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1                                              CTE and MRE are our new standard imaging modalities for
2                                              CTE can be caused by mutations in genes encoding EpCAM,
3                                              CTE elements of different species share sequence similar
4                                              CTE is characterized by intestinal epithelial cell dyspl
5                                              CTE-associated HAI-2 mutant proteins exhibited reduced a
6                                              CTE-containing vectors, produced in a Rev-independent pa
7                                            A CTE severity score, maximum standardized uptake value (S
8 mma that contain the zinc finger motif and a CTE display binding to core recognition sequences that i
9 ons within CTE sites identified by NMR and a CTE domain swapping experiment also confirmed the functi
10 ses the levels of unspliced RNA containing a CTE and specifically promotes the association of this RN
11 me association of unspliced RNA containing a CTE.
12  to be critical for CTE binding and define a CTE-interacting surface on this domain.
13               The simian retroviruses have a CTE which interacts with the cellular Tap export protein
14                                  Export of a CTE-containing lariat occurs when wild-type CTE, but not
15 ould not be viewed as a 'safer' version of a CTE.
16 n of its own intron-containing RNA through a CTE-mediated mechanism.
17 tions of either element that strongly affect CTE activity caused a marked delay of virus replication
18               For mutants strongly affecting CTE activity and splicing, unspliced RNA but not spliced
19    Visual interpretation of both PET/CTE and CTE images detected the presence of disease in all bowel
20                                  PET/CTE and CTE images were each visually assessed for Crohn disease
21 n treatment with brefeldin A, both the E and CTE proteins redistributed to punctate structures that c
22 support CTE-dependent nuclear RNA export and CTE binding.
23  in human Tap, rescues both CTE function and CTE binding.
24                       These localization and CTE analyses support the inference that MARCH6 and Doa10
25  link between TBE-related minisatellites and CTE.
26 7 of 410 patients) of patients referred, and CTE was the most common cause.
27 ects of these KH family proteins on RRE- and CTE (constitutive transport element of type-D retrovirus
28 licase activity, increased both Rev/RRE- and CTE-dependent gene expression and the levels of unsplice
29 -expression of Sam68 activates both RRE- and CTE-regulated reporter gene expression in human cells an
30 ding to CTE and were proposed to function as CTE co-factors (1,2).
31  RHA into nuclei dramatically inhibited both CTE- and Rev-dependent gene expression in human cells.
32  Tap cooperate in the nuclear export of both CTE- and RRE-containing RNA.
33 propose that RHA is required to release both CTE- and RRE-containing mRNA from spliceosomes before co
34 the residue found in human Tap, rescues both CTE function and CTE binding.
35 um C-reactive protein (0.82, P = 0.023), but CTE score did not.
36 ession of the human Tap protein, a candidate CTE cofactor.
37     In contrast to Cdc3 and Cdc12, the Cdc11 CTE, which recruits the nonessential septin Shs1, is dis
38 lar mRNAs with retained introns use cellular CTE equivalents to overcome restrictions to their expres
39                                  A conserved CTE asparagine residue is required for ubiquitylation an
40 emonstrated that unspliced intron-containing CTE RNA is efficiently exported to the cytoplasm in mamm
41 g CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichot
42                          The second critical CTE-interacting surface on Tap is defined by three previ
43 sented an important step for differentiating CTE from other neurodegenerative diseases.
44 er 1, 73%; reader 2, 65%) for distinguishing CTE from other causes.
45     Such selectivity suggests that the Doa10 CTE is involved in substrate discrimination and not gene
46 ividuals with neuropathologically documented CTE.
47 tion containing only the cytoplasmic domain (CTE) was efficiently localized to the Golgi complex, and
48  truncated EAAT2 and COOH terminus of EAAT2 (CTE).
49 lic cells to demonstrate ultra-low effective CTE with a wide temperature range.
