ライフサイエンスコーパス: AID

1 AID detection via tdTomato expression allowed tracking o

2 AID expression is tightly regulated in B cells and its o

3 AID is essential for the maturation of antibodies and ca

4 AID mediates class-switch recombination (CSR) and somati

5 AID was expressed in human primary keratinocytes in an i

6 AID-initiated DSBs at targets spread across activated S

7 AID-Pol II mutations are strongly favored in WRC and WGC

8 AID/APOBEC family enzymes are best known for deaminating

9 n initiation, we characterized the sigma(54) AID by NMR spectroscopy and other biophysical methods an

10 ium fluoride, we studied the NtrC1-sigma(54) AID complex using NMR spectroscopy.

11 construct of the Aquifex aeolicus sigma(54) AID that consists of two predicted helices and retains n

12 We found that deficient pS38 abated AID chromatin association and CSR but not mutation at My

13 In addition, through off-target activity, AID has a much broader effect on genomic instability by

14 frequencies of SHM in memory B cells from AD-AID patients and AID+/- subjects, who were unable to pre

15 ts with autosomal dominant AID mutations (AD-AID), asymptomatic AICDA heterozygotes (AID+/-), and pat

16 irectly or indirectly, potentially affecting AID expression and, consequently, genomic stability in B

17 Mice bearing a mutation in Aicda (AID(G133V)) that disrupts AID-G4 binding modeled the pat

18 Using lithium and an AID-S38 phospho mutant, we compared the role of pS38 in

19 ility in normal and neoplastic B cells by an AID-dependent mechanism.

20 indings in the clinical setting, we analyzed AID expression and PFs in a CLL cohort before and during

21 ptosis-control genes FAS/CD95, Caspase-2 and AID.

22 on, growth in response to BAFF or APRIL, and AID/Bcl-6 expression, as well as follicular CD4(+) cell

23 equences in regulating Ab gene diversity and AID targeting specificity.

24 wild-type AID localized to MHCII genes, and AID expression correlated with decreased MHCII expressio

25 ssion and translocation frequency to IGH and AID off-target sites in human chronic lymphocytic leukae

26 M in memory B cells from AD-AID patients and AID+/- subjects, who were unable to prevent the accumula

27 inducing both Igh germline transcription and AID expression.

28 end AIDS by 2030, with incidence of HIV and AIDs-related mortality rates both at less than one event

29 ed a mutational signature of BRCA and APOBEC/AID.

30 To test the ARF-AID system in a quantitative and sensitive manner, we me

31 gradation is substantially faster in the ARF-AID system.

32 ctive capability of a recombinase-associated AID subtype (rAID-1) that is present broadly in Bacteroi

33 Despite the functional link between AID and TET in epigenetic gene regulation, the role of A

34 tifs potentially function as spacers between AID deamination hotspots.

35 h DNA damage, suggesting that factors beyond AID association contribute to mutation targeting.

36 ntact-dependent interbacterial antagonism by AID systems helps to shape human gut microbiome ecology.

37 To directly map uracils created by AID/APOBEC enzymes, here we used uracil-DNA glycosylase

38 chromosome structure of TOP2A degradation by AID.

39 mutation hotspots are largely determined by AID deamination.

40 itch DNA recombination (CSR) is initiated by AID-introduced DSBs in the switch (S) regions targeted f

41 The mutability modulated by AID hotspots and coldspots changes correlated only weakl

42 anism by which processing of G:U produced by AID at the telomeres can eliminate B cells at risk of ge

43 man B-ALL are not preferentially targeted by AID.

44 biological insights, reporting evidence of c-AID activity among unmutated CLL cases or the absence of

45 ed heightened humoral responses (CD20, CD22, AID) in melanoma.

46 express Cre in germinal center (GC) B cells (AID-Cre).

47 omain of the cardiac L-type calcium channel (AID-TAT) on restoring mitochondrial metabolic activity,

48 In this study, we characterize AID-dependent break formation in J(H) introns from mouse

49 In chronic lymphocytic leukemia (CLL), AID is overexpressed in the proliferative fractions (PFs

50 nduced cytidine deaminase (AID) to construct AID-nCas9-Ung and found that it converts C to A with an

51 Moreover, G4 substrates induce cooperative AID oligomerization.

52 onal interference, and gene deletion (CRISPR-AID) in the yeast Saccharomyces cerevisiae.

