ライフサイエンスコーパス: CID

1 CID and HCD generated mainly glycosidic B/Y and C/Z clea

2 CID appeared after the divergence of protostomes and deu

3 CID assembly in prophase I is also conserved in female m

4 CID data suggests that facile metal-phosphate dissociati

5 CID infusion eliminated 85% to 95% of circulating CD3(+)

6 CID is most complementary, increasing the number of iden

7 CID MS/MS of [LGa2(betacas)](n+) revealed protection aga

8 CID of UO2(N3)Cl2(-) resulted in the loss of N2 to form

9 akaryocyte precursor (PEM) population, and a CID-independent macrophage population.

10 s in these expanded populations identified a CID-dependent bipotent erythrocyte-megakaryocyte precurs

11 Human RLTPR deficiency is a CID affecting at least the CD28-responsive pathway in T

12 Importantly, the additional CID-MS(2) data allows one to validate the glycan assignm

13 inal fluid, which were reduced by >90% after CID.

14 Although CID spectra (at a given collision energy) of source-acti

15 Although CIDs are more prevalent in the Middle East than Western

16 The most ancient CID/NCBD formed a relatively weak complex (Kd approximat

17 OCK8 deficiency from other forms of HIES and CIDs, study the mutational spectrum of DOCK8 deficiency,

18 Here we show that the APC CID interacts with alpha-catenin, a Hippo signaling regu

19 ptimal efficiency in nearly the same time as CID at low precursor charge state (z = +3) and becomes f

20 eficiency with multiple intestinal atresias (CID-MIA) is a rare hereditary disease characterized by i

21 with the mass spectrometer switching between CID and UVPD activation modes to obtain a complementary

22 core OS ions were subsequently activated by CID, high-energy collision-induced dissociation (HCD), o

23 The ions were then fully characterized by CID experiments and IRMPD spectroscopy.

24 by ion mobility (IM) and then dissociated by CID or SID for further structural analysis.

25 tic sulfide linkage cannot be broken down by CID with lab collision energy up to 50 eV while C(2)+ al

26 ix components undergo MS/MS fragmentation by CID, allowing noise-free detection of the analyte's surv

27 for the robust analysis of data generated by CID MS/MS of RNA oligomers.

28 SePh groups are reactivated and sequenced by CID.

29 rongly suggest that TTC7A gene defects cause CID-MIA.

30 requency and type of genetic defects causing CIDs in this region differ in comparison with those in o

31 eviously described an approach for combining CID with ion mobility mass spectrometry (IM-MS) for disp

32 Moreover, comparative CID fragmentation analysis between unmodified phosphopep

33 In comparison, CID spectra of {LGa2}(5+)-bound phosphoinositides genera

34 ence analysis more informative and complete (CID MS(2) is thus equivalent to CID MS(3)).

35 nstrate that centromeric nucleosomes contain CID dimers in vivo.

36 In contrast, CID of the complexes to the protonated basic AAs results

37 to further dissociation through conventional CID.

38 To investigate the role of differential CTD-CID interactions in the choice of termination pathway, w

39 Therefore, CTD-CID interactions target specific termination complexes t

40 Moreover, collision-induced decomposition (CID) spectra of precursor fluoride adducts of the bifunc

41 Chemotherapy-induced diarrhea (CID) is a relatively common adverse event in the treatme

42 CGS with a chemical inducer of dimerization (CID) expands total cells 99-fold, erythrocytes 70-fold,

43 l molecule chemical inducer of dimerization (CID), rapamycin.

44 ation of a chemical inducer of dimerization (CID; AP1903/Rimiducid).

45 the formation of H(+)(AA) as the only direct CID product.

46 rgy-resolved collision induced dissiciation (CID) experiments.

47 y low-energy collision-induced dissociation (CID) (40 V), and the type of sphingosine base was identi

48 fragments of collision-induced dissociation (CID) (b/y/a fragments) as well as electron capture/trans

49 obtained by collision induced dissociation (CID) and 351 nm ultraviolet photodissociation (UVPD).

50 ssed through collision-induced dissociation (CID) and collision-induced unfolding (CIU) as monitored

51 n signal) of collision-induced dissociation (CID) and electron transfer dissociation (ETD) processes.