50 A to Tap is direct and independent of either CTE or the nuclear transport domain of RHA.
51 V) by the constitutive RNA transport element CTE of the simian type D retroviruses.
52 s-acting constitutive transport RNA element (CTE) that has been shown to interact with the human TAP
53 ted but highly conserved C-terminal element (CTE) in Doa10; this cytosolically disposed 16-residue mo
54 e retroviral constitutive transport element (CTE) and also plays a critical role in the sequence nons
55 monkey virus constitutive transport element (CTE) and significant evidence that Tap also participates
56 by using the constitutive transport element (CTE) derived from Mason-Pfizer monkey virus for expressi
57          The constitutive transport element (CTE) encoded by simian type D retroviruses directs unspl
58              Constitutive transport element (CTE) facilitates retroviral RNA export by interacting wi
59 a cis-acting constitutive transport element (CTE) for simple retroviruses and by the trans-acting vir
60 by using the constitutive transport element (CTE) from Mason-Pfizer monkey virus (MPMV).
61 s (HBV), the constitutive transport element (CTE) of Mason-Pfizer monkey virus (MPMV), or the pre-mRN
62 laced by the constitutive transport element (CTE) of simian retrovirus type 1.
63          The constitutive transport element (CTE) of type D retroviruses mediates the nuclear export
64          The constitutive transport element (CTE) of type D retroviruses serves as a signal of nuclea
65 iated by the Constitutive Transport Element (CTE) of type D retroviruses.
66 cts with the constitutive transport element (CTE) of type D retroviruses.
67 a cis-acting constitutive transport element (CTE) that presumably interacts directly with cellular ex
68 at contain a constitutive transport element (CTE), a cis-acting 2-fold symmetric RNA stem-loop motif.
69 monkey virus constitutive transport element (CTE), an element that enables export of unspliced, intro
70 monkey virus constitutive transport element (CTE), in the RNA.
71 virus (MPMV) constitutive transport element (CTE)-containing RNAs is not inhibited by leptomycin B tr
72 virus (MPMV) constitutive transport element (CTE).
73 known as the constitutive transport element (CTE).
74 lar or viral constitutive transport element (CTE).
75 s known as a constitutive transport element (CTE).
76  bearing the constitutive transport element (CTE).
77 ting it is a constitutive transport element (CTE).
78 lopment of chronic traumatic encephalopathy (CTE) and Alzheimer's disease.
79            Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of
80            Chronic traumatic encephalopathy (CTE) refers to pathologic changes that have been found i
81  described chronic traumatic encephalopathy (CTE).
82 ficits, or chronic traumatic encephalopathy (CTE).
83 rticularly chronic traumatic encephalopathy (CTE).
84 iteria for chronic traumatic encephalopathy (CTE).
85   The activity of this Tap mutant to enhance CTE-mediated gene expression is also markedly reduced.
86 hy (PET/CTE), compared with CT enterography (CTE) alone, in the assessment of patients with Crohn dis
87 based imaging, specifically CT enterography (CTE) and magnetic resonance enterography (MRE), transcut
88 parable to computed tomography enterography (CTE).
89              Congenital tufting enteropathy (CTE) is a rare autosomal recessive diarrheal disorder pr
90              Congenital tufting enteropathy (CTE) is a severe autosomal recessive human diarrheal dis
91 o be due to a unique property of the ERalpha CTE, independent of HMGB-1/-2.
92 ations (FE) and charge-transfer excitations (CTE) coupled nonadiabatically to local intramolecular vi
93                                    Exogenous CTE peptide increased PR-binding affinity for PRE as did
94        The coefficient of thermal expansion (CTE) is a physical quantity that indicates the thermal e
95  Ultra-low coefficient of thermal expansion (CTE) is an elusive property, and narrow temperature rang
96 tween the coefficients of thermal expansion (CTE) of the consecutive device layers of field-effect tr
97 ating, its coefficient of thermal expansion (CTE) smoothly increases, leading to a room temperature C
98 ce translation of proteins from the exported CTE RNA.
99    The redox regulated C-terminal extension (CTE) and the associated alternate splicing mechanism, wh
100  and the impact of the C-terminal extension (CTE) by contrasting HP1a to its paralogue, HP1b.
101 d, except for Cdc10, a C-terminal extension (CTE) containing a predicted coiled coil.
