ライフサイエンスコーパス: NCL

1 NCL also regulates the biogenesis of specific microRNAs

2 NCL knockdown specifically reduced the ORF2 IRES activit

3 NCL overexpression increased EBNA1 binding to oriP and t

4 NCL repression of p53 translation utilizes both the 5'-

5 NCL RNA-binding domain K429 was critical for ATP and EBN

6 PL26, respectively, and that disruption of a NCL-NCL homodimer by RPL26 may be the switch between tra

7 After NCL, the lipid moiety is removed to yield an unmodified

8 us hydrazine to cleave the Ddae linker after NCL-based assembly.

9 ction can be disrupted by the addition of an NCL binding aptamer (AS1411).

10 EBNA1's N-terminal 100 aa and NCL's RNA-binding domains were critical for EBNA1/NCL in

11 A, is required for both NCL dimerization and NCL-mediated translational repression, and is the domain

12 ion was stronger between the entopallium and NCL.

13 to loss of PGRN contributes to both FTD and NCL pathology in a dose-dependent manner.

14 hilic deposits, suggesting that both FTD and NCL-like pathology are present in PGRN patient neurons a

15 es both the 5'- and 3'-UTRs of p53 mRNA, and NCL binds to the same 5'-3'-UTR interaction region that

16 tical interaction between DENV C protein and NCL that represents a potential new target for the devel

17 We confirmed reports that RPL26 and NCL interact with each other and then explored the poten

18 e describe, to our knowledge, the first anti-NCL single-chain fragment variable displaying antineopla

19 novel therapeutic target for GRN-associated NCL and FTD and highlight the emerging theme of defectiv

20 erts to arylthioesters that are efficient at NCL.

21 epresent the prototype of novel immune-based NCL-targeting drugs with clinical potential as diagnosti

22 sent work was to study the interplay between NCL and alpha(v)beta(3) by using biochemical, immunofluo

23 This immunoagent binds NCL on the cell surface, it is translocated into the cyt

24 in binding to p53 mRNA, is required for both NCL dimerization and NCL-mediated translational repressi

25 al repression and stress induction of p53 by NCL and RPL26, respectively, and that disruption of a NC

26 der telencephalon, nidopallium caudolateral (NCL) were simultaneously recorded.

27 g in birds is the nidopallium caudolaterale (NCL) and the mammalian equivalent is known as the prefro

28 ation area termed nidopallium caudolaterale (NCL) from crows that assessed and briefly memorized nume

29 elencephalic area nidopallium caudolaterale (NCL) while two crows (Corvus corone) performed a delayed

30 le neurons in the nidopallium caudolaterale (NCL), a pallial association area of the avian endbrain.

31 rons in the avian nidopallium caudolaterale (NCL), an endbrain structure that originated independentl

32 e-spanning proteins, whose deficiency causes NCL in mouse and man.

33 evidence on the association of genes causing NCL with retromer function and endosomal trafficking, re

34 al ligation and thiol-ene radical chemistry (NCL-TEC) on the resulting cysteine thiol has been invest

35 rompted the isolation of several sub-clones (NCL-1-12) to identify a more tractable and improved in v

36 vivo than its noncleavable (NC) analog, CMP-NCL-CA4.

37 t stem cells (iPSCs) for the two most common NCL subtypes: classic late-infantile NCL, caused by TPP1

38 hich the infantile NCL (INCL) and congenital NCL (CNCL) are the most lethal.

39 disease), which is second only to congenital NCL for its age of onset and devastating progression.

40 CLN3 is the most widely conserved NCL gene, suggesting that it has a basic eukaryotic cell

41 d working memory of numerosities in the crow NCL exhibiting several characteristics that are surprisi

42 mmunolabelling with the antibody (designated NCL-hamlet) demonstrated a polypeptide of approximately

43 ronal ceroid lipofuscinosces/Batten disease (NCL) is a devastating group of neurodegenerative disease

44 Excessive RPL26 disrupts NCL dimerization, and point mutations in the NCL-interac

45 Dorsal NCL contained relatively dense staining for TH, choline

46 d for investigating early mechanisms driving NCL pathogenesis.

47 RNA-binding domains were critical for EBNA1/NCL interaction.

48 generated the first CRISPR/Cas9 gene edited NCL model.

