ライフサイエンスコーパス: NBS

1 NBS bromination of 24 followed by lactone formation gave

2 NBS bromination, lithium halogen exchange, and alkylatio

3 NBS cell lines show a similar defect in ATR phosphorylat

4 NBS for cystic fibrosis is a cost-effective strategy and

5 NBS in these neuromuscular disorders should be implement

6 NBS would address the delays in diagnosis that prevent p

7 NBSs inserted near the replication terminus bound Noc-YF

8 Our survey reveals that 48.5% of the 132 NBS-LRR loci tested contain functional rice blast R gene

9 on of 2-(1-alkynyl)biphenyls with ICl, I(2), NBS, and p-O(2)NC(6)H(4)SCl.

10 containing cytochrome c, and monitored for 3-NBS leakage.

11 able Raman tracer 3-nitrobenzenesulfonate (3-NBS) were optically trapped, translated into a solution

12 spectra, temperature-controlled release of 3-NBS through vesicle membranes composed of pure 1,2-dipal

13 model compound, 3-nitrobenzene sulfonate (3-NBS), from individual optically trapped phospholipid ves

14 Here, we survey 332 NBS-LRR genes cloned from five resistant Oryza sativa (r

15 les, are shown to possess the 3gG2 gene in a NBS-LRR gene cluster background distinct from PI96983.

16 Here we show that RPS5, a NBS-LRR protein from Arabidopsis, is activated by AvrPph

17 hanisms by which pathogen molecules activate NBS-LRR proteins are poorly understood.

18 An NBS-promoted intramolecular electrophilic aromatic subst

19 ssified only one out of 18 AT carriers as an NBS carrier.

20 ese cycloadducts has been demonstrated by an NBS-MeOH mediated stereospecific efficient access to ful

21 An autonomous plasmid carrying an NBS array recruited Noc-YFP and conferred a severe Noc-d

22 Here, we describe an NBS specific UV photocrosslinking biotinylation method (

23 Fom-2 was predicted to encode an NBS-LRR type R protein of the non-TIR subfamily.

24 uggest that the positional specificity of an NBS is dependent on the promoter in question and is more

25 Purified Noc bound specifically to an NBS in vitro.

26 g was accomplished by linking a hapten to an NBS ligand with an ethylene glycol linker.

27 oups: usual care (n = 305), those viewing an NBS movie and brochure (n = 300), and those viewing both

28 o-(1-alkynyl)benzamides with ICl, I(2), and NBS.

29 nervous system is different between ATLD and NBS and likely explains their respective neuropathology.

30 Cells from ATLD and NBS patients are deficient in activation of the Atm prot

31 this activation depended on both the CC and NBS domains.

32 fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrop

33 e H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs.

34 c HGGs, respectively, including in DIPGs and NBS-HGGs.

35 ns in the NBS1 gene that encodes nibrin, and NBS cells are radiosensitive and defective in S-phase ch

36 with both a carboxylic acid nucleophile and NBS electrophile.

37 ance gene-like features, including S/TPK and NBS-LRR domains.

38 Following HU-induced replication arrest, NBS and ATR-Seckel cells show similarly impaired G2/M ch

39 iffer significantly (P < or = 0.001) between NBS carriers and controls.

40 genic exchange is dramatically lower between NBS-LRR sequences located in different chromosome region

41 1-(1-alkynyl)-2-(methylseleno)arenes by Br2, NBS, I2, ICl, PhSeCl, PhSeBr, and Hg(OAc)2.

42 aining propargylic alcohols by ICl, I2, Br2, NBS, and PhSeBr.

43 and ketones to react with I2, ICl, NIS, Br2, NBS, p-O2NC6H4SCl, or PhSeBr and various alcohols or car

44 ic acids with bromine or N-bromosuccinimide (NBS) in the presence of potassium carbonate as base, the

45 benzylic compounds with N-bromosuccinimide (NBS) is presented.

46 )iodo]benzene (PIFA) and N-bromosuccinimide (NBS) using cyanamidyl/arylcyanamidyl radicals as the ami

47 A protocol for the N-bromosuccinimide (NBS)- and trichloroisocyanuric acid (TCCA)-mediated synt

48 ing this work, attempted N-bromosuccinimide (NBS)-mediated cyclization of oxetane alcohol 17, prepare

49 ding of Pd(OAc)(2) using N-bromosuccinimide (NBS).

50 ieved by the addition of N-bromosuccinimide (NBS).

51 bromination of tetraphenylporphyrin (TPP) by NBS.