102 VirD2 proteins and the C-terminal extension (CTE) domain of Arabidopsis thaliana telomerase reverse t
103 g "AT-hook" within the C-terminal extension (CTE) flanking the DBD, which makes base-specific minor g
104 -box proteins, while a C-terminal extension (CTE) induces a second bend, resulting in RNA crimping.
105 We show here that this C-terminal extension (CTE) mediates in vivo localization of the protein to the
106 ction is mediated by a C-terminal extension (CTE) of the DNA binding domain and is unique to the estr
107 ally disordered carboxyl-terminal extension (CTE) of the DNA binding domain.
108 d ROR utilize a carboxyl-terminal extension (CTE) of the zinc finger DNA binding domain in their inte
109 as 25 amino acids in a C-terminal extension (CTE) participate in DNA binding.
110 2 was dependent on the C-terminal extension (CTE) region of the ER DNA binding domain (DBD) and corre
111  short flexible carboxyl terminal extension (CTE) that interacts with the minor groove flanking the P
112 ty is dependent on the C-terminal extension (CTE), amino acid sequences adjacent to the zinc finger c
113 tes are located in the C-terminal extremity (CTE) of the receptor following its palmitoylation site.
114 proposal that HAP95 specifically facilitates CTE-mediated gene expression by directly binding to RHA.
115                             Signatures of FE/CTE mixing and the extent of electron/hole separation ar
116 rs a repressive conformation of the flexible CTE enabling it to bind to preferred sequences flanking
117 A (RHA) as a potential cellular cofactor for CTE.
118 ment of pathological diagnostic criteria for CTE represented an important step for differentiating CT
119  repeat domain were found to be critical for CTE binding and define a CTE-interacting surface on this
120 efines a surface on Tap that is critical for CTE binding.
121 ch regions of this sequence are critical for CTE function, mutations in the downstream DR were genera
122  RBT represents the greatest risk factor for CTE pathological features, although clinicopathological
123 s to TBE in the regions that are neutral for CTE function.
124 ng and nuclear localization are required for CTE activation.
125 udy was to identify the gene responsible for CTE.
126 ns in the gene for EpCAM are responsible for CTE.
127  a prospective study of a cohort at risk for CTE.
128 ic RNA binding domain that is sufficient for CTE binding but inadequate to support CTE function.
129                 The sumoylated CTE fragment (CTE-SUMO-1) accumulates in the spinal cord of these mice
130 show that the Tap gene contains a functional CTE in its alternatively spliced intron 10.
131 report the crystal structure of a functional CTE RNA-binding domain of human Tap, including the N-ter
132 ntaining RNA through the use of a functional CTE within intron 10.
133 s a shuttle protein that binds to functional CTE in vitro and in vivo.
134 ed by heterologous RNA export elements, e.g. CTE of simian type D retroviruses.
135 polyamides in both the upstream minor groove CTE site and the minor groove of the ERE half-site.
136 ing to the CTE, indicating that DNA and HMGB-CTE interactions are mutually exclusive.
137            We conclude that a transient HMGB-CTE interaction alters a repressive conformation of the
138  homologous to the core TAP-binding sites in CTE.
139 ses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropath
140 on during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI.
141 rexpression of HAP95 significantly increases CTE-dependent gene expression but has no effect on gener
142  blocked p15 binding only modestly inhibited CTE-dependent nuclear RNA export.
143      Accordingly, the measured instantaneous CTE of polystyrene resin varied from 5.86 x 10(-5) degre
144 ved and recorded to derive the instantaneous CTE of the packaged LED under different injected current
145 etric complex with Cdc12, independent of its CTE.
146                                         Like CTE, TBE is an active nuclear export signal.
147 t the use of conventional materials with low CTE.
148  conserved Asn residue (N890A) in the MARCH6 CTE stabilized the normally short lived enzyme to the sa
149              Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms
150 y virus constitutive transport element (MPMV CTE)-dependent nuclear RNA export or on the expression o
151  with retained introns that contain the MPMV CTE (constitutive transport element).
152 on from a pNL4-3 provirus that used the MPMV CTE for RNA export.