52 oes top-down collision-induced dissociation (CID) and electron transfer dissociation (ETD) with hybri

53 hods such as collision-induced dissociation (CID) and electron transfer dissociation (ETD).

54 modes (e.g., collision-induced dissociation (CID) and electron-transfer dissociation (ETD)).

55 omparison to collision induced dissociation (CID) and higher energy collision dissociation (HCD) in a

56 o those from collision induced dissociation (CID) and higher energy collision dissociation (HCD) with

57 rotein using collision-induced dissociation (CID) and subjecting them to ion mobility separation (IMS

58 alysis using collision-induced dissociation (CID) as the fragmentation method.

59 followed by collision-induced dissociation (CID) at 1.5 keV in a collision cell filled with argon ga

60 aration, and collision-induced dissociation (CID) can be used to finally elucidate the complete struc

61 Collision-induced dissociation (CID) causes preferential cleavage of the phospho-ester b

62 The adjusted collision induced dissociation (CID) conditions generate specific Y-ions in the yield of

63 Beam-type collision-induced dissociation (CID) data of intact glycopeptides isolated from mouse li

64 gainst which collision-induced dissociation (CID) data of modified oligonucleotides can be compared.

65 xhibits poor collision-induced dissociation (CID) efficiency for multiple reaction monitoring (MRM) d

66 o complement collision-induced dissociation (CID) experiments.

67 onsisting of collision-induced dissociation (CID) followed by 193 ultraviolet photodissociation (UVPD

68 ty separated collision-induced dissociation (CID) followed by high resolution mass spectrometry (TIMS

69 metry and by collision-induced dissociation (CID) following nuclease P1 digestion of the DNA moiety t

70 on (RDD) and collision induced dissociation (CID) following separation by liquid chromatography was u

71 th in-source collision induced dissociation (CID) for the mass spectrometric (MS) detection and imagi

72 parent ions, collision induced dissociation (CID) fragment ions, reduced mobility (Ko), mass flight t

73 to observed collision induced dissociation (CID) fragmentation inefficiency, developing sensitive li

74 he in-source collision-induced dissociation (CID) fragmentation patterns of authentic standards, to t

75 by standard collision-induced dissociation (CID) fragmentation spectra.

76 ), in-source collision-induced dissociation (CID) fragmentation, and photolysis were used to analyze

77 t feature of collision-induced dissociation (CID) fragmentation, but targeted analysis of MS1 pairs u

78 pectrum from collision-induced dissociation (CID) is explained by the metabolite's predicted CID MS/M

79 Collision-induced dissociation (CID) is the dominant method for probing intact macromole

80 onventional, collision-induced dissociation (CID) MS(2) spectra.

81 sts in using collision induced dissociation (CID) multistage mass spectrometry (MS(2) and MS(3)) expe

82 lytic cycle, collision induced dissociation (CID) of [(phen)M(O2CCH3)](+) yields the organometallic c

83 The collision-induced dissociation (CID) of a range of deprotonated fatty acid standards was

84 We show that collision-induced dissociation (CID) of pHis peptides produces prominent characteristic

85 urements and collision-induced dissociation (CID) of the intermediate complex confirm the well-protec

86 Collision-induced dissociation (CID) of these cationic modified lipids enables class ide

87 achieved by collision induced dissociation (CID) of UO2(N3)Cl2(-) in a quadrupole ion trap mass spec

88 generational collision-induced dissociation (CID) on a miniature mass spectrometer and emphasize usef

89 nonselective collision induced dissociation (CID) on a time-of-flight mass spectrometer.

90 ns formed by collision-induced dissociation (CID) on the basis of charge state and size-to-charge rat

91 coupled with collision-induced dissociation (CID) or radical-driven fragmentation techniques such as

92 age of using collision-induced dissociation (CID) post-UVPD: radical ions are produced following irra

93 gh efficient collision-induced dissociation (CID) procedure could be obtained by simply manipulating

94 complex via collision-induced dissociation (CID) produces a Schiff base product anion.

95 ncluding collisionally induced dissociation (CID) products, and a quantitative examination of the spe

96 ions, while collision induced dissociation (CID) spectra assisted structural elucidation.

97 pectra [e.g. Collision Induced Dissociation (CID) spectra of tryptic peptides], their performance oft

98 ft time, and collision induced dissociation (CID) spectrum.