52 previously described TIR-X, TIR-NBS, and CC-NBS groups.

53 1.2 and Vat arthropod resistance genes as CC-NBS-LRR (coiled coil-nucleotide binding site-leucine ric

54 Here, we demonstrate that unlike most CC-NBS-LRR R genes, HRT/rrt-mediated resistance is dependen

55 encoded an N-terminal coiled-coil motif (CC-NBS-LRR, or CNL).

56 leotide-binding site-leucine-rich repeat (CC-NBS-LRR) family and is activated by AvrPphB-mediated cle

57 hat it affects (TIR-NBS-LRR as opposed to CC-NBS-LRR).

58 into adulthood following introduction of CF NBS because considerable resources have been devoted to

59 lessons learned from the past 20 years of CF NBS: standardized protocols for all patients identified

60 The cystic fibrosis (CF) NBS program is a successful model for NBS.

61 -T and ATLD while microcephaly characterizes NBS.

62 these cyclizations in combination with cheap NBS as a bromine source to give bromoenol lactones in hi

63 Comparative studies with the coiled-coil-NBS-LRR genes RPS2, RPM1, and RPS5 and isogenic P. syrin

64 ulting in the NBS targeting affinity column (NBS(IBA)).

65 ntaining DNA hyperreplicated in T-containing NBS-deficient cells by comparison with T-containing, Nbs

66 lly applied for the age determination of CRM NBS 947 and other sulfate and oxide plutonium samples.

67 In the past decade, NBS has undergone rapid expansion and an unprecedented n

68 Nine women stated that they had declined NBS (all the usual care group; P < .001).

69 We demonstrate NBS in ovarian, uterine and lung cancer cohorts from The

70 hanisms of evolution for the large, diverse, NBS-LRR gene family.

71 protocols for all patients identified by DMD NBS, longitudinal follow-up in multidisciplinary clinics

72 se disorders with particular emphasis on DMD NBS, because of the likely approval of new gene-modifyin

73 rect classification of individuals as either NBS carriers or noncarriers in a training set with 25 in

74 nduced reaction of the substrate with excess NBS.

75 ame is true for other pathogens, many extant NBS-LRR genes retain functionality.

76 proach coupled with liquid-phase extraction (NBS-LPE) was developed and applied to the extraction of

77 Cystic fibrosis NBS has now moved on from the development phase and is e

78 al recombination located within the flanking NBS-LRR genes would have removed Pc, the clustering of c

79 s (CF) NBS program is a successful model for NBS.

80 a benthamiana, that miR482 targets mRNAs for NBS-LRR disease resistance proteins with coiled-coil dom

81 tion care, and transplantation protocols for NBS identified infants with SCID, as well as infants wit

82 lthough all groups showed strong support for NBS, the percentage of women who were "very supportive"

83 The lessons learned from NBS will provide important insights as we move into the

84 Furthermore, NBS has revealed the incidence, causes, and follow-up of

85 tine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcrip

86 zations have been performed using I(2), ICl, NBS and PhSeCl as electrophiles.

87 If NBS for FXS is developed, it must be carried out with cl

88 In NBS-LPE, only a small amount of apple flesh (ca. 10mg) w

89 Nbs1, the protein defective in NBS, functions in ataxia telangiectasia mutated protein

90 ings using instruments currently deployed in NBS laboratories.

91 unequal events to generate LRR diversity in NBS-LRR loci.

92 transgenes lacking the Atm binding domain in NBS fibroblasts.

93 ith 53BP1 and gammaH2AX foci, do not form in NBS cells, do form in AT cells and do not correlate with

94 as dramatically reduced after irradiation in NBS cells expressing the nibrin DeltaAtm transgenes rela

95 tion are not clear, because the mutations in NBS and ATLD cells result in global effects on the MRN c

96 exed with Rad50, localized to the nucleus in NBS fibroblasts, and associated with chromatin.

97 transgene with a C-terminal NLS sequence in NBS fibroblasts.

98 nduced DNA rereplication and tetraploidy, in NBS-deficient but not NBS-proficient cells.

99 Incorporating NBS education into prenatal care is broadly supported by

100 to show that most duplication of individual NBS-LRR sequences occurs at close physical proximity to

101 segments comprising the novel intermolecular NBS are next to helices that likely move with channel op

102 for the identified baby, which would justify NBS even in the absence of medical benefit to the child.

103 60-bp region within the approximately 3.7-kb NBS-LRR genes.