153  for HIV-1 Rev and demonstrate that the MPMV CTE nuclear RNA export pathway uses a distinct, Crm1-ind
154 o the Tap/Nxf1 pathway, utilized by the MPMV CTE, through the expression of a RevM10-Tap fusion prote
155             The presence and accumulation of CTE-SUMO-1 is specific to ALS mice, since it does not oc
156                Conversely, the activation of CTE by Tap in quail cells was inhibited by a transdomina
157       Surprisingly, even very low amounts of CTE RNA block export of normal mRNAs, apparently through
158 ia are developed, the clinical assessment of CTE should be informed by modern research that is of rel
159 study population, most frequently because of CTE.
160 iomarkers of pathological characteristics of CTE and longitudinal tracking with neuropsychological ev
161 anism, and clinicopathological correlates of CTE reflect the current reliance on postmortem case seri
162 rkers in diagnosis, and existing criteria of CTE are reviewed.
163  mild TBI and autopsy-confirmed diagnosis of CTE.
164                               Enhancement of CTE function was not seen when a Sam68 point mutant (G17
165 proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior partici
166 ave been implicated in the nuclear export of CTE-containing RNA.
167  binds to CTE and mediates nuclear export of CTE-containing RNAs.
168 ling and the Tap-dependent nuclear export of CTE-containing RNAs.
169 an replace Nxt1 to enhance the expression of CTE-containing mRNA and promote its association with pol
170 ion in quail cells, in which the function of CTE is dependent on the expression of a functional human
171 vidence about the clinical manifestations of CTE has been accumulating via post-mortem medical record
172 ique information about the manifestations of CTE, including clinical and preclinical stages.
173 tion, characterization, and/or prediction of CTE.
174  of NXF1:NXT1 facilitates the recognition of CTE-RNA and promotes its nuclear export.
175  Tap inhibited RHA-mediated up-regulation of CTE function in mammalian cells.
176 review discusses the state of the science of CTE and raises considerations for researching and interp
177                Neuropathological severity of CTE was distributed across the highest level of play, wi
178 similarly in the RNA secondary structures of CTE and TBE.
179 mportant for RHA binding, transactivation of CTE, and nuclear cytoplasmic shuttling.
180 mote polysome association and translation of CTE-RNA, we investigated the effect of 9G8 on cytoplasmi
181 y paralleled the effects of the mutations on CTE activity.
182                                  Research on CTE would benefit greatly from incorporating principles
183 t HAP95 synergizes significantly with RHA on CTE-mediated reporter gene expression and promotes nucle
184 s enterocolic fistula, not evident on PET or CTE alone.
185                                          PET/CTE also may reveal clinically significant findings, suc
186                                          PET/CTE and CTE images were each visually assessed for Crohn
187            Visual interpretation of both PET/CTE and CTE images detected the presence of disease in a
188  combined (18)F-FDG PET/CT enterography (PET/CTE), compared with CT enterography (CTE) alone, in the
189 and underwent abdominal-pelvic (18)F-FDG PET/CTE using neutral oral and intravenous contrast medium.
190                       Low-dose (18)F-FDG PET/CTE, compared with CTE, may improve the detection and gr
191                  The effective dose from PET/CTE was 17.7 mSv for the first 4 patients and 8.31 mSv f
192 ith biopsies within 27 d (mean, 12 d) of PET/CTE.
193 ) of 13 patients, (18)F-FDG uptake using PET/CTE revealed active inflammation in a bowel segment not
194 RNA analysis showed that cytoplasmic Gag-Pol-CTE RNA levels were only slightly enhanced by the additi
195 parate risk scores were developed to predict CTE (defined as the composite of stent thrombosis or myo
196 BE has properties expected from a primordial CTE.
197 eveal the importance of the steroid receptor CTE for DNA binding affinity and functional response to
198      At the present time, evidence regarding CTE has not been confirmed in a prospective study of a c
199 ear transport domain of RHA and up-regulates CTE-mediated gene expression.