99 pon ion trap collision-induced dissociation (CID) to yield products that reveal fatty acid chain leng

100 le of source collision-induced dissociation (CID) was used to completely analyze radiological dispers

101 iments using collision induced dissociation (CID) were employed for initial characterization of the d

102 tion method, collision-induced dissociation (CID) with low-mass target gases, typically leads to unfo

103 om in-source collision-induced dissociation (CID), (2) in-depth evaluation of in-source adducts forme

104 tides during collision-induced dissociation (CID), a data dependent neutral-loss-triggered EThcD acqu

105 try, such as collision-induced dissociation (CID), and data analysis algorithms.

106 try (IM-MS), collision-induced dissociation (CID), and hydrogen/deuterium exchange (HDX)-MS.

107 techniques: collision-induced dissociation (CID), beam-type CID (HCD), electron-transfer dissociatio

108 ombinations: collision-induced dissociation (CID), beam-type CID (HCD), electron-transfer dissociatio

109 alternating collision-induced dissociation (CID), ETD, and higher-energy collisional dissociation (H

110 ragmented by collision-induced dissociation (CID), followed by IMS analysis.

111 sulting from collision-induced dissociation (CID), higher-energy C-trap dissociation (HCD), and elect

112 1-16), using collision induced dissociation (CID), higher-energy collision induced dissociation (HCD)

113 e a combined collision induced dissociation (CID), higher-energy collisional dissociation (HCD), and

114 tperformed collisional induced dissociation (CID), higher-energy collisional dissociation (HCD), and

115 tion method, collision induced dissociation (CID), often provides limited structural information from

116 on (HCD) and collision induced dissociation (CID), provided the complete sequence of the glycan struc

117 Upon Collision Induced Dissociation (CID), several spectrometric fragment-ion signals were ob

118 ques such as collision induced dissociation (CID), the cleavage propensity after absorption of UV lig

119 zation (ESI)-collision-induced dissociation (CID)-FTICR MS was applied to identify protein isoforms t

120 lel ion trap collision induced dissociation (CID)-MS(2) data acquisition to the original HCD-product

121 provided by collision-induced dissociation (CID)-MS3 fragmentation.

122 pecies using collision-induced dissociation (CID).

123 conventional collision induced dissociation (CID).

124 RNase B by collisional-induced dissociation (CID).

125 tified using collision-induced dissociation (CID).

126 ination with collision-induced dissociation (CID).

127 ions under collisional-induced dissociation (CID).

128 pattern upon collision-induced dissociation (CID).

129 y low-energy collision-induced dissociation (CID).

130 ry (IMS) and collision-induced dissociation (CID).

131 o sequential collision-induced dissociation (CID).

132 ng (CIU) and collision-induced dissociation (CID).

133 Collision-induced dissociation (CID-MS/MS) revealed differences in the gas-phase stabili

134 n-induced or electron transfer dissociation (CID and ETD).

135 CD95 domain called calcium-inducing domain (CID) and the Src homology 3 domain of phospholipase Cgam

136 ack the conserved catenin inhibitory domain (CID), which is essential for beta-catenin proteolysis.

137 rs, occupies chromosomal interacting domain (CID) boundaries and that Mediator in chromatin associate

138 C-terminal domain (CTD)-interacting domain (CID) proteins are involved in two distinct RNApII termin

139 C-terminal domain (CTD)-interacting domain (CID).

140 C-terminal domain (CTD)-interacting domain (CID).

141 -terminus of Pol II (CTD-interacting domain, CID).

142 two interacting disordered protein domains, CID and NCBD.

143 rrangements, which have been observed during CID.

144 The observation of UO2Cl2(-) during CID is most likely due to the absence of an energy barri

145 ngosine base was identified by higher energy CID (80 V).

146 Gly and Ala is observed as the lowest-energy CID pathway for the (Gly)H(+)(18C6) and (Ala)H(+)(18C6)

147 d types of spectra (including CID, HCD, ETD, CID/ETD and HCD/ETD spectra of trypsin, LysC or AspN dig

148 a target analyte's unique fragment following CID.

149 ndem mass spectrometry (LC-MS/MS) assays for CID resistant compounds is especially challenging.

