ライフサイエンスコーパス: NES

1 NES initiates and terminates the transfer of plasmids th

2 NES-containing proteins are involved in numerous cellula

3 NES-GFP expression declined following satellite cell act

4 NESs are short stretches of 8-15 amino acids with regula

5 follows: a highly conserved NES in helix 12 (NES-H12) and two additional NES sequences spanning helix

6 led a database named NESdb that contains 221 NES-containing CRM1 cargoes that were manually curated f

7 Finally, we also tested CRM1-binding of 40 NESs that were found in the 56 structures.

8 ensional structures are now available for 68 NESs within 56 different cargo proteins.

9 ely, our data demonstrate the existence of a NES in E1A that is modulated by the phosphorylation of t

10 KI vies with CRM1/exportin 1 for access to a NES, and assembly of a CaMKI-14-3-3 zeta-CCTalpha comple

11 NES in helix 12 (NES-H12) and two additional NES sequences spanning helix 3 and helix 6, respectively

12 structures of CRM1 bound to eight additional NESs which reveal diverse conformations that range from

13 Analysis of all NES structures show 5-6 distinct backbone conformations

14 All NESs also participate in main chain hydrogen bonding wit

15 Additionally, upon overexpression, the ALX NES mutant was found to be impaired in inhibiting TCR/CD

16 erminus, (1)MKFKLHV(7), also functions as an NES (termed N-NES) in a chromosome region maintenance 1

17 We previously engineered an NES-negative ICP27 mutant, dLeu, that replicates poorly

18 Finally we show that the addition of an NES directly to the 60S ribosomal subunit protein Rpl3 p

19 p75(NTR)), PAX3, SOX9, AP2B1 (AP-2beta), and NES, generated a phenotypic footprint of endothelial NCD

20 rotein, and promoter activity in NES-B3T and NES-B10T cells, but not in NES-G2T or NES-G4T cells.

21 us (normal esophageal squamous [NES]-B3T and NES-B10T) and without Barrett's esophagus (NES-G2T and N

22 Two fluorescent CAD constructs, NLS-CAD and NES-CAD, were prepared that incorporated strong nuclear

23 o the differential diagnosis of epilepsy and NES.

24 and without Barrett's esophagus (NES-G2T and NES-G4T) to study effects of acid and bile salts on expr

25 We propose that Rev multimerization and NES masking regulates Rev's trafficking to and retention

26 ic sequence that resides between the NLS and NES clusters.

27 Importantly, the NLS- and NES-dependent shuttling of Cby modulates the dynamic int

28 In transfected cells, both wild-type and NES mutant VHS-RNases effectively degraded cellular mRNA

29 ar localization and export signals (NLSs and NESs) to mediate nucleocytoplasmic trafficking, a proces

30 ar localization and export signals (NLSs and NESs).

31 The nuclear export signal of AR (NES(AR)) has an important role in AR intracellular traff

32 ay of peptide sequences that can function as NESs.

33 cruitment to the 40S pre-ribosome-associated NES-containing adaptor Rio2.

34 smission by the nicking enzyme in S. aureus (NES), which is essential for conjugative transfer.

35 RSV replication, we created viruses bearing NES mutant Gag proteins.

36 otein kinase A inhibitor (PKIA) CRM1-binding NESs into AMPKalpha.

37 Previously we have shown that CRM1 binds NESs in both polypeptide orientations.

38 50 and 100 J/m(2)) caused DNA damage in both NES and BAR-T cells but significantly increased apoptosi

39 Mutual and unique gene expression by NES-GFP+ cells from hindlimb and diaphragm muscles demon

40 and function of Scd5p-DeltaCT is restored by NES addition.

41 Fusions of the CALM NES (NES(CALM)-AF10) or NES motifs from heterologous pro

42 The CALM NES is essential for CALM-AF10-dependent Hoxa gene up-re

43 ansfer (FRET)-based reporter yellow cameleon NES-YC3.6 and the intensity-based sensor R-GECO1.

44 analyses, we identified an active canonical NES element within the E1A protein spanning amino acids

45 In HEK293 cells, NES mutations decrease overall Htt aggregation but incre

46 e nuclear export is mediated via a consensus NES sequence and Crm1, as evidenced by leptomycin B (LMB

47 port signal (NES) that resembles a consensus NES.