200 structively determine the spatially resolved CTE of the packaged LED device, which offers significant
201  prepared from mutant G93A-SOD1 mice reveals CTE to be of a higher molecular weight than expected bec
202            Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms
203 nding surface of the HP1a CSD plus its short CTE provide the needed discrimination among HP1a's partn
204                               The sumoylated CTE fragment (CTE-SUMO-1) accumulates in the spinal cord
205  demonstrate that quail Tap fails to support CTE function because it cannot bind the CTE.
206 ev NES rescues the ability of Tap to support CTE function, this substitution also confers sensitivity
207 nt for CTE binding but inadequate to support CTE function.
208 d these mutants for their ability to support CTE-dependent nuclear RNA export and CTE binding.
209 NP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distributi
210 utive patients referred because of suspected CTE.
211 nal American football players with suspected CTE (n = 14) and compared results with those of cognitiv
212 ubstitutions for surface residues in the Tap CTE-binding domain and tested these mutants for their ab
213 key virus-CTE or the recently discovered Tap-CTE.
214 hly increases, leading to a room temperature CTE that is similar to that of ZrW(2)O(8) and positive t
215        Previously, we have demonstrated that CTE function displays species specificity, that is, the
216                In contrast, we observed that CTE-mediated expression from human immunodeficiency viru
217 ue samples from G93A-SOD1 mice, we show that CTE-SUMO-1 is targeted to promyelocytic leukemia nuclear
218 athological evidence of CTE, suggesting that CTE may be related to prior participation in football.
219                  This evidence suggests that CTE is manifested clinically by changes in cognition (es
220                                          The CTE has two symmetric structures, either of which suppor
221                                          The CTE interacts directly with the Tap protein (also known
222                                          The CTE of both ER subtypes was also shown to be required fo
223                                          The CTE RNA and an RNA containing the RRE of HIV-1 (plus Rev
224 tween active site residues of Rv0805 and the CTE that determine its association with the cell wall.
225 rotein interaction between HMGB-1/-2 and the CTE.
226 port CTE function because it cannot bind the CTE.
227 of minor groove DNA contacts mediated by the CTE and by changing the helical geometry of DNA such tha
228 ement of the essential Rev regulation by the CTE generated a virus variant that retained its replicat
229                Replacement of Rev-RRE by the CTE provides a novel approach to dramatically lower the
230 s; and indicate that the bend induced by the CTE results primarily from a steric block.
231 ytoplasmic utilization of RNA containing the CTE.
232 red to systems that were based on either the CTE alone or Rev and RRE for expression of both the pack
233 ficantly enhance the affinity of Tap for the CTE in vitro and readily formed a ternary complex with T
234 mmation per bowel segment was higher for the CTE score (0.79, P < 0.0001) than the SUVmax ratio (0.62
235                                 However, the CTE (only 4 residues in HP1a as compared with 87 residue
236 tal deletion of phosphoacceptor sites in the CTE affected proper receptor regulation.
237 osphorylation of Ser and Thr residues in the CTE of the receptor in a redundant fashion, able to inco
238 on in the helicase core and the other in the CTE-that may help displace or sequester the opposite RNA
239 n displays species specificity, that is, the CTE functions in human but not quail cells.
240 al coherence tomography (OCT) to measure the CTE of an InGaN-based (lambda = 450 nm) high-power LED e
241 from naturally intronless genes, but not the CTE or RRE from intron-containing genes, significantly e
242 o dissect the functional significance of the CTE (residues 88-112) in the context of the complete hVD
243   These studies reveal the importance of the CTE and HMGB-1/-2 for ERalpha and ERbeta interaction wit
244                        The importance of the CTE for binding JDP2 was confirmed by peptide competitio
245 to the role and functional importance of the CTE for co-activator interactions.
246 raction correlates with a requirement of the CTE for maximal HMGB-1/-2 enhancement of DNA binding in
247 red with Tap-mediated transactivation of the CTE function in quail cells, in which the function of CT
248                         The structure of the CTE is stabilized both by interactions with the DNA and
249 th a Cdc3-Cdc12 complex independently of the CTE of either protein.