53 We demonstrate the application of CRISPR-AID not only to increase the production of beta-carotene

54 compounds in the PubChem bioassay database (AID: 1508591).

55 Guided by single guide (sg)RNAs, dCas9-AID-P182X (AIDx) directly changed cytidines or guanines

56 Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specific gene expression,

57 nary precursors, the antibody gene deaminase AID and the RNA/DNA editing enzyme APOBEC1 (A1).

58 in an activation-induced cytidine deaminase (AID) and H2AX-dependent fashion.

59 ed by activation-induced cytidine deaminase (AID) and requires base excision repair (BER) and mismatc

60 that activation-induced cytidine deaminase (AID) and ten-eleven-translocation (TET) family members r

61 es of activation-induced-cytidine deaminase (AID) and the A-T mutator, DNA polymerase eta, respective

62 on of activation-induced cytidine deaminase (AID) between heterologous challenges of West Nile, Japan

63 Activation-induced cytidine deaminase (AID) converts cytosine into uracil to initiate somatic h

64 Activation-induced cytidine deaminase (AID) generates U:G mismatches in Ig genes that can be co

65 enous activation-induced cytidine deaminase (AID) in engineered cells allowed for Ig class switching

66 Activation-induced cytidine deaminase (AID) initiates both class switch recombination (CSR) and

67 Activation-induced cytidine deaminase (AID) initiates immunoglobulin (Ig) class switch recombin

68 Activation-induced cytidine deaminase (AID) initiates somatic hypermutation and class switch re

69 Activation-induced cytidine deaminase (AID) is a B-cell-specific enzyme that targets immunoglob

70 Activation-induced cytidine deaminase (AID) is a genome-mutating enzyme that initiates class sw

71 Activation-induced cytidine deaminase (AID) is a mutator enzyme that targets immunoglobulin (Ig

72 binds activation-induced cytidine deaminase (AID) that catalyzes SHM, we tested AID interactions with

73 used activation-induced cytidine deaminase (AID) to construct AID-nCas9-Ung and found that it conver

74 human activation-induced cytidine deaminase (AID) to identify genes preventing R loops.

75 nt of activation-induced cytidine deaminase (AID) to Ig switch regions (S regions).

76 ng of activation-induced cytidine deaminase (AID) to immunoglobulin (Ig) loci promotes antibody class

77 9 to recruit variants of cytidine deaminase (AID) with MS2-modified sgRNAs, we can specifically mutag

78 nduce activation-induced cytidine deaminase (AID)(2) and I-promoter transcription, with 3' IgH regula

79 ed by activation-induced cytidine deaminase (AID), the activity of which leads to DNA double-strand b

80 Activation-induced cytidine deaminase (AID), the enzyme responsible for induction of sequence v

81 nzyme activation-induced cytidine deaminase (AID), which is required in affinity maturation.

82 on of activation-induced cytidine deaminase (AID)-instigated DNA double-strand breaks into the IgH lo

83 rgone activation-induced cytidine deaminase (AID)-mediated somatic hypermutation (SHM) following neur

84 e DNA activation-induced cytidine deaminase (AID).

85 nzyme Activation-induced cytidine Deaminase (AID).

86 y the activation-induced cytidine deaminase (AID).

87 il by activation-induced cytidine deaminase (AID).

88 on of activation-induced cytidine deaminase (AID).

89 that activation-induced cytidine deaminase (AID, encoded by AICDA) links chronic inflammation and sk

90 srupt activation-induced cytidine deaminase (AID; Aicda) directly in BXSB zygotes.

91 on of activation-induced cytidine deaminase (AID; also known as AICDA) in precursor B-cells.

92 on of activation-induced cytosine deaminase (AID).

93 Activation-induced deoxycytidine deaminase (AID) initiates somatic hypermutation (SHM) in immunoglob

94 in patterns of activation-induced deaminase (AID) and apolipoprotein B mRNA editing catalytic polypep

95 Activation-induced deaminase (AID) and apolipoprotein B mRNA-editing enzyme catalytic

96 Activation-induced deaminase (AID) can drive lymphomagenesis by generating off-target

97 roteins induce activation-induced deaminase (AID) expression in activated B cells.