48 inding domain as follows: a highly conserved NES in helix 12 (NES-H12) and two additional NES sequenc

49 st demonstration of evolutionarily conserved NESs in all T-box proteins in conjunction with NLSs indi

50 In contrast, NES-CAD was confined to the cytoplasm, and Thr-456 remai

51 The plasticity of the CRM1-NES interaction is not well understood, as there are man

52 re efficient cargo release in the cytoplasm, NESs have evolved to display low affinity for Crm1.

53 al structures of CRM1 bound to two different NESs with unusual sequences showed the NES peptides bind

54 activity was remarkably tolerant of diverse NES sequences, including supraphysiological NES (SNES) p

55 d NES-B10T) and without Barrett's esophagus (NES-G2T and NES-G4T) to study effects of acid and bile s

56 n AID, indicating that all the CSR-essential NES motif functions evolutionarily predated CSR activity

57 s to form a motif reminiscent of established NES.

58 gher sensitivity and precision over existing NES prediction tools upon comparative analysis using exp

59 sequence logos, and agreement with existing NES consensus sequences revealed strong preferences for

60 clear localization (NLS) and nuclear export (NES) signals.

61 Interestingly cells expressing NES mutants exhibit reduced survival after X-irradiation

62 ous exportin and it provides a new basis for NES prediction.

63 As control for NES activity, we show that while GFP-Wdr68 exhibited a p

64 ied structural and sequence determinants for NES orientation.

65 ent forms of psychotherapy are effective for NES.

66 LocNES scans query proteins for NES consensus-fitting peptides and assigns these peptide

67 ent manner and that it contains a functional NES that is sufficient to direct the export of an NLS-co

68 e nucleus, whether it possesses a functional NES, and to determine if nuclear Crk II affects cell cyc

69 first time that 1) survivin has a functional NES; 2) nuclear accumulation of overexpressed survivin c

70 this study, we characterize a new functional NES (175LLSIPELQCLNI186) in the transactivation (TA) dom

71 ures for real NESs might be useful in future NES prediction efforts.

72 The H2+NES ERalpha mutant does not maintain nuclear translocati

73 es did not bind CRM1, hence illustrating how NESs are easily misidentified.

74 ctures of natural, experimentally identified NESs and of false-positive NESs that were generated from

75 ctures showed that experimentally identified NESs are more likely than the false positives to adopt a

76 hobic positions of experimentally identified NESs but not of false positives.

77 ive analysis using experimentally identified NESs.

78 In addition to Tbx5, we identified NESs in all T-box proteins and demonstrated interaction

79 arboring a germline mutation in IkappaBalpha NES.

80 NA (mRNA), protein, and promoter activity in NES-B3T and NES-B10T cells, but not in NES-G2T or NES-G4

81 ucture resulted in a significant decrease in NES-H12 activity.

82 orientations results in a large expansion in NES consensus patterns and therefore a corresponding exp

83 ty in NES-B3T and NES-B10T cells, but not in NES-G2T or NES-G4T cells.

84 ut significantly increased apoptosis only in NES cells.

85 kappaB, Bcl-2, cIAP-1, XIAP, and survivin in NES cells but increased the levels of those proteins in

86 ization, whereas mutation of each individual NES only partially increases the nuclear localization.

87 inor groove-targeted polyamide that inhibits NES with low micromolar efficacy.

88 quires a cooperative action of the intrinsic NES, 14-3-3, and the CRM1 nuclear export receptor.

89 ch occupy different extents of the invariant NES-binding groove.

90 mechanism by which Rev transiently masks its NES peptide, thereby biasing its trafficking to and rete

91 vin can be separated through mutation of its NES.

92 gests that this region may function as a key NES in other nuclear receptors.

93 At P6, hRPCs continued to express VIM, KI67, NES, PAX6, SOX2, GNL3, and SIX6.

94 l developmental genes: VIM (vimentin), KI67, NES (nestin), PAX6, SOX2, HES5, GNL3, OTX2, DACH1, SIX6,

95 em cells were detected, including BMI1, KIT, NES, NOTCH1, and SIX2.

96 dation of Id2, because a p204 mutant lacking NES lost these activities.

97 (iii) In infected cells, VHS-RNase lacking NES degraded the short-lived AU-rich mRNAs but not the s

98 binding beyond the generally low affinity LR-NES.

99 f the leucine-rich nuclear export signal (LR-NES).

100 tite manner by means of an amino-terminal LR-NES and its nucleotide-binding domain.

