ライフサイエンスコーパス: CID

1 CID appeared after the divergence of protostomes and deu

2 CID data suggests that facile metal-phosphate dissociati

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

4 CID is most complementary, increasing the number of iden

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

6 CID of the charge-reduced precursors results in extensiv

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

8 CID outperforms existing chromatin interaction detection

9 CID tools such as the FK506-binding protein-FKBP-rapamyc

10 CID was identified in 115 (51%) of 225 RSCA cases: long

11 CIDs transporting positive charge upward (a) occurred at

12 A total of 1096 CIDs transporting negative charge upward and 8 CIDs tran

13 ltiple-stage tandem mass spectrometry (MS(3) CID) provides supplementary and valuable structural info

14 years of age, HCM was the most common (33%) CID.

15 Ds transporting negative charge upward and 8 CIDs transporting positive charge upward were analyzed.

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

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

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

19 In addition, CID also outperforms other methods in discovering chroma

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

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

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

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

24 on, which enabled us to separate and analyze CID and ECD fragmentation simultaneously.

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

26 The resultant ETD and CID spectra were used for the identification of the inta

27 was demonstrated using hybrid UVPD-MS/MS and CID-MS(3) on a diagnostic pair of product ions.

28 o intrinsically disordered domains, NCBD and CID, likely emerged in an ancestral deuterostome organis

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

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

31 We characterize the on-board CID process by comparing the fragments generated from a

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

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

34 dem mass spectrometry (MS2) fragmentation by CID in the ion trap.

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

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

37 alysis of the avidin tetramer is possible by CID in tandem-TIMS.

38 SePh groups are reactivated and sequenced by CID.

39 COMBINES-CID provides an efficient, cost-effective solution for e

40 l binders-enabled selection of CID (COMBINES-CID) method broadly applicable to different ligands.

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

42 ntified after RSCA was LQTS; the most common CID cause of RSCA for those >40 years of age was HCM.

43 The commonest CID identified after RSCA was LQTS; the most common CID

44 Moreover, comparative CID fragmentation analysis between unmodified phosphopep

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

46 to further dissociation through conventional CID.

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

48 ents affected by combined immune deficiency (CID), a group of disorders caused by genetic defects tha

49 work and for the first time, we demonstrate CID in a field asymmetric time of flight ion mobility sp

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

51 Chemically induced dimerization (CID) systems, in which two proteins dimerize only in the

52 , we used chemically inducible dimerization (CID) assays in tandem with CRISPR KO lines to systematic

53 Chemically inducible dimerization (CID) uses a small molecule to induce binding of two diff

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

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

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

57 ce context of compact intracloud discharges (CIDs) is examined using their electric field waveforms a

58 thod called Chromatin Interaction Discovery (CID) to overcome this limitation with an unbiased cluste

59 roportion of each cardiac inherited disease (CID) causing resuscitated sudden cardiac arrest (RSCA) o

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

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

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

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

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

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

66 ate, we show collision-induced dissociation (CID) and electron-transfer dissociation (ETD) on each pr

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

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

69 on (HCD) and collision-induced dissociation (CID) are employed to provide complementary structural in

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

71 h we perform collision-induced dissociation (CID) at pressures in the millibar range.

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

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

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

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

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

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

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

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

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

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

82 on (SID) and collision-induced dissociation (CID) for Fourier transform ion cyclotron resonance mass

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

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

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

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

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

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

89 Collision induced dissociation (CID) is a widely used technique in mass spectrometry to

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

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

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

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

94 S results in collision-induced dissociation (CID) of avidin tetramers into compact monomers, dimers,

95 generated by collision-induced dissociation (CID) of disaccharides can retain the anomeric configurat

96 Collision-induced dissociation (CID) of MALDI-generated ozonide ions (with yields in the

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

98 Collision-induced dissociation (CID) of the resulting demethylated PC product anions all

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

100 Collision induced dissociation (CID) of these phosphorylated oligosaccharides produces s

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

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

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

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

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

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

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

108 pon ion-trap collision-induced dissociation (CID) to generate product ion spectra unique to individua

