding sequence (TMPRSS2:ERG) in urine, noninvasive
238 response, binds to androgen receptor at the ERG gene breakpoint and inhibits both the juxtaposition
239 emistry to assess oncoprotein encoded by the ERG gene as the established surrogate of ERG fusion gene
241 inine 761 highlights a mechanism for how the ERG oncogene may coax AR towards inducing proliferation
242 diabetic rats was assessed by monitoring the ERG b-wave and oscillatory potentials, Muller cell react
245 ism in prostate tumor cell lines we show the ERG-mediated up-regulation of the prostanoid receptors E
250 issues showed that the presence of a TMPRSS2-ERG rearrangement was highly correlated with lower level
255 his study, we analyzed the status of TMPRSS2-ERG fusion genes and interstitial genes in tumors from a
256 ized two mouse models recapitulating TMPRSS2-ERG insertion or deletion events in the background of pr
257 tumour growth, and ERF loss rescues TMPRSS2-ERG-positive prostate cancer cells from ERG dependency.
259 l prostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expres
260 ss along with other genes within the TMPRSS2-ERG interstitial region contributes to disease progressi
265 alyzed in case-case comparisons (296 TMPRSS2:ERG fusion-positive versus 256 fusion-negative cases) an
268 selectively isolating and adsorbing TMPRSS2:ERG mRNA onto bare gold electrodes without requiring any
269 hat combined measurement of PCA3 and TMPRSS2:ERG (T2:ERG) RNA in the urine after digital rectal exami
270 negative (OR = 0.53, P = 0.0007) and TMPRSS2:ERG fusion-positive PrCa (OR = 1.30, P = 0.0016), respec
271 ferences have been described between TMPRSS2:ERG fusion-positive and fusion-negative prostate cancer
272 ical utility by accurately detecting TMPRSS2:ERG in a collection of 17 urinary samples obtained from
273 is that prostate cancers that harbor TMPRSS2:ERG may be etiologically distinct from fusion-negative c
274 9962 (17q24), which were enriched in TMPRSS2:ERG fusion-negative (OR = 0.53, P = 0.0007) and TMPRSS2:
275 or the candidate target gene SOX9 in TMPRSS2:ERG fusion-positive PrCa, which was not evident in TMPRS
278 pared the transcriptional effects of TMPRSS2:ERG expression in a transgenic mouse model with those of
279 ts, such as the multiple variants of TMPRSS2:ERG fusion gene mutations in prostate cancer (PCa), are
281 ta-analysis showed the prevalence of TMPRSS2:ERG fusions in prostate cancer to be highest in men of E
282 stematic review and meta-analysis of TMPRSS2:ERG fusions in relation to race, Gleason score, and tumo
283 ) in urine, noninvasive screening of TMPRSS2:ERG mRNA in patient urine samples could improve the spec
284 emical assay for direct detection of TMPRSS2:ERG mRNA in PCa urinary samples by selectively isolating
287 equence and the ERG coding sequence (TMPRSS2:ERG) in urine, noninvasive screening of TMPRSS2:ERG mRNA
290 ays for identifying multiple urinary TMPRSS2:ERG variants are potentially useful to aid in early canc
291 of a discovery set of 552 cases with TMPRSS2:ERG data and 7650 unaffected men from five centers we ha
292 an independent set of 669 cases with TMPRSS2:ERG data was established to replicate the top five candi
298 d that 47 of 262 (18%) prostate cancers were ERG-positive, and being negative for ERG staining was as
299 I: 0.37, 0.81; P-trend = 0.004) but not with ERG-negative disease (HR: 0.96; 95% CI: 0.62, 1.50; P-tr
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