101 The LR-NES interface explains the consensus hydrophobic pattern

102 The LR-NES is a combined alpha-helical-extended structure that

103 s an acidic patch on CRM1 adjacent to the LR-NES site.

104 ong-term neuroepithelial-like stem cells (lt-NES) from pluripotent cell lines.

105 Mutation of both N-NES and LZ-NES results in a predominant nuclear localization, where

106 (NES) in the leucine zipper domain (named LZ-NES).

107 on is not well understood, as there are many NES sequences that seem incompatible with structures of

108 Remarkably, the Mcm2-Mcm3 NLS and the Mcm3 NES are sufficient to form a transport module that recap

109 s (MPeMSCs) express stem cell markers c-MYC, NES and VEGFR2 and in the presence of matrix components

110 Mutation of both N-NES and LZ-NES results in a predominant nuclear localiza

111 e activities of a dominant N-terminal NES (N-NES) and a distinct C-terminal NLS (C-NLS).

112 Further, mutation of N-NES enhances the transcriptional activity of ATF2, sugge

113 FKLHV(7), also functions as an NES (termed N-NES) in a chromosome region maintenance 1 (CRM1)-depende

114 the shorter P3-P5 isoforms, which lack the N-NES, are believed to be nuclear through the activity of

115 in P3, concomitant with truncation of the N-NES, to become the principal targeting signal conferring

116 Specifically, the N-NES-containing isoforms P1 and P2 are cytoplasmic, where

117 S), which, intriguingly, overlaps with the N-NES.

118 may lie in the interplay between neighboring NES and SUMOylation motifs.

119 Fusions of the CALM NES (NES(CALM)-AF10) or NES motifs from heterologous proteins

120 driven by regulatory elements of the nestin (NES) gene within mouse satellite cells, which permitted

121 In primary cultured neurons, NES mutations increase nuclear accumulation and increase

122 t NIC tagged to a nuclear export signal (NIC-NES), restored autophagy and suppressor function in Notc

123 The discovery of multiple NLS/NES motifs in Nrf2 and the redox sensitivity of NESTA im

124 Functional NLSs, NES, and GSK3-beta-dependent phosphorylation regulate it

125 cificity filter that prevents binding of non-NES peptides.

126 activity of ATF2, suggesting that the novel NES negatively regulates the transcriptional potential o

127 The Nrf2 NES was sensitive to leptomycin B and could function as

128 The Nrf2-NES appeared to be redox-insensitive.

129 sitive, the redox insensitivity of this Nrf2-NES indicates the importance of Keap1 retention as a key

130 The Nurr1 NES was sensitive to CRM1 and could function as an indep

131 effective communication of the diagnosis of NES.

132 s information about experimental evidence of NES-mapping and CRM1-mediated nuclear export.

133 ay, we also found that ectopic expression of NES mutants can complement for depletion of endogenous s

134 cance of the heterogeneous manifestations of NES.

135 The large conformational range of NES backbones explains the lack of a fixed pattern for i

136 se, clinical manifestations and treatment of NES.

137 t research has improved our understanding of NES as a biopsychosocial disorder.

138 t S6 is cytoplasmic, due to the unmasking of NES.

139 The binding of NESs to CRM1 in both orientations results in a large exp

140 Due to the diverse and complex nature of NESs, reliable prediction of the signal remains a challe

141 Furthermore, our mutagenesis studies on NES-H12 suggest that altered shuttling of thyroid hormon

142 Fusions of the CALM NES (NES(CALM)-AF10) or NES motifs from heterologous proteins (ABL1, Rev, PKIA,

143 3T and NES-B10T cells, but not in NES-G2T or NES-G4T cells.

144 Identification of mutations in mapped NLS or NES domains in heterotaxy patients demonstrates the func

145 Disruption of either the NLS or NES sequences of nibrin significantly altered the cellul

146 cells expressing K17 mutations in its NLS or NES signals exhibited an increase in levels of nuclear p

147 he UBA and either the Nxt1-binding domain or NESs.

148 rminal NES, which cooperates with five other NES elements to exclude MRTF-A from the nucleus.

149 ogether, these results indicate that the p10 NES domain of Gag is critical for virus replication and

150 Gag mutants containing deletions of the p10 NES or mutations of critical hydrophobic residues at pos

151 wly identified monomerization-dependent PCNA NES.