49 tly inhibited nucleolin expression, enhanced NCL mRNA association with argonaute-containing complexes

50 ected against the full-length human ERalpha (NCL-ER-6F11), calcium-binding proteins calbindin-D(28k),

51 was accomplished through a menu of extended NCL followed by metal free dethiylation.

52 e linker can be cleaved in one pot following NCL or desulfurization.

53 PSAP is an underlying disease mechanism for NCL and FTLD due to GRN mutations.

54 points postinfection, suggesting a role for NCL in viral morphogenesis.

55 ents reveal a surprisingly critical role for NCL K429 in EBNA1 episome maintenance and transcription,

56 nt of gene therapies targeting the brain for NCLs caused by defects in transmembrane proteins has bee

57 lementation have shown promising results for NCLs caused by lysosomal enzyme deficiencies.

58 nce linking NCL genes to AD, and discuss how NCL, AD, and PD converge on a shared molecular pathway.

59 In NCL, lysosomes accumulate autofluorescent proteolipid in

60 ed with the survival of patients with HCC in NCL although the therapeutic options differ from those f

61 Data on patients with HCC in NCL in advanced stages are scarce.

62 Only a minority of patients with HCC in NCL lacked any sign of hepatic damage.

63 More than 25% of patients with HCC in NCL presented with extrahepatic metastases.

64 performed comparing 93 patients with HCC in NCL to 571 patients with HCC in liver cirrhosis (LC) wit

65 influencing survival in patients with HCC in NCL were analyzed.

66 Patients with HCC in NCL were diagnosed at older age and in more advanced tum

67 sent in the majority of patients with HCC in NCL.

68 nal peptide-thioesters, key intermediates in NCL.

69 ffects that are similar to those observed in NCL.

70 We contend that NMD targets PTCs in NCL gene transcripts for degradation.

71 widespread pathology similar to that seen in NCL.

72 alpha-thioesters that were directly used in NCL without purification.

73 argonaute-containing complexes, and induced NCL RNA transport to PBs.

74 Infantile NCL (INCL), the most severe form of NCL, is caused by mu

75 of all disease causing alleles in infantile NCL, the most common of which worldwide is the p.R151X m

76 most severe form of the disease is infantile NCL (INCL).

77 to that which occurs in human late infantile NCL.

78 The gene for variant late-infantile NCL (vLINCL), CLN6, was previously mapped to chromosome

79 common NCL subtypes: classic late-infantile NCL, caused by TPP1(CLN2) mutation, and juvenile NCL, ca

80 n an ovine model of a variant late-infantile NCL, there is abnormal expression of sleep homeostasis.

81 d Cln6(nclf) model of variant late-infantile NCL.

82 models of NCL: Ppt1(-/-) model of infantile NCL and Cln6(nclf) model of variant late-infantile NCL.

83 rred with a suspected diagnosis of infantile NCL who had normal PPT activity.

84 arious types of NCLs, of which the infantile NCL (INCL) and congenital NCL (CNCL) are the most lethal

85 The infantile NCL (INCL) is the most devastating neurodegenerative LSD

86 ns in CLN1 primarily manifest with infantile NCL (INCL or Haltia-Santavuori disease), which is second

87 missense mutations associated with infantile NCL showed no residual enzyme activity, whereas mutation

88 lity of two novel KDM1A-specific inhibitors (NCL-1 and NCD-38) to promote differentiation and apoptos

89 Interestingly, NCL is expressed on the surface of actively proliferatin

90 ine cerebellar cells derived from a juvenile NCL model (CLN3) showed enrichment of endogenous KCTD7.

91 caused by TPP1(CLN2) mutation, and juvenile NCL, caused by CLN3 mutation.

92 nical history is characteristic for juvenile NCL.

93 l mutant (Cln3(-/-)) mouse model of juvenile NCL (JNCL) that revealed a delayed onset neurodegenerati

94 er, mutations in CLN3 are linked to juvenile NCL (JNCL), the latest onset and mildest form of NCL in

95 patients originally diagnosed with juvenile NCL.