98 Activation-induced deaminase (AID) functions by deaminating cytosines and causing U:G

99 Activation-induced deaminase (AID) initiates antibody gene diversification by creating

100 s initiated by activation-induced deaminase (AID), which deaminates cytosine to uracil in DNA.

101 (SHM) enzyme, Activation Induced Deaminase (AID), which overlaps the CpG methylation site.

102 es ["activity-regulated inhibitor of death" (AID) genes] including the transcription factor (TF) NPAS

103 of CTNNBL1 with AID, resulting in decreased AID in the nuclei of patient EBV-transformed B cell line

104 hat MMSET-II inactivation leads to decreased AID recruitment and DSBs at the upstream donor Smu regio

105 program, increased cell death, and defective AID expression.

106 currence of acquired interbacterial defence (AID) gene clusters in Bacteroidales species that reside

107 question, we apply an Auxin-Induced Degron (AID) system to distinguish roles of basket nucleoporins

108 The auxin-inducible degron (AID) system enables rapid depletion of target proteins w

109 on of PICH using the auxin-inducible degron (AID) system resulted in the retention of SUMO2/3-modifie

110 mitosis, we used the auxin-inducible degron (AID) system to rapidly degrade the protein at different

111 The auxin-inducible degron (AID) system was developed as a tool to achieve rapid and

112 mately 20% of the acute infectious diarrhea (AID) episodes worldwide, often by producing heat-stable

113 equence of treatment for autoimmune disease (AID) and an emerging clinical phenomenon.

114 is (TA) is an even rarer autoimmune disease (AID), both of which present with inflammatory vasculitis

115 ies in autoimmune and inflammatory diseases (AID) have uncovered hundreds of loci mediating risk.

116 The pathogenesis of autoimmune diseases (AIDs) is not only attributed to genetic susceptibilities

117 mutation in Aicda (AID(G133V)) that disrupts AID-G4 binding modeled the pathology of hyper-IgM syndro

118 We found that these earliest-diverged AID orthologs are active cytidine deaminases that exhibi

119 gulatory domains, the autoinhibitory domain (AID) and calmodulin-binding domain (CBD), which block th

120 inal sigma(54) activator interacting domain (AID).

121 t patients, patients with autosomal dominant AID mutations (AD-AID), asymptomatic AICDA heterozygotes

122 -GC B-cell lymphomas, the role of downstream AID-associated DNA repair pathways in the pathogenesis o

123 ngle-stranded, thereby creating an effective AID substrate.

124 e switch (S) region is a much more efficient AID deamination target than the V region.

125 ARF is absent from previously engineered AID systems but is a critical component of native auxin

126 Consistently, PI3Kdelta inhibitors enhanced AID expression and translocation frequency to IGH and AI

127 In this study, we examined AID footprints across the entire length of an engineered

128 We find that the existing AID / APOBEC hotspots have a large impact on retrotransp

129 individual B cells that previously expressed AID are located within the LN cortex, in an area close t

130 he proliferation of tumor B cells expressing AID.

131 We demonstrated that Tg mice expressing AID in the skin spontaneously developed skin squamous ce

132 Odds ratio (OR) assessment for AID-directed therapies.

133 ructures are not necessary intermediates for AID access.

134 osis constitute an essential time window for AID-induced deamination, and provide a novel DNA damage

135 a trade-off for its physiological function, AID also contributes to tumor development through its mu

136 direct targeting and induction of functional AID by EBNA3C, suggest a novel role for EBV in the etiol

137 tures of maltose binding protein (MBP)-fused AID alone and in complex with deoxycytidine monophosphat

138 em enables us to easily and rapidly generate AID-based conditional knockout cells in a wide range of

139 lobulin switch regions are particularly good AID substrates in vitro.

140 (AD-AID), asymptomatic AICDA heterozygotes (AID+/-), and patients with uracil N-glycosylase (UNG) de

141 a clinically used therapeutic, induced high AID pS38 levels.

142 to the lungs of patients suffering from HIV/AIDs.

143 cal and/or sexual IPV and emotional IPV, HIV/AIDs knowledge and behaviors, decision-making, and gende

144 However, AID also deaminates nonimmunoglobulin genes, and failure

145 However, AID is mostly cytoplasmic, and how and exactly when it a

146 However, AID occupancy does not directly correlate with DNA damag

147 Here, we produced active human AID and revealed its preferred recognition and deaminati

148 ontrol of another mutagenic deaminase, human AID, and provides a rationale for its regulation.