152 Comparison of minus and plus NESs identified structural and sequence determinants for

153 enhances association with Rev-RRE and poises NES binding sites to interact with a Rev oligomer.

154 ntally identified NESs and of false-positive NESs that were generated from the database in order to i

155 n B or independent mutation of the potential NES (NESm) abolished Wee1 nuclear export.

156 efore a corresponding expansion of potential NESs in the proteome.

157 These findings led to a new and more precise NES consensus.

158 ased signal change compared with ratiometric NES-YC3.6 in response to several stimuli.

159 Such distinguishing features for real NESs might be useful in future NES prediction efforts.

160 tch arrangement of overlapping, co-regulated NES/NLS sequences is vital to delineating the critical r

161 ring structure of a full-length, 665-residue NES-DNA complex.

162 tform to study the effects of modulating Rev NES identity, number, position, or strength on Rev subce

163 The leucine-rich NES is recognized by the export receptor Crm1 to mediate

164 K17, we defined and validated a leucine-rich NES that mediated CRM1 binding for export.

165 Oxidative stress inactivates Keap1's NES, allowing entry of both Keap1 and Nrf2 into the nucl

166 ot accumulate in plant nuclei (SAP11DeltaNLS-NES) was able to bind and destabilize TCP transcription

167 s about (psychogenic) nonepileptic seizures (NES) over the past two decades.

168 g homology to known nuclear export sequence (NES) domains.

169 demonstrate that a nuclear export sequence (NES) in Keap1 is required for termination of Nrf2-antiox

170 ive, CRM1-dependent nuclear export sequence (NES) in the AMPK catalytic subunit (AMPKalpha).

171 The N-terminal nuclear export sequence (NES) of inhibitor of nuclear factor kappa B (NF-kappaB)

172 that N17 acts as a nuclear export sequence (NES) within Htt exon and when fused to yellow fluorescen

173 that constitute the nuclear export sequence (NES).

174 ear localization (NLS) and export sequences (NES).

175 omer that displays nuclear export sequences (NESs) for recognition by the Crm1-Ran(GTP) nuclear recep

176 device based on nano-electrostatic sieving (NES) mechanism that is facilitated by multi-nanofluidic

177 identify a canonical nuclear export signal (NES) ((537)LKKQLSTLYL(546)) located in the leucine zippe

178 tify a Crm1-dependent nuclear export signal (NES) adjacent to the Mcm3 NLS.

179 ated by an N-terminal nuclear export signal (NES) and a C-terminal nuclear localization signal (NLS).

180 experiments with hBVR nuclear export signal (NES) and nuclear localization signal (NLS) mutants demon

181 p27(KIP1) lacks a nuclear export signal (NES) and requires an adaptor for CRM1 binding for nuclea

182 including a divergent nuclear export signal (NES) and two nuclear localization signals (NLSs).

183 ce 1 (CRM1)-dependent nuclear export signal (NES) at the AID C terminus is necessary for CSR, and has

184 more, we identified a nuclear export signal (NES) at the N terminus (AAs 176-192) that contributes to

185 VHS-RNase contains a nuclear export signal (NES) but not a nuclear localization signal.

186 the zebrafish, that a Nuclear Export Signal (NES) fusion protein (GFPNESWdr68) failed to support cran

187 rted a CRM1-dependent nuclear export signal (NES) in E1A that is conserved in the group C adenoviruse

188 osing or activating a nuclear export signal (NES) in the C terminus of p53.

189 studies identified a nuclear export signal (NES) in the intervening region of Keap1 comprised of hyd

190 basic region and one nuclear export signal (NES) in the leucine zipper domain (named LZ-NES).

191 cin B (LMB)-dependent nuclear export signal (NES) in the p10 domain.

192 and a CRM1-dependent nuclear export signal (NES) in the SUMO protease SENP2.

193 larly to the NLS, the nuclear export signal (NES) is not apparent in the primary sequence, but assemb

194 The leucine-rich nuclear export signal (NES) is the only known class of targeting signal that di

195 ed for exposing p53's nuclear export signal (NES) is unnecessary for p53 nuclear export.

196 calization involved a nuclear export signal (NES) located from Ile-11 to Ile-23 in the PCNA sequence.