96 en ruled out for mutations in the nine known NCL-associated genes, suggesting that additional genes r

97 The NEXUS Class Library (NCL) is a collection of C++ classes designed to simplify

98 Native chemical ligation (NCL) affords an N-linked chitobiose glycoprotein analogu

99 Although native chemical ligation (NCL) and related chemoselective ligation approaches prov

100 of the machine via native chemical ligation (NCL) demonstrates that even challenging 15- and 19-membe

101 e broad utility of native chemical ligation (NCL) in protein synthesis has fostered a search for meth

102 Native chemical ligation (NCL) is widely applicable for building proteins in the l

103 as performed using native chemical ligation (NCL) of a C-terminal peptide thioester and an N-terminal

104 n order to perform native chemical ligation (NCL) of two peptide fragments.

105 obes combining the native chemical ligation (NCL) reaction with solid phase peptide synthesis (SPPS).

106 sn(36) by means of native chemical ligation (NCL) to give the full sequence of diptericin epsilon.

107 escribe the use of native chemical ligation (NCL) to rapidly prepare phospholipids spontaneously from

108 ive and reversible native chemical ligation (NCL) which can take place at N-(methyl)-cysteine residue

109 In one approach, native chemical ligation (NCL), short, unprotected peptides are connected through

110 ue was achieved by native chemical ligation (NCL).

111 eptide by means of native chemical ligation (NCL).

112 on can facilitate native chemical ligations (NCLs) between a peptide-thioester - in which the thioest

113 predicted to contain a non-conserved linker (NCL) sequence flanked by highly conserved N- and C-termi

114 fficking, review the recent evidence linking NCL genes to AD, and discuss how NCL, AD, and PD converg

115 n disease or neuronal ceroid lipofuscinoses (NCL) are a group of genetic neurodegenerative diseases t

116 The neuronal ceroid lipofuscinoses (NCL) are progressive neurodegenerative disorders with on

117 mal dominant neuronal ceroid lipofuscinoses (NCL) CLN4 is caused by mutations in the synaptic vesicle

118 Neuronal ceroid-lipofuscinoses (NCL) are autosomal recessive disorders that form the mos

119 The neuronal ceroid lipofuscinoses (NCLs) are a group of autosomal recessive neurodegenerati

120 The neuronal ceroid lipofuscinoses (NCLs) are a group of devastating monogenetic lysosomal d

121 The neuronal ceroid lipofuscinoses (NCLs) are a group of fatal, monogenic neurodegenerative

122 Human neuronal ceroid lipofuscinoses (NCLs) are a group of genetic neurodegenerative diseases

123 The neuronal ceroid lipofuscinoses (NCLs) are a group of inherited and incurable neurodegene

124 Neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative lysosom

125 The neuronal ceroid lipofuscinoses (NCLs) are common neurodegenerative disorders of childhoo

126 Neuronal ceroid lipofuscinoses (NCLs) are neurodegenerative storage diseases characteriz

127 Neuronal ceroid lipofuscinoses (NCLs) are the most common childhood neurodegenerative LS

128 Neuronal ceroid lipofuscinoses (NCLs) are the most common hereditary neurodegenerative d

129 Neuronal ceroid lipofuscinoses (NCLs) comprise a heterogeneous group of metabolic storag

130 The neuronal ceroid lipofuscinoses (NCLs), also known as Batten disease, are a group of auto

131 Neuronal ceroid lipofuscinoses (NCLs), as a group, represent one of the most common (one

132 The neuronal ceroid lipofuscinoses (NCLs), more commonly referred to as Batten disease, are

133 ncluding the neuronal ceroid lipofuscinoses (NCLs).

134 Neuronal ceroid lipofuscinoses (NCLs; Batten disease) are collectively the most frequent

135 Neuronal ceroid lipofuscinosis (NCL) comprises approximately 13 genetically distinct lys

136 atients with neuronal ceroid lipofuscinosis (NCL) develop neurodegeneration characterized by vision l

137 se models of neuronal ceroid lipofuscinosis (NCL) exhibit many features of the human disorder, with w

138 Neuronal ceroid lipofuscinosis (NCL) is a genetically heterogeneous group of lysosomal d

139 te infantile neuronal ceroid lipofuscinosis (NCL) is an inherited disorder characterized by progressi

140 Neuronal ceroid lipofuscinosis (NCL) is one of the most prevalent neurodegenerative diso

141 ses known as neuronal ceroid lipofuscinosis (NCL) or Batten disease has been identified.

142 h variant of neuronal ceroid lipofuscinosis (NCL) or Batten disease, due to defects in a putative new

143 tive disease neuronal ceroid lipofuscinosis (NCL), accumulated throughout the CNS but not in visceral

144 Neuronal ceroid lipofuscinosis (NCL), commonly referred to as Batten disease, is a group

145 me (KRS) and neuronal ceroid lipofuscinosis (NCL).