149 escribed the biochemical properties of human AID and found that it is an unusual enzyme in that it ex

150 o damage from either the expression of human AID or increased oxidative stress.

151 Finally, using a hyperactive AID variant, we mutagenize loci both upstream and downst

152 and nonclonal mutations arise within non-Ig AID target genes in the combined absence of UNG and MSH2

153 ferred nucleic acid substrates, illuminating AID targeting mechanisms during CSR and SHM.

154 Importantly, AID-TAT was rapidly targeted to the heart, and not retai

155 f these effects were completely abrogated in AID-deficient B cells.

156 gs indicate a crucial role for G4 binding in AID targeting and suggest that AID activity may extend b

157 dings, we observe a complete block in CSR in AID(S38A/S38A)MSH2(-/-) mouse B cells that correlates wi

158 d demonstrate that M2 primarily functions in AID-expressing cells to facilitate MHV68 dissemination t

159 b, showed increased somatic hypermutation in AID off-targets.

160 on is almost negligible at the JH4 intron in AID(S38A/S38A)MSH2(-/-) mouse B cells, and, consistent w

161 ith this, NP-specific affinity maturation in AID(S38A/S38A)MSH2(-/-) mice is not significantly elevat

162 spho mutant, we compared the role of pS38 in AID activity at the Ig switch region and off-target Myc

163 The prolonged survival in AID-deficient BXSB mice appears attributed primarily to

164 Here, we analyzed B cell tolerance in AID-deficient patients, patients with autosomal dominant

165 dies on microbiota-autoimmunity interplay in AIDs are urgently needed and underway to explore novel a

166 wt mice were treated with active or inactive AID-TAT.

167 A eukaryotic transcription system including AID has not been reported previously.

168 nically approved kinase inhibitors, increase AID expression and genomic instability in normal and neo

169 Moreover, although ibrutinib increases AID expression in a CLL cell line, it is unable to do so

170 from idelalisib in their potential to induce AID in treated patients.

171 Moreover, the rate of auxin-induced AID degradation is substantially faster in the ARF-AID s

172 of Sox2 in splenic B cells severely inhibits AID expression and CSR, whereas deletion of Sox2 increas

173 passive transfer of antinucleosome IgG into AID(-/-)MRL/lpr mice elevated autoantibody levels and pr

174 gh-affinity IgA antibodies with mice lacking AID-enabled Ig affinity maturation, we found that IgA de

175 Igh locus AID-initiated lesions are processed by error-free and er

176 We discuss possible mechanisms AID and APOBEC viral targets have adopted to escape the

177 sed with Rosa26-loxP-tdTomato reporter mice (AID(Cre)-Rosa26(tdTomato)) to monitor B cells having und

178 Importantly, we analyzed monoallelic AID deamination footprints on both DNA strands occurring

179 ring CSR, as the AID phosphorylation mutant, AID(S38A), cannot interact with APE1, a BER protein.

180 -associated autoinflammatory diseases (NLRP3-AIDs) include conditions of various severities, due to g

181 The phenotypic spectrum of NLRP3-AIDs appears to be related to the germinal/mosaic status

182 ism to limit the tumor promoting activity of AID when it overwhelms uracil excision repair.

183 uses or retrotransposons and, in the case of AID, changing antibody sequences to drive affinity matur

184 omain suppresses constitutive degradation of AID-tagged proteins.

185 ted loop extrusion juxtaposes proper ends of AID-initiated donor and acceptor S-region DSBs for delet

186 extent ibrutinib, enhanced the expression of AID and increased somatic hypermutation and chromosomal

187 d elevation in RAG1 while high expression of AID marked pre-B-ALL lacking common cytogenetic changes.

188 distinct BCR repertoire, high expression of AID, high sensitivity to PAMPs, and the ability to produ

189 portantly, the reduction in the formation of AID-accessible ssDNA in cells lacking H3.3 is independen

190 tors or ibrutinib increased the formation of AID-dependent tumours in pristane-treated mice.

