ライフサイエンスコーパス: NES

1 NES exhibits systemic and local accumulation of immunosu

2 NES initiates and terminates the transfer of plasmids th

3 NES-containing proteins are involved in numerous cellula

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 osomal proteins (false discovery rate <0.25; NES, 1.95).

8 cellular matrix (false discovery rate <0.25; NES, 2.25).

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

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

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

12 localization of RPW8.2 by tagging it with a NES led to lethal cell death.

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

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

15 t that understanding how CRM1(E571K) affects NES binding provides a platform for identifying cargoes

16 A), as determined by the PKA reporter, AKAR4-NES, and induced phosphorylation of vasodilator-stimulat

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

18 All NESs also participate in main chain hydrogen bonding wit

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

20 tein sequences, whether the motif acts as an NES (true positive) or not (false positive).

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

22 Furthermore, we have identified an NES-containing nucleocytoplasmic shuttling domain (aa 19

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

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

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

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

27 o the differential diagnosis of epilepsy and NES.

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

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

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

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

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

33 ay of peptide sequences that can function as NESs.

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

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

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

37 ht-forward approach to identify CRM1-binding NES sequences by analysis of their structural prerequisi

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

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

40 50 and 100 J/m(2)) caused DNA damage in both NES and BAR-T cells but significantly increased apoptosi

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

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

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

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

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

50 cargoes, suggesting limitations with current NES prediction methods.

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

52 Better defined NES should also allow meaningful mapping of cancer-relat

53 pithelial stem (hbNES) cells or iPSC-derived NES cells, which display a range of aggressive phenotype

54 iPSC-derived NES tumors develop quickly with leptomeningeal dissemina

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

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

57 ding affinities and structures of 27 diverse NESs for wild-type and E571K CRM1 with structure-based b

58 ancer (TNBC), including neutrophil-enriched (NES) and macrophage-enriched subtypes (MES).

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

60 s to form a motif reminiscent of established NES.

61 001, FDR P = 0.005], and cholesteryl esters (NES = -1.77, P = 0.005, FDR P = 0.02), and phosphatidylc

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

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

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

65 Extracted NES are scored for reliability by combining sequence-bas

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

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

68 ied structural and sequence determinants for NES orientation.

69 ent forms of psychotherapy are effective for NES.

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

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

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

73 ed candidate cooperating mutations in Gorlin NES cells, with mutation of DDX3X or loss of GSE1 both a

74 We found that Gorlin NES cells formed tumors in mouse cerebellum mimicking hu

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

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

77 These findings demonstrate that human NES cells provide a potent experimental resource for dis

78 The confidently identified NES candidate motifs were checked for overlap with cance

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

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

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

82 ive analysis using experimentally identified NESs.

83 arboring a germline mutation in IkappaBalpha NES.

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

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

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

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

88 ut significantly increased apoptosis only in NES cells.

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

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

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

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

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

94 Retransplantation of tumor-isolated NES (tNES) cells resulted in accelerated tumor formation

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

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

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

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

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

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

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

102 binding beyond the generally low affinity LR-NES.

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

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

105 The LR-NES interface explains the consensus hydrophobic pattern

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

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

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

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

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

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

112 3CA with the neuronal stem/progenitor marker NES was associated with poor prognosis in PN GBM patient

113 While most NESs bind the two CRM1 similarly, NESs from Mek1, eIF4E-

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

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

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

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

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

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

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

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

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

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

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

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

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

127 Nfkbia(NES/NES) CD8 T cells harboring a mutated IkappaBalpha nu

128 Consequently, CD8 T cells in Nfkbia(NES/NES) mice poorly expand during viral infection, and

129 at the antiviral CD8 T cell defect in Nfkbia(NES/NES) mice was cell intrinsic.

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

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

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

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

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

135 ructures of CRM1 bound to various classes of NES peptides, we adopted, for the first time, the struct

136 effective communication of the diagnosis of NES.

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

138 cance of the heterogeneous manifestations of NES.

139 Prediction of NES is of great interest in many aspects of research inc

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

141 Orthotopic transplantation of NES cells generated from Gorlin syndrome patients, who a

142 se, clinical manifestations and treatment of NES.