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

110 generated by collision-induced dissociation (CID) together with a floppiness parameter defined based

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

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

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

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

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

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

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

118 1-16), using collision induced dissociation (CID), higher-energy collision induced dissociation (HCD)

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

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

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

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

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

124 n low-energy collision-induced dissociation (CID), traditional ESI-MS/MS fails to define fatty acyl r

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

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

127 oupling with collision-induced dissociation (CID)-MS/MS strategy provides a new tool for unsaturated

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

129 pattern upon collision-induced dissociation (CID).

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

131 pecies using collision-induced dissociation (CID).

132 conventional collision induced dissociation (CID).

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

134 tified using collision-induced dissociation (CID).

135 ination with collision-induced dissociation (CID).

136 n when using collision-induced dissociation (CID).

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

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

139 m which its (13)C-isotopologue distribution (CID) is quantified.

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

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

142 ptide binding to the CTD-interacting domain (CID) of RPRD1A and RPRD1B proteins in isothermal calorim

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

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

145 A CTD interaction domain (CID) from the protein Nrd1 can partially substitute for

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

147 delineate chromosomally interacting domains (CIDs).

148 to TAD-like chromosomal interaction domains (CIDs) but do not display A/B compartment-type organizati

149 two interacting disordered protein domains, CID and NCBD.

150 improve mean sequence coverage dramatically (CID-only 15% vs chimeric 33%), even during discovery-bas

151 rrangements, which have been observed during CID.

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

153 of the glycopeptides at low collision energy CID to produce linkage-specific Y-ions.

154 a target analyte's unique fragment following CID.

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

156 ranging from 16 to 19 km vs. 6 to 16 km for CIDs transporting negative charge upward and (b) had con

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

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

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

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

161 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autosomal recessive (AR) hyper-I

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

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

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

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

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

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

168 s that have poor fragmentation efficiency in CID.

169 nsitivity in flythrough mode, 7x increase in CID sensitivity for protonated leucine enkephalin (m/z 5

170 tigate the generality of anomer retention in CID by exploring different fragmentation channels in gly

171 ucing the number of electrodes, (2) increase CID and SID sensitivity by lengthening the collision cel

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

173 mes of Sulfolobus archaea are organized into CID-like topological domains in addition to previously d

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

175 GM NLDN-reported peak currents for isolated CIDs (33 kA) were similar to those initiating normal lig

176 The percentages of isolated CIDs transporting negative charge upward decreased from

177 Some of our isolated CIDs could be viewed as precursors, because they apparen

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

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

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

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

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

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

184 First, in negative ion mode, CID of mass-selected GPL anions generates fatty acyl car

185 inity ancestral and high-affinity human NCBD/CID interactions.

186 val rate rather than those with nonsyndromic CIDs.

187 when Set1/COMPASS is recruited via the Nrd1 CID, histone H2B ubiquitylation is still required for ef

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

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

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

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

192 with RAG deficiency and with other forms of CID has revealed distinct abnormalities in central and p

193 However, only a handful of CID systems exist and creating one with the desired sens

194 ne enkephalin (m/z 556), and 14x increase of CID sensitivity of 53 kDa streptavidin tetramer.

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

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

197 icacy of octreotide LAR in the prevention of CID.

198 a combinatorial binders-enabled selection of CID (COMBINES-CID) method broadly applicable to differen

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

200 tudy the mobility and vibrational spectra of CID fragments from two human milk oligosaccharides.

201 ir were the most common underlying causes of CIDs.

202 ompanied by an increase of the percentage of CIDs preceding (initiating) normal lightning events from

203 The treatment of CIDs with allogeneic hematopoietic stem cell transplanta

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

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

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

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

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

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

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

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

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

213 difficult HSCT decisions in patients with P-CID.