191 The generation of AID off-target mutagenic activity in precursor B-cells d

192 ines to the other three bases independent of AID hotspot motifs, generating a large repertoire of var

193 nfected primary B cells for the induction of AID mRNA and protein.

194 ivated by functional EBNA3C and induction of AID.

195 Mechanisms of AID targeting and catalysis remain elusive despite its c

196 lymphocyte populations as in other models of AID deficiency as well as increased populations of CD73(

197 nce of G4 recognition and oligomerization of AID in CSR.

198 Median time from onset of AID to diagnosis of myeloid neoplasm was 8 (interquartil

199 identify a novel role for phosphorylation of AID at serine 38 in mismatch repair-dependent CSR and af

200 Phosphorylation of AID at serine 38 was previously hypothesized to regulate

201 , our data implicate intrinsic preference of AID for structured substrates and uncover the importance

202 We also analyzed the presence of AID hotspots and coldspots at different points in lineag

203 germinal center B cells but preservation of AID(+) B cells.

204 e investigated the biochemical properties of AID from a sea lamprey, nurse shark, tetraodon, and coel

205 Central to the recruitment of AID to the IgV genes are factors that regulate the gener

206 proteins contribute to optimal resolution of AID-induced DSBs.

207 T in epigenetic gene regulation, the role of AID loss in hematopoiesis and myeloid transformation rem

208 While SBS85 is a denoted signature of AID in lymphoid cells, the etiologies of SBS37 and SBS39

209 ith data in the murine context, silencing of AID in human bone marrow cells skews differentiation tow

210 ently, we solved the functional structure of AID and demonstrated that these properties are due to no

211 nded DNA (ssDNA), the enzymatic substrate of AID Here, we report that chicken DT40 cells lacking vari

212 that telomeres are off-target substrates of AID and that B cell proliferation depends on protective

213 Preferential targeting of AID-mediated DSBs to S sequences is critical for allowin

214 However, the downstream targets of AID action mediating neuroprotection remained so far unk

215 and SHM are regulated by phosphorylation on AID serine38 (pS38), but the role of pS38 in off-target

216 break (DSB) formation is as low as even one AID deamination event on both DNA strands.

217 sk for GCA and for GCA and TA with any other AID based on the Swedish hospital diagnoses up to years

218 ngs were diagnosed with GCA, TA or any other AID.

219 GCA was associated with 10 other AIDs and TA was associated with 6 other AIDs; both share

220 ther AIDs and TA was associated with 6 other AIDs; both shared associations with polymyalgia rheumati

221 both GCA and TA with such a number of other AIDs provide evidence for polyautoimmunity among these d

222 We next test the effect of premature AID expression from earliest pro-B-cell stages in B-cell

223 , Ninth Revision, coded diagnosis of primary AID who were seen at 2 centers from January 1, 2004, to

224 In a large population with primary AID, azathioprine exposure was associated with a 7-fold

225 ls in the switch region, although processive AID deaminations are evident in some molecules.

226 ubset of patients with evidence of prolonged AID activity during the pre-malignant phase, indicating

227 uggest a role for the HMT MMSET in promoting AID-mediated DNA breaks during CSR.

228 RAD-AID's three-pronged integrated strategy for AI adoption

229 This strategy derives from RAD-AID's more-than-a-decade experience as a nonprofit organ

230 infrastructure developments occur while RAD-AID delivers phased introduction, testing, and scaling o

231 gher doses over a broad physiological range, AID and Blimp1 expression, CSR, somatic hypermutation an

232 Here, we reconstitute AID-catalyzed deamination during Pol II transcription el

233 the CLL PFs and, interestingly, also reduces AID expression, which correlates with dampened AKT and J

234 These results suggest that Sox2 may regulate AID expression in class-switched B cells to suppress gen

235 rally highly toxic, mechanisms that regulate AID expression are of much relevance to CSR and genomic

236 exon sequences and their ability to regulate AID deamination and subsequent repair process.

237 equence-intrinsic properties, which regulate AID deamination and affect the preferential access of do

238 Altering the timing of cell cycle-regulated AID nuclear residence increases DNA damage at off-target

239 3-kinase delta (PI3Kdelta) pathway regulates AID by suppressing its expression in B cells.