150 a and superior or comparable with others for CID and HCD spectra.

151 Furthermore, CID dimerization and centromeric targeting require a res

152 of spectra or even for spectral pairs (e.g. CID/ETD spectral pairs).

153 This combined IM-HDX-CID methodology provides a comprehensive view of GA self

154 are defined by PubChem Compound Identifiers (CIDs); ligand capture also includes peptides and clinica

155 Combined immunodeficiencies (CIDs) and "atypical" SCID show reduced, not absent T-cel

156 Combined immunodeficiencies (CIDs) are diseases of defective adaptive immunity with d

157 Combined immunodeficiencies (CIDs) form a heterogeneous group of inherited conditions

158 liarities about combined immunodeficiencies (CIDs) in the Middle East.

159 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autosomal recessive (AR) hyper-I

160 Combined immunodeficiency (CID) is a T-cell defect frequently presenting with recur

161 Combined immunodeficiency (CID) is characterized by severe recurrent infections wit

162 Combined immunodeficiency (CID) refers to inborn errors of human T cells that also

163 lish SOCE cause a combined immunodeficiency (CID) syndrome that is accompanied by autoimmunity and no

164 s, resulting in a combined immunodeficiency (CID) without endocrine or ectodermal manifestations.

165 associated with a combined immunodeficiency (CID), leading to increased susceptibility to infections.

166 Using IMS CID MS/MS, applied here for the first time to gangliosid

167 is present both before and after culture in CID media, although site-specific qPCR of transposon jun

168 s that have poor fragmentation efficiency in CID.

169 rent from the ubiquitous monomer ejection in CID.

170 ct monomers and dimers, which we observed in CID experiments of high charge states of SAP, accessed b

171 Naphthenic ring-openings were observed in CID, leading to formation of olefinic structures.

172 e for all tested types of spectra (including CID, HCD, ETD, CID/ETD and HCD/ETD spectra of trypsin, L

173 An initial CID event performed on an R-LPS precursor produced spect

174 ro binding of purified SSRP1 or its isolated CID domain to a methylated DNA fragment containing alter

175 ion trap collision-induced dissociation (IT-CID) and negative electron transfer (NET)-CID.

176 en conducted to define the limitations of IT-CID in sequencing such 2'-chemically modified oligonucle

177 ce coverage can be achieved by performing IT-CID on multiple charge states.

178 We found that IT-CID is sufficient in characterizing oligonucleotide sequ

179 Unlike IT-CID, NET-CID mainly generates a noncomplementary d/w ion

180 gave limited backbone fragmentation with IT-CID, largely due to dominant fragmentation at the DNA re

181 with isothermal titration calorimetry (ITC), CID MS/MS, and density functional theory (DFT).

182 ary to recruit GANP, which requires both its CID and MCM3AP domains, together with nucleoporin Nup153

183 fferent to distinguish the isomeric ligands, CID can establish the relative abundance of each ligand

184 s within the instrument: these factors limit CID capability.

185 and granulomatous/autoimmune manifestations (CID-G/AI), produce a broad spectrum of autoantibodies.

186 In this manner, CID affords additional selectivity during high resolutio

187 mune cell homeostasis, thereby promoting MIA-CID development.

188 l and intestinal features of 6 unrelated MIA-CID patients.

189 IT-CID) and negative electron transfer (NET)-CID.

190 Unlike IT-CID, NET-CID mainly generates a noncomplementary d/w ion series.

191 Information from NET-CID of different charge states is not fully redundant su

192 Furthermore, we found that NET-CID did not show preferential dissociations at the DNA r

193 This work demonstrates that the NET-CID is a valuable tool to provide high sequence coverage

194 val rate rather than those with nonsyndromic CIDs.

195 Thus, the Nrd1 CID couples Ser(P)-5 CTD not only to termination, but al

196 Surprisingly, replacing the Nrd1 CID with that from Rtt103 reduces binding to Rrp6/Trf4,

197 Trf4, and RNA transcripts terminated by Nrd1(CID(Rtt103)) are predominantly processed by core exosome

198 Nrd1 with the CID from Rtt103 (Nrd1(CID(Rtt103))) causes read-through transcription at many

199 diagnosis of "atypical" SCID and 14 of 51 of CID.