146 n, infantile neuronal ceroid lipofuscinosis (NCL).

147 r, infantile neuronal ceroid lipofuscinosis (NCL).

148 age disorder neuronal ceroid lipofuscinosis (NCL).

149 clusions and neuronal ceroid lipofuscinosis (NCL).

150 ge disorder, neuronal ceroid lipofuscinosis (NCL).

151 ine model of neuronal ceroid lipofuscinosis (NCL, Batten disease) caused by a mutation in CLN5 In hum

152 a family of neuronal ceroid lipofuscinosis (NCLs) diseases.

153 hy (SMA) and neuronal ceroid lipofuscinosis (NCLs).

154 HCC is diagnosed in the non-cirrhotic liver (NCL).

155 We show that many NCL neurons encode information about visual stimuli and

156 Lentivirus shRNA-mediated NCL depletion substantially reduced EBNA1 recruitment to

157 orization of numerosities in working memory, NCL activity predicted the crows' number discrimination

158 preclinical studies using orthotopic models, NCL-1 and NCD-38 significantly reduced GSCs-driven tumor

159 Moreover, NCL silencing impaired lymphoblastoid cell line growth.

160 was rescued by reintroducing the non-mutated NCL proteins.

161 otechnology Characterization Laboratory (NCI-NCL) have jointly developed multiple standard operating

162 ective article would like to present the NCI-NCL and EUNCL multi-step approach of incremental complex

163 the homing pigeon caudolateral neostriatum (NCL).

164 his process, suppressor-26 (sup-26) and NHL (NCL-1, HT2A, and LIN-41 repeat) domain-containing-2 (nhl

165 me) but not in the caudolateral nidopallium (NCL) or hippocampus.

166 The caudolateral nidopallium (NCL, the avian analogue of the mammalian prefrontal cort

167 Nucleolin (NCL) is a nucleocytoplasmic protein involved in many bio

168 Nucleolin (NCL) was identified to be EBNA1 associated.

169 RPL4 and Nucleolin (NCL) were a scaffold for an EBNA1-induced oriP complex.

170 proteins (hnRNPs) R, Q and L, and nucleolin (NCL), appeared to interact specifically with the ORF2 IR

171 In contrast, nucleolin (NCL) suppresses the translation of p53 mRNA and its indu

172 The multifunctional protein nucleolin (NCL) is overexpressed on the surface of activated endoth

173 the multifunctional host protein nucleolin (NCL).

174 Here we find that nucleolin (NCL), a major nucleolar protein, posttranscriptionally r

175 uR was found to interact with the nucleolin (NCL) 3'UTR and specifically promoted nucleolin translati

176 As a lysosomal storage disease, all 13 of NCL's causative genes affect endolysosomal function, and

177 This suggests that sustained activity of NCL neurons is a neuronal correlate of visual working me

178 This work expands the application of NCL to the formation of phospholipid membranes.

179 et cells, and it abrogates the biogenesis of NCL-dependent miRNAs.

180 ion of lipofuscin deposits characteristic of NCL, thus providing the first direct demonstration that

181 We found that the RNA-binding domain of NCL participates in binding to p53 mRNA, is required for

182 anslational repression, and is the domain of NCL that interacts with RPL26.

183 affected by a molecularly undefined form of NCL characterized by infantile-onset progressive myoclon

184 (JNCL), the latest onset and mildest form of NCL in children.

185 in a mouse model of CLN6 disease, a form of NCL with a deficiency in the membrane-bound protein CLN6

186 nfantile NCL (INCL), the most severe form of NCL, is caused by mutations in the Ppt1 gene, which enco

187 s affected in a late infantile-onset form of NCL.

188 Cln3 (-/-) mouse model of a juvenile form of NCL.

189 disease and may be applied to other forms of NCL caused by transmembrane protein deficiencies in the

190 gliosis is a characteristic of all forms of NCL, but it is unclear whether glial activation precedes

191 of the molecularly uncharacterized forms of NCL, we report here the structure and chromosomal locali

192 associated phenotypes common to all forms of NCL.

193 s were identified, suggesting other forms of NCL.

194 re at least 13 genetically distinct forms of NCL.