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

215 44 patients) and nonsyndromic (352 patients) CIDs.

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

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

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

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

220 2 GOF mutations produce a nonfully penetrant CID phenotype through a different pathophysiologic mecha

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

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

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

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

225 (PubChem CID: 8815); trans-anethole (PubChem CID: 637563); Myristicin (PubChem CID: 4276); Safrole (P

226 nol (PubChem CID: 853433); Caffeine (PubChem CID: 2519); Dicyclohexylmethanol (PubChem CID: 78197).

227 em CID: 2519); Dicyclohexylmethanol (PubChem CID: 78197).

228 Estragole (PubChem CID: 8815); trans-anethole (PubChem CID: 637563); Myrist

229 afrole (PubChem CID: 5144); Eugenol (PubChem CID: 3314); Methyl eugenol (PubChem CID: 7127); Acetyl e

230 (PubChem CID: 3314); Methyl eugenol (PubChem CID: 7127); Acetyl eugenol (PubChem CID: 7136); trans-Is

231 (PubChem CID: 7127); Acetyl eugenol (PubChem CID: 7136); trans-Isoeugenol (PubChem CID: 853433); Caff

232 CID: 5610); Tyramine hydrochloride (PubChem CID: 66449); Poly(vinyl chloride) (PubChem SID: 24864273

233 ubChem CID: 7136); trans-Isoeugenol (PubChem CID: 853433); Caffeine (PubChem CID: 2519); Dicyclohexyl

234 e (PubChem CID: 637563); Myristicin (PubChem CID: 4276); Safrole (PubChem CID: 5144); Eugenol (PubChe

235 SID: 24864273); Tricresyl phosphate (PubChem CID: 6529); sodium phosphotungstate tribasic hydrate (Pu

236 sticin (PubChem CID: 4276); Safrole (PubChem CID: 5144); Eugenol (PubChem CID: 3314); Methyl eugenol

237 s studied in this article: Tyramine (PubChem CID: 5610); Tyramine hydrochloride (PubChem CID: 66449);

238 tructures that were linked to 65,957 PubChem CIDs and to over 878,966 PubMed articles.

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

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

241 diation collision-induced dissociation (SORI-CID).

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

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

244 Finally, we developed an in-source CID ramping (InCIDR) method to analyze the intensity cha

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

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

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

251 Subsequent CID of charge-inverted fatty acyl complex cations yielde

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

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

254 alone and richer fragmentation patterns than CID alone.

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

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

257 We applied the CID system to a sensitive sandwich enzyme-linked immunos

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

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

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

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

262 We expect that the CID method will be valuable in characterizing 3D chromat

263 CPVT was the CID most likely to present with RSCA and HCM the least.

264 The CIDs were categorized based on whether they were isolate

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

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

267 Only one-third of RSCA cases due to CID occurred while exercising.

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

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

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

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

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

273 lycan units show different stabilities under CID/HCD fragmentation.

274 ld of phosphate-retaining sequence ions upon CID.

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

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

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

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

279 collision induced dissociation/193 nm UVPD (CID/UVPD) approach was implemented to pinpoint the locat

280 In this work, a hybrid UVPD-CID approach known as activated-electron photodetachment

281 While various CID tools are available, chemically inducible trimerizat

282 ies and positions, which is not possible via CID of the precursor lipid cations.

283 itional condition to what is achievable with CID, CIT expands the types of manipulation in single liv

284 and immunological phenotypes associated with CID.

285 Of 725 probands from the CIDRNZ with CID, the proportion presenting with RSCA was: CPVT, 9 (5

286 This strategy was complemented with CID for the de novo elucidation of unknown CLs in biolog

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

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

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

290 A genetic diagnosis in patients with CID was made in 48 (49%) of 98 tested.

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

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

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

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

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

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

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

298 study describes the profile of patients with CIDs presenting with RSCA; their data were collected by

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