250 that an RNA comprised almost entirely of the CTE of Mason-Pfizer monkey virus (CTE RNA) is exported e
251  accurate and immediate determination of the CTE of packaging materials is gaining importance because
252  Rv0805 and a truncated mutant devoid of the CTE produce different phenotypic effects when expressed
253               Functional conservation of the CTE was investigated in the human ortholog of Doa10, MAR
254                 We tested the ability of the CTE, the WPRE, and introns to enhance expression of E2.
255 pport hTAP's role as an export factor of the CTE-containing mRNAs.
256 P (hTAP) protein promoting the export of the CTE-containing mRNAs.
257 ding affinity for PRE as did deletion of the CTE.
258 affinity difference is also dependent on the CTE.
259 ily formed a ternary complex with Tap on the CTE.
260 receptors, and this interaction requires the CTE.
261 mination among HP1a's partners, and that the CTE is important for differentiating the interactions of
262 sults with the yeast enzyme suggest that the CTE is involved in the recognition and/or ubiquitylation
263                        Here we show that the CTE of PR contains a specific binding site for HMGB that
264   Two host proteins bind specifically to the CTE but not to non-functional variants, making these pro
265 ecific PRE DNA inhibited HMGB binding to the CTE, indicating that DNA and HMGB-CTE interactions are m
266                                    While the CTE and RRE primarily enhance nucleocytoplasmic export,
267 onal importance of JDP2 interaction with the CTE for enhancement of PR transcriptional activity.
268 Vmax (0.67, P = 0.013), as compared with the CTE score (0.62, P = 0.024).
269  To identify residues that interact with the CTE, we have introduced 38 alanine substitutions for sur
270 nvolved in binding of JDP2 reside within the CTE.
271 of candidate symptoms in retired athletes to CTE is complicated by the presence of multiple premorbid
272  protein (Tap) were identified as binding to CTE and were proposed to function as CTE co-factors (1,2
273 llular mRNA export factor, directly binds to CTE and mediates nuclear export of CTE-containing RNAs.
274 all diagnostic yield of MRE is comparable to CTE.
275                                  Compared to CTE the image quality is not quite as good, and there is
276 , we show that quail cells are refractory to CTE function but become highly permissive upon expressio
277 fers significant advantages over traditional CTE measurement techniques.
278  produced using a combination RNA transport (CTE and Rev-Rev response element)-based packaging system
279                     These engineered tunable CTE thin film can be applied to minimize thermal fatigue
280                                          Two CTE-binding proteins, RNA helicase A (RHA) and Tap, have
281               Here, we report that these two CTE-binding proteins interact with each other in vitro a
282  CTE-containing lariat occurs when wild-type CTE, but not a mutant form, is inserted into the pre-mRN
283 go on to show that insertion of an ultrathin CTE buffer layer mitigates this problem and can help ach
284 mmation in a bowel segment not evident using CTE (n = 2) or revealed an enterocolic fistula missed wi
285 id indicator of neuropathologically verified CTE.
286 ely of the CTE of Mason-Pfizer monkey virus (CTE RNA) is exported efficiently from Xenopus oocyte nuc
287 taining either the Mason-Pfizer monkey virus-CTE or the recently discovered Tap-CTE.
288 euroimaging or laboratory evaluations, while CTE currently only can be definitively diagnosed postmor
289       A family with 2 children affected with CTE was identified.
290 erpreting cognitive outcomes associated with CTE and for developing preventive treatment programs.
291 ing the clinical syndrome(s) associated with CTE and the necessary and sufficient symptoms needed for
292 se that has been cognitively associated with CTE.
293    Low-dose (18)F-FDG PET/CTE, compared with CTE, may improve the detection and grading of active inf
294 t RNA helicase A functionally interacts with CTE and contains a bidirectional nuclear transport domai
295  revealed an enterocolic fistula missed with CTE (n = 1).
296  of the Agrobacterium bait proteins, or with CTE.
297 angiography for distinguishing patients with CTE from those with other causes.
298 l features of deceased football players with CTE.
299                       Point mutations within CTE sites identified by NMR and a CTE domain swapping ex
300 6 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87

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