195 Finally, inhibition of NCL using guanosine-rich aptamers reduces the levels of

196 Knockdown of NCL with small interfering RNA (siRNA) or treatment of c

197 uanosine-rich aptamers reduces the levels of NCL-dependent miRNAs and their target genes, thus reduci

198 The inherent limitations of NCL are discussed with insights from the mechanistic sta

199 ) determine the cell surface localization of NCL downstream of the RPTPbeta/zeta/c-Src signaling casc

200 tein is feasible using the combined logic of NCL and metal-free dethiylation (MFD).

201 x-dependent apoptosis in this mouse model of NCL, combined Bax- and CD-deficient mice were generated.

202 olvement of interneurons in a mouse model of NCL.

203 the brains of two different mouse models of NCL: Ppt1(-/-) model of infantile NCL and Cln6(nclf) mod

204 o provide a thorough mechanistic overview of NCL and extended methods.

205 ast two neurochemically distinct portions of NCL.

206 ide was more abundant in ventral portions of NCL.

207 nd to be densest in intermediate portions of NCL.

208 ) play in the instigation and progression of NCL pathogenesis.

209 and cell-cycle regulation in both strains of NCL mice.

210 ve have been reported recently in subsets of NCL patients.

211 CLN5 deficiency causes a subtype of NCL, referred to as CLN5 disease.

212 that its expression correlates with that of NCL-dependent miRNAs.

213 dentified as the cause of different types of NCL, with ages at onset ranging from around birth to adu

214 ing to five overlapping clinical variants of NCL.

215 tion reported in clinical childhood forms of NCLs.

216 e first clinical signs in childhood forms of NCLs.

217 II have been reported in several subtypes of NCLs.

218 enes (called CLNs) underlie various types of NCLs, of which the infantile NCL (INCL) and congenital N

219 ath to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expre

220 nucleolar protein fibrillarin, dependent on NCL-1.

221 ent study of a sibling pair with adult onset NCL and retinal degeneration showed linkage to the regio

222 this gene may be a candidate for adult-onset NCL.

223 mutations also cause a rare, infantile-onset NCL subtype designated as CLN14.

224 isease-modifying therapies for either FTD or NCL, in part because of a poor understanding of how muta

225 Transfection with CLN8 but not other NCL genes corrected growth and apoptosis in CLN9-deficie

226 nd sequencing of the coding regions of other NCL genes was negative.

227 vides a possible explanation for overlapping NCL-like pathology observed in patients with mutations i

228 r regression, premature death, and prominent NCL-type storage material.

229 The native chemical ligation reaction (NCL) involves reacting a C-terminal peptide thioester wi

230 in the nclf mouse, which manifests recessive NCL-like disease, disclosed a third lesion-an extra base

231 n the NCL-interacting region of RPL26 reduce NCL-RPL26 interactions and attenuate both RPL26 binding

232 s were developed that allowed the sequential NCL-TEC process to proceed in high yield.

233 uronal populations in the mnd/mnd mouse show NCL-like pathological changes.

234 The ligation strategies (NCL, Staudinger, KAHA, KATs, etc.) that could involve bo

235 yielding thioester peptides and subsequently NCL reaction.

236 Positive correlation of cell surface NCL and alpha(v)beta(3) expression was also observed in

237 d as a biomarker for the use of cell surface NCL antagonists as anticancer agents.

238 inhibition of cell migration by cell surface NCL antagonists was observed only in cells expressing al

239 Interestingly, cell surface NCL localization was detected only in cells expressing a

240 ty mediated this phenomenon and cell surface NCL was found to interact with both alpha(v)beta(3) and

241 Immunoprecipitation of MS2-tagged NCL 3'UTR was used to screen for endogenous repressors o

242 We also found that NCL is able to oligomerize, consistent with a model in w

243 3'UTR bearing MS2 RNA hairpins revealed that NCL RNA was mobilized to processing bodies (PBs) after s

244 These data show that NCL and KRS may share etiological features and implicate

245 We also show that NCL is commonly overexpressed in human breast tumors and

246 Here we show that NCL-1/TRIM2/Brat tumour suppressor extends lifespan and

247 The results suggest that NCL may consist of multiple subdivisions.

248 malian orders, we know very little about the NCL across the avian clade.

249 rsal arcopallial tract that runs between the NCL and the arcopallium.