200 mmunity posttransplant and administration of CID can eliminate them from both peripheral blood and th

201 We wanted to identify the genetic cause of CID in 2 siblings, the products of a first-cousin marria

202 In most cases, the cause of CID remains unknown.

203 o determine the underlying genetic causes of CID-MIA by analyzing the exomic sequences of 5 patients

204 A combination of CID and ion mobility spectrometry was applied for the fi

205 Comparison of CID spectra of R-LPS ions with varying lipid A and core

206 An autosomal recessive form of CID is associated with homozygous mutations in MALT1.

207 Using immunoprecipitation of CID mononucleosomes and cysteine crosslinking, we demons

208 a result that cannot be achieved by means of CID using standard collision energies.

209 otide (octreotide LAR) for the prevention of CID in this population.

210 icacy of octreotide LAR in the prevention of CID.

211 AR did not prevent or reduce the severity of CID.

212 obility separation (IMS) or another stage of CID to fragment the ions.

213 ir were the most common underlying causes of CIDs.

214 in the awareness, diagnosis, and therapy of CIDs in the region and the research opportunities, espec

215 The treatment of CIDs with allogeneic hematopoietic stem cell transplanta

216 ovo on the CID spectra and that of UVnovo on CID or UVPD spectra alone.

217 D (High Energy Collision Dissociation) only, CID (Collision Induced Dissociation)/HCD (High Energy Co

218 Our results show that optimized CID fragmentation enables DIA of IgG glycoforms and sugg

219 MS fragments for MS(3) analysis using HCD or CID increased the sequence coverage to 89%.

220 split-kinases can be activated by orthogonal CIDs in mammalian cells.

221 We further demonstrate that the orthogonal CIDs, abscisic acid and gibberellic acid, can be used to

222 resent profound combined immunodeficiency (P-CID), for which outcome data are insufficient for unambi

223 The P-CID study for the first time characterizes a group of pa

224 we recruited nontransplanted patients with P-CID aged 1 to 16 years to compare natural histories of s

225 difficult HSCT decisions in patients with P-CID.

226 As presented here, the methods for paired CID/UVPD spectral acquisition and interpretation constit

227 44 patients) and nonsyndromic (352 patients) CIDs.

228 the associated phosphorylation of the PCF11 CID act to promote transcript release from chromatin-ass

229 Furthermore, mutation of the Pcf11 CID results in Nrd1 retention on chromatin, delayed degr

230 Furthermore, phosphorylation of the PCF11 CID weakens its interaction with Pol II.

231 The novel HCD-pd-CID/ETD workflow combines the best possible decision tre

232 2 GOF mutations produce a nonfully penetrant CID phenotype through a different pathophysiologic mecha

233 We generated a cell-penetrating CID peptide that prevented Th17 cell transmigration and

234 class information without having to perform CID in positive mode.

235 llenge in the typical MRM method due to poor CID fragmentation of the analyte.

236 ) is explained by the metabolite's predicted CID MS/MS spectrum.

237 din-3-yl)ethyl)f uran-2-carboxamide, Pubchem CID: 46897844).

238 the need for conducting MS(3) or sequential CID (collision-induced dissociation)- and ETD (electron

239 biallelic mutations in CARD11 causing severe CID, the R30W defect results in a less profound yet prom

240 Source CID significantly enhanced the signal for metal ions by

241 Source CID spectra yielded reasonably accurate isotopic ratios

242 seeds when analyzed under similar in-source CID conditions.

243 DEFFI-MS and in-source CID enabled isotopic and molecular speciation of inorgan

244 S signal response as a function of in-source CID potential demonstrated contrasting trends for the de

245 of retention times, mass spectra, in-source CID spectra, and enzymatic hydrolysis to authentic stand

246 od utilizing LC-MS/MS coupled with in-source CID that is highly selective and sensitive to PEG-relate

247 We utilize in-source CID to enhance ion collisions with atmospheric gas, ther

248 By switching the source CID on and off between scans, all major constituents in

249 ic fragmentations observed for each species, CID experiments performed after the mobility separation

250 This type of charting of specific CID reaction pathways can offer value to selected reacti

251 duced dissociation tandem mass spectrometry (CID MS/MS), the underlying mechanism remains unknown.