197 putative leucine-rich nuclear export signal (NES) motif that overlaps with the PHD-Bromo interaction

198 ovel CRM1-independent nuclear export signal (NES) motifs in the ligand-binding domain as follows: a h

199 tion signal (NLS) and nuclear export signal (NES) motifs, and constitutively shuttles between the nuc

200 Nucleus export signal (NES) of p204 is required for the p204-enhanced cytoplasm

201 ibitin; fusion of the nuclear export signal (NES) of prohibitin to green fluorescence protein led to

202 (NLS) sequences and a nuclear export signal (NES) sequence whose functions were confirmed by mutagene

203 rities to a canonical nuclear export signal (NES) that also binds CRM1/exportin 1.

204 e describe for Tbx5 a nuclear export signal (NES) that is recognized by the CRM1 export protein.

205 that CALM contains a nuclear export signal (NES) that mediates cytoplasmic localization of CALM-AF10

206 151 is adjacent to a nuclear export signal (NES) that resembles a consensus NES.

207 xclusion, driven by a nuclear export signal (NES) that restricts GEN1 actions to mitosis when the nuc

208 otypical leucine-rich nuclear export signal (NES) to GFP as a cargo model and expressed the fluoresce

209 A functional nuclear export signal (NES) was identified in the C terminus of the protein (am

210 addition, a putative nuclear export signal (NES) was identified, and mutation of it also inhibited n

211 Additionally, a novel nuclear export signal (NES) was identified, which included residues L526 and L5

212 A nuclear export signal (NES) was previously identified within the p10 domain of

213 yptic CRM-1-dependent nuclear export signal (NES) within ZIC3, and identify a mutation within this re

214 ng its Crm1-dependent nuclear export signal (NES), all functioned in export.

215 ion signal (bNLS) and nuclear export signal (NES), as well as to a fluorescent protein for microscopy

216 and harbors a masked nuclear export signal (NES), the transdominant negative mutant S6 is cytoplasmi

217 The nuclear export signal (NES)-binding groove of CRM1 is able to drive a chemical

218 We compiled >200 nuclear export signal (NES)-containing CRM1 cargoes in a database named NESdb.

219 ses a normally buried nuclear export signal (NES)-like sequence.

220 n using an N-terminal nuclear export signal (NES).

221 otypical leucine-rich nuclear export signal (NES).

222 ein Nmd3 to provide a nuclear export signal (NES).

223 signal and C-terminal nuclear export signal (NES).

224 ntify a rev-like nuclear exportation signal (NES) in the central domain of survivin and demonstrate t

225 basic region and a nuclear exporting signal (NES) in the leucine zipper domain of Nrf2.

226 expression of the nuclear exporting signal (NES)-fused form of Rb caused disruption of sarcomeric or

227 and two leucine-rich nuclear export signals (NES) in its ligand binding domain.

228 presence of three nuclear exclusion signals (NESs) in the PRMT5 protein.

229 Classical nuclear export signals (NESs) are short cognate peptides that direct proteins ou

230 inds highly variable nuclear export signals (NESs) in hundreds of different cargoes.

231 taining leucine-rich nuclear export signals (NESs) through complex formation with RanGTP.

232 recognition of their nuclear export signals (NESs), which are highly variable in sequence and structu

233 us to Crm1-dependent nuclear export signals (NESs).

234 s, NLSs) and export (nuclear export signals, NESs).

235 Sorted NES-GFP+ cells exclusively acquired a myogenic fate, eve

236 trate the first identification of a specific NES within CIITA and place it among the other protein do

237 telomerase-immortalized esophageal squamous (NES) and Barrett's (BAR-T) epithelial cell lines.

238 ett's esophagus (normal esophageal squamous [NES]-B3T and NES-B10T) and without Barrett's esophagus (

239 tation (minus) to that of previously studied NESs (plus).

240 NES sequences, including supraphysiological NES (SNES) peptides that otherwise arrest CRM1 transport

241 se, patients with the night eating syndrome (NES) and persons without an eating disorder were assesse

242 m the cell nucleus by CRM1, and the Takifugu NES can substitute for the equivalent region in human AI

243 ation of mutant p53s required the C-terminal NES and an intact ubiquitination pathway.

244 iated export of AMPKalpha via its C-terminal NES provides an additional mechanism for cells to use in

245 n promotes nuclear export via the C-terminal NES.

246 t in vivo for the AMPKalpha carboxy-terminal NES, as transgenic Drosophila expressing AMPKalpha lacki

247 ween the activities of a dominant N-terminal NES (N-NES) and a distinct C-terminal NLS (C-NLS).