250 ologically different subareas constitute the NCL in these songbirds.

251 droxylase (TH)-dense region that defines the NCL.

252 ver, protein sequencing failed to detect the NCL.

253 We recorded single-neuron activity from the NCL of crows performing a delayed match-to-sample task w

254 Thus, sustained activity in the NCL actively processes information for the upcoming beha

255 NCL dimerization, and point mutations in the NCL-interacting region of RPL26 reduce NCL-RPL26 interac

256 ermore, while recombinant RB47 including the NCL did not display endoribonuclease activity in vitro,

257 ease activity in vitro, versions lacking the NCL displayed strong activity.

258 The purpose of making the NCL available is to encourage the use of the NEXUS forma

259 s that comparable to the PFC in mammals, the NCL in birds varies considerably across species.

260 lay phase, indicating a dominant role of the NCL in numerical working memory.

261 tudy aimed to describe the trajectory of the NCL in pigeon, chicken, carrion crow and zebra finch.

262 is showed that whereas the trajectory of the NCL in the chicken is highly comparable to the pigeon, t

263 The selectivity of the NCL reaction makes in situ membrane formation compatible

264 The findings suggest that the NCL plays a role in learning arbitrary associations, a c

265 tags and protein sequencing showed that the NCL was excised from a full-length recombinant substrate

266 episome binding and maintenance, whereas the NCL C-terminal K380 and K393 induced oriP DNA H3K4me2 mo

267 The NCLs, although relatively rare, share many pathological

268 in vitro and/or in vivo efficacy across the NCLs with an emphasis on targets of action.

269 important early pathological targets in the NCLs and has identified two proteins, VDAC1 and Pttg1, w

270 y onset and rapid disease progression in the NCLs suggests that one or more key cellular processes ar

271 tic axonal and synaptic vulnerability in the NCLs.

272 tic basis and ultrastructural changes in the NCLs.

273 out PPT2 as the causative gene in any of the NCLs at defined chromosomal loci.

274 JNCL is the most common of the NCLs, a group of disorders with infant or childhood onse

275 understand the genetic underpinnings of the NCLs, we performed whole-exome sequencing on DNA samples

276 esis of all 20 natural amino acids and their NCL reactions.

277 Therefore, NCL is an attractive target for antineoplastic treatment

278 Herein, we report that three NCL disease forms with similar tissue pathology are conn

279 in were homogeneously distributed throughout NCL.

280 Binding of 4LB5 to NCL on the cell surface of a variety of breast cancer an

281 any peptide or expressed protein amenable to NCL.

282 usality from the direction of entopallium to NCL and from ROT to entopallium.

283 ely processing color information from ROT to NCL, relayed by entopallium, and blue could trigger the

284 arcinoma HeLa cells, analysis of a traceable NCL 3'UTR bearing MS2 RNA hairpins revealed that NCL RNA

285 expression profiles existed between the two NCL models studied, 2 of the 15 proteins examined (VDAC1

286 We present a family with typical NCL pathology in which we performed exome sequencing and

287 ed to be orthologous to the genes underlying NCL in nclf mice and in South Hampshire and Merino sheep

288 sights into the mechanisms by which EBV uses NCL and RPL4 to establish persistent B-lymphoblastoid ce

289 gest that selective targeting of KDM1A using NCL-1 and NCD-38 is a promising therapeutic strategy for

290 Pharmacological inhibition of KDM1A using NCL-1 and NCD-38 significantly reduced the cell viabilit

291 knowledge this is the first example of using NCL to generate phospholipids de novo.

292 ic form of Parkinson's disease (PD), whereas NCL is a lysosomal storage disorder.

293 1 binding to oriP and transcription, whereas NCL K429A was deficient.

294 ligomerize, consistent with a model in which NCL stabilizes this double-stranded RNA structure.

295 While NCL is one of the most popular tools for synthesizing pr

296 These findings are consistent with NCL acting as an IRES trans-acting factor (ITAF) for ORF

297 The RPL4 N terminus cooperated with NCL-K429 to support EBNA1 and oriP-mediated episome bind

298 proximately 8% of individuals diagnosed with NCL by conservative clinical and histopathologic criteri

299 al preparation was developed, co-loaded with NCL-240, a small-molecule inhibitor of the PI3K/mTOR pat

300 Neuropathological analysis of patients with NCL shows accumulation of intracellular autofluorescent