252 duced dissociation tandem mass spectrometry (CID MS/MS), which produces a complex dataset of oligomer

253 Patients with syndromic CIDs had a significantly lower 5-year survival rate rath

254 However, in patients with syndromic CIDs, autosomal recessive mutations in ataxia-telangiect

255 nificantly better chiral discrimination than CID.

256 g protein complexes with less unfolding than CID.

257 D nucleosomes are octameric in vivo and that CID dimerization is essential for correct centromere ass

258 The results of this study confirm that CID involves the unfolding of the protein complex via se

259 Taken together, our findings suggest that CID nucleosomes are octameric in vivo and that CID dimer

260 The CID experiments generated fragment ions predominantly fr

261 bind to Sac3 approximately 100-550; and the CID region in which Cdc31 and two Sus1 chains bind to Sa

262 multiple complementary spectra, such as the CID/UVPD pairs, into peptide fragmentation site predicti

263 and C57/Sle1Sle2Sle2 mice was blocked by the CID 1067700 compound, which specifically targeted Ras-re

264 e the most prevalent reaction pathway in the CID.

265 nce exceeds that of PEAKS and PepNovo on the CID spectra and that of UVnovo on CID or UVPD spectra al

266 In benchmarks on the CID/UVPD data, UVnovo assigned correct full-length seque

267 Nrd1 with the CID from Rtt103 (Nrd1(CID(Rtt103))) causes read-through

268 d by high resolution mass spectrometry (TIMS-CID-MS) for epimer analysis.

269 nd diversity of ETD mass spectra compared to CID counterparts.

270 In contrast to CID, the phosphorylation site of histidine, arginine, an

271 nd complete (CID MS(2) is thus equivalent to CID MS(3)).

272 Mass selection and subsequent ion trap CID of the lipid anions allows for the characterization

273 These anions also fragment upon ion trap CID to yield product ions indicative of chain lengths an

274 lision-induced dissociation (CID), beam-type CID (HCD), electron-transfer dissociation (ETD), and the

275 lision-induced dissociation (CID), beam-type CID (HCD), electron-transfer dissociation (ETD), ETciD,

276 itially proceed via the so-called "typical" (CID) dissociation route.

277 ld of phosphate-retaining sequence ions upon CID.

278 The major losses upon CID on the adduct, [(phen)M(C6H11O2)](+), are 1-butene f

279 Native phosphoinositide ions yielded upon CID in the negative ion-mode predominantly product ions

280 structure elucidation was accomplished using CID.

281 entation characteristics were analyzed using CID and ETD tandem mass spectrometry.

282 ns and protein complexes, our workflow using CID-MS/MS acquisition performs with high confidence, sco

283 Eighty-two patients from 60 families with CID and the phenotype of AR-HIES with (64 patients) and

284 mbers belonging to 5 unrelated families with CID-MIA.

285 oteins that have been shown to interact with CID boundaries, such as Sth1, Ssu72 and histone H4.

286 utations in ORAI1 in unrelated kindreds with CID, autoimmunity, ectodermal dysplasia with anhidrosis,

287 ar and immunologic analysis of patients with CID, anhidrosis, and ectodermal dysplasia of unknown eti

288 enetic aberration in 4 related patients with CID, early-onset asthma, eczema, and food allergies, as

289 resent at detectable levels in patients with CID-G/AI who had a history of severe viral infections.

290 ed whole-exome sequencing on 5 patients with CID-MIA and 10 healthy direct family members belonging t

291 the TTC7A gene in 8 unrelated patients with CID-MIA and demonstrated that the TTC7A protein is expre

292 cing in 3 additional unrelated patients with CID-MIA revealed biallelic deleterious mutations in 2 of

293 ain 7A (TTC7A) on 3 additional patients with CID-MIA.

294 pheral lymphoid tissues from 2 patients with CID-MIA.

295 Recognizing patients with CID/HIES is of clinical importance because of the differ

296 Five consecutive patients with CIDs and chronic viral infections underwent an allogenei

297 us option for the treatment of patients with CIDs at high risk of GVHD, infection, or both in an HLA-

298 characterize the categories of patients with CIDs in Iran clinically and genetically.

299 ry data were obtained from 696 patients with CIDs.

300 methods, here we show that the fission yeast CID-protein Seb1 is essential for termination of protein