104 e 151-amino-acid sequence missing from known NBS-LRR proteins at the N terminus.

105 logenetic analyses of A. thaliana and legume NBS-LRR sequences demonstrate that Rpg1-b and RPM1 are n

106 ce translocated to new chromosome locations, NBS-LRR gene copies have a greater likelihood of escapin

107 Moreover, NBS cells fail to retain ATR in the nucleus following HU

108 ging the dogma and principle of the national NBS program: screen only if you can intervene.

109 on and tetraploidy, in NBS-deficient but not NBS-proficient cells.

110 es (up to five from: Fmoc, Boc Alloc, pNZ, o-NBS, and Troc), together with the right concourse of the

111 eptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants.

112 To demonstrate the applicability of NBS-LPE, AsA levels at different sampling points in a si

113 We describe the cloning of a cluster of NBS-LRR resistance gene candidates from MLG F of the vir

114 e have been notably shifted: the delta13C of NBS 22 oil is -30.03 per thousand.

115 f 1-formyldipyrromethane with 2 mol equiv of NBS at -78 degrees C led to an isomeric mixture of the d

116 undergoes bromination (with 1 molar equiv of NBS in THF) both in ring B (7-position) and at the 15-po

117 For each substrate, only 1.05 equiv of NBS was necessary to fully transform the benzylic starti

118 cess allows pathogen-inducible expression of NBS-LRR proteins and that it contributes to a novel laye

119 Arguments in favor of NBS include benefits of early intervention and follow-up

120 A substantial fraction of NBS-deficient fibroblasts reinitiate DNA replication in

121 The 45-year history of NBS has demonstrated its benefits, as well as the import

122 the study of infants identified by means of NBS for SCID who received care at the University of Cali

123 those derived from multiple mouse models of NBS express a hypomorphic NBS1 allele that exhibits impa

124 , and behavior with respect to opting out of NBS or DBS for their child.

125 this article, we discuss the future path of NBS for these disorders with particular emphasis on DMD

126 In the presence of NBS 3-methylindole reacted with various imidazoles to gi

127 ess of dimethyl disulfide in the presence of NBS gave the 4-methylthio-thiophenes as sole products.

128 on inhibition by Noc requires recruitment of NBS DNA to the cell membrane and is dependent on its abi

129 iodine as a halogen source, while the use of NBS gave exclusively the 4-butylselenyl-selenophenes.

130 program, use of the TREC assay performed on NBS cards was able to identify infants with T-cell lymph

131 ormally regulate telomere protection (ATM or NBS) also led to higher frequencies of telomere formatio

132 Using NCS or NBS (N-chloro- or N-bromosuccinimide) and 5 mol % Pd(OAc

133 hat is known to inhibit ATP binding in other NBS-LRR proteins blocked activation of RPS5, whereas a s

134 re unsuccessful, electrophiles, particularly NBS, enabled the coupling reaction to occur in good yiel

135 ls were carriers for at least one pathogenic NBS allele.

136 ce proteins are detected indirectly by plant NBS-LRR proteins from modifications the virulence protei

137 the amino-terminal and LRR domains of plant NBS-LRR proteins.

138 athogen-associated molecular patterns, plant NBS-LRR proteins detect pathogen-associated proteins, mo

139 ce and generates clusters of closely related NBS-LRR sequences.

140 nucleotide binding site-leucine-rich repeat (NBS-LRR) disease resistance genes.

141 nucleotide binding site-leucine rich repeat (NBS-LRR) encoding disease resistance genes located at a

142 nucleotide-binding site-leucine-rich repeat (NBS-LRR) family are used for pathogen detection.

143 nucleotide-binding site-leucine-rich repeat (NBS-LRR) protein Prf.

144 Nucleotide binding site-leucine-rich repeat (NBS-LRR) proteins mediate pathogen recognition in both m

145 nucleotide-binding site-leucine-rich repeat (NBS-LRR) proteins that are structurally related to prote

146 nucleotide binding site-leucine-rich repeat (NBS-LRR) proteins.

147 nucleotide binding site-leucine rich repeat (NBS-LRR) resistance proteins of plants (R-proteins) and

148 n sub-class of RPW8-encoding genes, the RPW8-NBS-encoding genes.

149 evolved faster than the NBS domains in RPW8-NBSs.

150 e August 2010, California has conducted SCID NBS.