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

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

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

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

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

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

149 3T and NES-B10T cells, but not in NES-G2T or NES-G4T cells.

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

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

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

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

154 wly identified monomerization-dependent PCNA NES.

155 05, FDR P = 0.02), and phosphatidylcholines (NES = -1.72, P = 0.01, P = 0.03) were negatively enriche

156 er binding affinity than (Hs)CRM1 toward PKI-NES and significant differences in affinities toward pot

157 Finding more plausible NES functioning regions among the vast array of consensu

158 be useful for determining the most plausible NES region in the context of the whole protein sequence

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

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

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

162 Possible NES candidate regions are extracted from the cancer-rela

163 178 sequences are predicted to have possible NES motifs containing cancer-related mutations at their

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

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

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

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

168 finding a feature that can distinguish real NES motifs from false positives is desired to improve th

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

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

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

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

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

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

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

176 iation with WD [normalized enrichment score (NES) = 2.01, P = 0.001, FDR P = 0.005], and cholesteryl

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

178 ng groove, suggesting that binding of select NESs may be altered.

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

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

181 located within the nuclear export sequence (NES) of human RGS14.

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

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

184 sequence (NLS) and nuclear export sequence (NES), suggesting a role in nucleo-cytoplasmic transport.

185 that constitute the nuclear export sequence (NES).

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

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

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

189 s, we have identified nuclear export signal (NES) (19)LSLRELAI(26) of p17.

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

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

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

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

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

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

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

197 consensus pattern of Nuclear Export Signal (NES) is a short sequence motif that is commonly identifi

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

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

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

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

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

203 Nuclear export signal (NES) motifs function as essential regulators of the subc

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

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

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

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

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

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

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

211 151 is adjacent to a nuclear export signal (NES) that resembles a consensus NES.

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

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

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

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

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

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

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

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

220 RM1 is located in its nuclear export signal (NES)-binding groove, suggesting that binding of select N

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

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

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

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

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

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

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

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

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

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

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

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

233 LSs), as well as the nuclear export signals (NESs), in RPW8.2 is critical for the activation of cell

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

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

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

237 While most NESs bind the two CRM1 similarly, NESs from Mek1, eIF4E-transporter, and RPS2 showed >10-f

238 d that large affinity changes seen with some NES peptides (of Mek1 and RPS2) do not always translate

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

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

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

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

243 rate <0.25; normalized enrichment statistic [NES], 2.15).

244 PS) cell-derived human neuroepithelial stem (NES) cells generated from a Gorlin syndrome patient carr

245 Here, we evaluated neuroepithelial stem (NES) cells, representative of cerebellar progenitors.

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

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

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

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

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

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

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

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

254 Taken together, we demonstrate that NES cells derived from Gorlin patients can be used as a

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

256 The NES device exhibits polarity selectivity on the analytes

257 The NES device is fabricated by standard photolithography an

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

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

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

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

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

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

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

265 acids (aa 19 to 40) of p17 that comprise the NES can modulate both p17 and hnRNP A1 interaction and n

266 onservation and structural similarity in the NES-binding cleft region, (Sc)CRM1 exhibits 16-fold lowe

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 rgo proteins, containing the location of the NES consensus patterns with the disordered propensity pl

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

272 time, the structure-based prediction of the NES motifs bound to the CRM1's binding groove.

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 Whereas expression of the NES-containing C-terminal domain of RPW8.2 in the cytopl

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

278 red from high false positive rates since the NES consensus patterns are quite commonly observed in pr

279 the two EHM-targeting signals along with the NES-containing C-terminal domain.

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

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

282 These NESs have multiple charged side chains binding close to

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 equence determined the functionality of this NES.

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

290 15 and Siah2 form a complex with AR, through NES(AR).

291 are frequently located in close proximity to NESs.

292 A MES-to-NES conversion mediated acquired ICB resistance of initi

293 We transduced NES cells with MYCN, observing medulloblastoma upon orth

294 Consistent with eIF4E-transporter NES binding weaker to CRM1(E571K), eIF4E-transporter was

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

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

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.