248 y of an autonomous Crm1-dependent N-terminal NES, which cooperates with five other NES elements to ex

249 Further studies demonstrate that NES-mediated nuclear export of Nrf2 is required for degr

250 ng and functional assays also indicated that NES masking underpins Rev's well-known tendency to accum

251 The NES device exhibits polarity selectivity on the analytes

252 The NES device is fabricated by standard photolithography an

253 The NES in KLF5 directs a fused green fluorescence protein t

254 The NES N-terminal relaxase-DNA complex crystal structure re

255 The NES-GFP model reveals unique transcriptional activity wi

256 Antibodies against the NES-like sequence recognize misfolded SOD1, but not nati

257 Both the NLS and the NES are located in the nonhomologous domains of SENP2 an

258 e phosphorylation of the S89 residue and the NES plays a role for an efficient viral replication in t

259 scaffold to optimally present RanGTP and the NES to Crm1, therefore, triggering 40S pre-ribosome expo

260 ion about sequence and structure of both the NES and the cargo protein, as well as information about

261 s then transported out of the nucleus by the NES in Keap1.

262 By modeling FRAP data, we calculate the NES affinity for the export machinery and the maximum ra

263 ince Apoptin fragments containing either the NES or the NLS fail to differentially localize in transf

264 Consistent with a role for the NES sequence in viral replication, this cluster of hydro

265 ing SENP2 in the nucleus by mutations in the NES impairs its polyubiquitination, whereas a cytoplasm-

266 the shuttling is blocked by mutations in the NES or by treating cells with leptomycin B.

267 he acidic C-terminal TAD, which includes the NES motif, or by leptomycin B-mediated inhibition of the

268 The CRM1 C-terminal domain lacking the NES-binding groove interacts with tetrameric p53, and th

269 elf-association acts to transiently mask the NES peptide(s), thereby biasing Rev's trafficking into t

270 h the NPC is dependent on recognition of the NES by Crm1, their interaction with Crm1 is not strictly

271 Disruption of the NES consensus sequence relocalizes mutant SOD1 to the nu

272 howed that the replication efficiency of the NES mutant adenovirus was up to 500-fold lower than that

273 We found that 16 of the NES peptides did not bind CRM1, hence illustrating how N

274 Mutation of the NES sequence in nibrin slowed the turnover of phosphoryl

275 hat seem incompatible with structures of the NES-bound CRM1 groove.

276 Disruption of either the NLS or the NES in nsP2 compromised essential viral functions.

277 hin the noncatalytic domain, but outside the NES, influence its function.

278 erent NESs with unusual sequences showed the NES peptides binding the CRM1 groove in the opposite ori

279 Delivery of a peptide corresponding to the NES of prohibitin prevented the export of prohibitin to

280 re mediated by domains that overlap with the NES and NLS sequences, respectively.

281 ions of specific leucine residues within the NES disrupt the normal subcellular distribution of the f

282 TF2 requires function of at least one of the NESs.

283 This NES motif is highly conserved in widely divergent specie

284 However, this NES, located at the inner face of the PCNA trimer, was n

285 lear localization of KLF5 by inhibiting this NES activity, and enhances the ability of KLF5 to stimul

286 Drosophila expressing AMPKalpha lacking this NES fail to rescue lethality of AMPKalpha null mutant fl

287 Mutation of leucine residue 238 of this NES motif abolished the interaction between CRM1 and TRI

288 n either one or two leucine residues of this NES sequence abolished the nuclear exclusion of the LZTS

289 equence determined the functionality of this NES.

290 export carrier protein CRM1 recognizes this NES-like sequence and exports misfolded SOD1 to the cyto

291 15 and Siah2 form a complex with AR, through NES(AR).

292 are frequently located in close proximity to NESs.

293 ine residues in agreement with a traditional NES consensus sequence.

294 Furthermore, two NES were characterized in the ligand binding domain, who

295 yribosomes, we constructed a mutant in which NES was ablated.

296 iferase transcriptional reporter assays with NES mutant Tbx5 forms demonstrated retention in the nucl

297 from 2 studies, each involving patients with NES and control subjects.

298 ic and management pathways for patients with NES are likely to emerge in the near future.

299 imental work has revealed that patients with NES have increased levels of physiological arousal at re

300 f normal-weight and overweight subjects with NES.