151 A newborn blood screening (NBS) test that could identify infants with a profound de

152 states and countries, of newborn screening (NBS) by tandem mass spectrometry, IVA can now be diagnos

153 plementation of universal newborn screening (NBS) for cystic fibrosis (CF), the timing and magnitude

154 Newborn screening (NBS) for SCID permits identification of affected infants

155 permits population-based newborn screening (NBS) for severe combined immunodeficiency (SCID).

156 currently not included in newborn screening (NBS) panels in the United States as it does not meet the

157 Newborn screening (NBS) represents the largest volume of genetic testing.

158 candidates for universal newborn screening (NBS).

159 ions commonly assessed by newborn-screening (NBS, n = 39) programs, genes associated with age-related

160 approaches to newborn blood spot screening (NBS) education are ineffective.

161 performance of newborn blood spot screening (NBS) has been continually assessed and its use has gradu

162 h HRR for three seasons: nonbreeding season (NBS), early and late breeding seasons (LBSs), to account

163 tified a consensus Noc-binding DNA sequence (NBS), and have shown that Noc is targeted to about 70 di

164 protein Noc binds to specific DNA sequences (NBSs) scattered around the chromosome and helps to prote

165 a coiled-coil (CC), nucleotide-binding site (NBS) and leucine-rich repeat (LRR) class resistance (R)

166 ance genes encoding nucleotide binding site (NBS) and leucine-rich repeat (LRR) domain-containing pro

167 tance proteins with nucleotide binding site (NBS) and leucine-rich repeat (LRR) motifs.

168 erred by genes with nucleotide binding site (NBS) and leucine-rich repeat (LRR) or serine/threonine p

169 e-like genes with a nucleotide-binding site (NBS) and leucine-rich repeats (LRRs) (Nbs1-Pi9-Nbs6-Pi9)

170 taining a conserved nucleotide-binding site (NBS) domain, 13 imperfect leucine-rich repeats (LRRs), a

171 adjacent conserved nucleotide binding site (NBS) found on the Fab of IgE Abs.

172 The nucleotide binding site (NBS) is an under-utilized, highly conserved binding site

173 to the coiled-coil nucleotide binding site (NBS) Leu-rich repeat (LRR) class of R genes, they share

174 localization of the nucleotide-binding site (NBS) on Kir6.x channels and how nucleotide binding gates

175 The conserved nucleotide binding site (NBS), found within the Fab variable domain of antibodies

176 nd evolution of the nucleotide-binding site (NBS)-encoding gene family and receptor-like kinase (RLK)

177 the key role of the nucleotide binding site (NBS)-encoding gene family in resistance to Verticillium

178 in-1 receptor (TIR)-nucleotide binding site (NBS)-Leu-rich repeat (LRR) class of disease resistance (

179 a coiled-coil (CC)-nucleotide-binding site (NBS)-leucine-rich repeat (LRR) protein, which possessed

180 asymmetry in their nucleotide-binding sites (NBS) unlike most of their human counterparts.

181 However, some NBS-LRR proteins directly bind pathogen proteins.

182 s determined with a network-based statistic (NBS) approach.

183 We used the network-based statistic (NBS) to compare large-scale connectivity between groups

184 Network Based Statistics (NBS) also revealed strong and consistent evidence that s

185 MRI) analyzed with network-based statistics (NBS) and graph-theoretical methods.

186 e we introduce network-based stratification (NBS), a method to integrate somatic tumor genomes with g

187 binding site-leucine rich repeat) subfamily NBS-LRR resistance proteins, as well as several resistan

188 escribed condition, Narcotic Bowel Syndrome (NBS)/Opioid-Induced GI Hyperalgesia, is characterized by

189 bility syndromes Nijmegen breakage syndrome (NBS) and ataxia telangiectasia (AT) share many overlappi

190 tivity disorders Nijmegen breakage syndrome (NBS) and ataxia-telangiectasia-like disorder (ATLD), res

191 Human Nijmegen breakage syndrome (NBS) cells and those derived from multiple mouse models

192 latory effect in Nijmegen breakage syndrome (NBS) cells.

193 that carriers of Nijmegen Breakage Syndrome (NBS) have a distinct gene expression phenotype that diff

194 Nijmegen breakage syndrome (NBS) is characterised by microcephaly, developmental del

195 Nijmegen breakage syndrome (NBS) is characterized by radiation hypersensitivity, chr

196 The disorder Nijmegen breakage syndrome (NBS) results from mutations in the NBS1 gene that encode

197 langiectasia and Nijmegen breakage syndrome (NBS), respectively, are essential elements in the cellul

198 ike disorder and Nijmegen breakage syndrome (NBS), respectively.

199 order (ATLD) and Nijmegen breakage syndrome (NBS), respectively.

200 isease (ATLD) or Nijmegen breakage syndrome (NBS).

201 also present in Nijmegen breakage syndrome (NBS)1.

202 These findings demonstrate that NBS-LRR genes can condition disease susceptibility and r

203 lation screening and studies have shown that NBS for FXS is feasible, the idea is still controversial

204 Our result shows that NBS carriers have a specific gene expression phenotype.

205 The NBS did not identify group differences in network connec

206 The NBS indicated that, compared with controls, depressed ad

207 The NBS protein Nbs1 is not only a downstream target of AT m

208 The NBS-mediated radical bromination of the N,N-di-tert-buto

209 ochure (n = 300), and those viewing both the NBS and DBS movies and brochures (n = 296).

210 hest in the NBS group (94%), followed by the NBS + DBS group (86%) and was lowest in the usual care g

211 o promote the exchange of ADP for ATP by the NBS domain, which activates 'downstream' signaling, by a

212 esults presented in this study establish the NBS(IBA) column as a viable small-molecule-based affinit

213 nce and on the face of the DNA helix for the NBS relative to that of RNA polymerase.

214 BA), which has a monovalent affinity for the NBS with a K(d) ranging between 1 and 8 muM, to ToyoPear

215 a Lewis base catalysis, is disclosed for the NBS-mediated oxidation of alcohols.

216 s to define the peptide segments forming the NBS on Kir6.x channels and show that unique N- and C-ter

217 ied in whole blood from individuals from the NBS cohort and RA patients from 2 independent cohorts.

218 (HDLc) were observed in individuals from the NBS cohort and RA patients from the Nijmegen cohort homo

219 Furthermore, the NBS(IBA) column consistently yielded >95% antibody recov

220 group (77% retention), and 221 women in the NBS + DBS group (75% retention).

221 d's sample withdrawn after testing: 3 in the NBS + DBS group and 2 in the usual care group (P = .25).

222 group, 79% in the NBS group, and 75% in the NBS + DBS group, a significant between-group difference

223 usual care group (70% retention), 231 in the NBS group (77% retention), and 221 women in the NBS + DB

224 ho were "very supportive" was highest in the NBS group (94%), followed by the NBS + DBS group (86%) a

225 were 69% in the usual care group, 79% in the NBS group, and 75% in the NBS + DBS group, a significant

226 An amino acid substitution in the NBS site of RPS5 that is known to inhibit ATP binding in

227 d 8 muM, to ToyoPearl resin resulting in the NBS targeting affinity column (NBS(IBA)).

228 HRRs for males in the LBS and females in the NBS.

229 It was then incorporated into the NBS-LRR protein to create a main sub-class of RPW8-encod

230 Nbs1, the NBS protein, forms a tight complex with Mre11 and Rad50,

231 BShutU, requires that the TnGTAT half of the NBS be on the promoter-proximal (downstream) side of the

232 pproximately 3 microL of whole blood) of the NBS card.

233 with greater Ka/Ks values than those of the NBS domains indicated that they evolved faster than the

234 at laboratory tests are just one part of the NBS system.

235 Potential advantages of the NBS(IBA) platform are improved antibody batch quality, e

236 -frame stop codons and lie downstream of the NBS-encoding exon.

237 nalyzed the phylogenetic distribution of the NBS-LRR domain architecture, used maximum-likelihood met

238 forces contributing to the formation of the NBS-LRR gene cluster.

239 gene that, paradoxically, is a member of the NBS-LRR resistance gene family.

240 The extant distribution and diversity of the NBS-LRR sequences has been generated by extensive duplic

241 e promoter-proximal (downstream) side of the NBS.

242 ere selectively captured and retained on the NBS(IBA) column and were successfully eluted by applying

243 indicated that they evolved faster than the NBS domains in RPW8-NBSs.

244 We propose that the NBS clinical features represent the result of these comb

245 nity chromatography method that utilizes the NBS as a target for selectively purifying antibodies fro

246 ive targeting of a specific IgE, whereas the NBS ligand enhances avidity for the IgE.

247 It remains unclear whether the NBS-LRR architectures were innovations of plants and ani

248 CC domains both coimmunoprecipitate with the NBS domain but not with each other.

249 g that the LRR domain must coevolve with the NBS domain.

250 However, the NBSs from the ureD promoter (ureDp) and codB promoter (c

251 ated nonconsensus amino acid residues in the NBSs to its consensus counterpart and studied its effect

252 This degeneracy of the NBSs is very intriguing and needs explanation in terms o

253 Therefore, NBS furnished direct conversion to the isoquinoline-5,8-

254 ubjects whose condition was detected through NBS led to the identification of one recurring mutation,

255 ong to the Toll/Interleukin-1 receptor (TIR)-NBS-LRR (TNL) class.

256 consisting of the entire portion of the TIR, NBS, and LRR domains but lacks the C-terminal domain of

257 One such gene (a TIR-NBS-LRR gene, RT4-4) was selected for functional analysi

258 ontains a gain-of-function mutation in a TIR-NBS-LRR type R gene.

259 RCT1 is a TIR-NBS-LRR-type resistance (R) gene in Medicago truncatula

260 in the class of R genes that it affects (TIR-NBS-LRR as opposed to CC-NBS-LRR).

261 ggest that the generation of alternative TIR-NBS-LRR R gene transcripts is of general biological sign

262 ed by RIL 46, a constitutively expressed TIR-NBS-LRR gene was identified as the candidate for nematod

263 th Toll/Interleukin-1 Receptor homology (TIR-NBS-LRR, or TNL), and those that encoded an N-terminal c

264 ons suggest that two or more related non-TIR-NBS-LRR gene products are likely involved in the allelic

265 We have identified a large cluster of TIR-NBS-LRR sequences associated within this locus, which ex

266 eotide-binding site/leucine-rich repeat (TIR-NBS-LRR) class of plant R genes and confers broad-spectr

267 eotide-binding site/leucine-rich repeat (TIR-NBS-LRR) class of plant resistance (R) proteins.

268 eotide binding site/leucine-rich repeat (TIR-NBS-LRR) class of resistance (R) genes, confers resistan

269 teins in the previously described TIR-X, TIR-NBS, and CC-NBS groups.

270 For each tissue, NBS identifies subtypes that are predictive of clinical

271 trated feasibility of a 2-tiered approach to NBS with screening by creatine kinase (CK) levels in dri

272 ses on the knowledge instrument in regard to NBS were 69% in the usual care group, 79% in the NBS gro

273 lithium carbonate and +1.95 per thousand to NBS 19 calcium carbonate.

274 TREC NBS in California has achieved early diagnosis of SCID a

275 e sought to report the first 2 years of TREC NBS in California.

276 nfants younger than 3.5 months who underwent NBS and had confirmed CF, with a gestational age of at l

277 disease among infants with CF who underwent NBS has not been well described.

278 of life among infants with CF who underwent NBS.

279 Since initiation of universal NBS for CF, significant improvement has occurred in nutr

280 ormed into a bromomethyl derivative 13 using NBS.

281 oesterification of a series of alkenes using NBS and a variety of carboxylic acids, and the oxidation

282 er T-lymphopenic disorders detected by using NBS.

283 l-protected alkyl amines are developed using NBS as the brominating reagent and catalytic amount of C

284 V photocrosslinking biotinylation method (UV-NBS(Biotin)) for the oriented immobilization of antibodi

285 Taken together, the UV-NBS(Biotin) method provides a universal, site-specific i

286 The UV-NBS(Biotin) method yielded surfaces with significantly e

287 While NBS shares overlapping characteristics with ataxia telan

288 Treatment of 1 with NBS afforded the 15-bromo analogue in 70% yield.

289 ined in high yield by bromination of 2d with NBS.

290 PY derivatives via electrophilic attack with NBS was developed.

291 egioselective electrophilic bromination with NBS to give the 15-bromo analogue (MeO-BC-Br15) in 85% y

292 s strictly localized by the interaction with NBS sites in vivo.

293 Treatment of these intermediates with NBS initiates a novel oxidative rearrangement that resul

294 atment of the 5-methoxybacteriochlorins with NBS gave regioselective 15-bromination when no pyrrolic

295 the immune defects observed in patients with NBS and related disorders.

296 er states were treated, and 42 patients with NBS-identified non-SCID T-cell lymphopenia were followed

297 2010 through October 2016, 32 patients with NBS-identified SCID and leaky SCID from California and o

298 pin)-substituted allylic alcohols react with NBS to afford (E)-alpha,beta-unsaturated aldehydes in 51

299 of the nitro group followed by reaction with NBS resulted in the formation of the required pentacycli

300 he intermediate boronate complex reacts with NBS triggering the 1,2-migration of the group on boron t