240 TNNBL1 plays an important role in regulating AID-dependent antibody diversification in humans.

241 However, precise mechanisms regulating AID deamination frequency remain incompletely understood

242 For use in mammalian cells, we replaced AID with rat APOBEC1 (APOBEC-nCas9-Ung).

243 chemical and structural approaches to report AID-preferred nucleic acid substrates, illuminating AID

244 method that incorporates the super-sensitive AID system and the single-step method provides a powerfu

245 The super-sensitive AID system enabled more than a 1000-fold reduction of th

246 step method coupled with the super-sensitive AID system enables us to easily and rapidly generate AID

247 Here, we describe a super-sensitive AID system that incorporates the synthetic auxin derivat

248 on frequency to the Igh locus and to several AID off-target sites.

249 age to the B-cell genome during CSR and SHM, AID induces unwanted (and sometimes oncogenic) mutations

250 king the Mlp1/2 nuclear basket proteins show AID-dependent genomic instability and replication defect

251 l knockout mouse strain with the GC-specific AID-Cre transgenic strain.

252 Surprisingly, AID(S38A/S38A)UNG(-/-) mouse B cells also cannot complet

253 Here we show that, surprisingly, AID genetic deletion does not affect B-ALL development i

254 Although off-target AID activity also contributes to oncogenic point mutatio

255 Off-target AID association also occurs, which causes oncogenic muta

256 marinus cytidine deaminase-based CBE Target-AID(4) induce less editing of RNA.

257 ion-induced cytidine deaminase (nCas9-Target-AID) systems to mutagenize Nicotiana tabacum protoplasts

258 tivated downstream acceptor S-region targets AID-generated deamination lesions at, potentially, any o

259 eaminase (AID) that catalyzes SHM, we tested AID interactions with the CTNNBL1 M466V variant.

260 We found that AID deamination occurs predominantly at WRC hot spots (w

261 We found that AID generates few and mostly isolated uracils in the swi

262 These results indicate that AID and TET2 share common effects on myeloid and erythro

263 We propose that AID-induced damage at telomeres acts as a fail-safe mech

264 We also reveal that AID-TAT treatment of precardiomyopathic cTnI-G203S mice,

265 Recent studies have revealed that AID's DNA mutator activity is regulated by the RNA exoso

266 Here, we show that AID is transiently in spatial contact with genomic DNA f

267 G4 binding in AID targeting and suggest that AID activity may extend beyond Ig loci to regulate the e

268 other types of human cancer, suggesting that AID-mediated, CpG-methylation dependent mutagenesis is a

269 The AID / APOBEC genes are a family of cytidine deaminases t

270 The AID system is useful for investigating the physiological

271 The AID/APOBEC enzymes deaminate cytosines in single-strande

272 The AID/APOBEC family enzymes convert cytosines in single-st

273 othesized to regulate BER during CSR, as the AID phosphorylation mutant, AID(S38A), cannot interact w

274 tic modification approach has identified the AID/RAD51 axis as a target for a potentially clinically

275 he CBD common to all isoforms, but lacks the AID.

276 and it was shown that transactivation of the AID gene (AICDA) is associated with EBNA3C binding to hi

277 abled more than a 1000-fold reduction of the AID inducer concentrations in chicken DT40 cells.

278 APOBEC3G (A3G) belongs to the AID/APOBEC protein family of cytidine deaminases (CDA) t

279 t amino acid sequence divergence among these AID orthologs is predicted to manifest as notable struct

280 uggest that infections promote B-ALL through AID-independent mechanisms, providing evidence for a new

281 Thus, AID activity can be differentially targeted by phosphory

282 Ab) binding affinity to DIII proteins, timed AID deletion, single-cell RNA sequencing, and lineage tr

283 e in BER and could potentially contribute to AID-initiated antibody diversification through this acti

284 G-quadruplex (G4) nucleic acid structures to AID targeting in vivo.

285 smatch repair or uracil glycosylase (UNG) to AID-initiated U:G mismatches.

286 as systems (SaCas9, Cas12a, and nCas9-Traget AID) using either a one-step or a two-step transfection

287 e-wide analyses also revealed that wild-type AID localized to MHCII genes, and AID expression correla

288 Utilizing AID-TAT to modulate cardiac metabolic activity may be be

289 gut microbiota have been reported in various AIDs, and increasing evidence suggests that disturbed gu

290 n be used to investigate how, when and where AID is targeted.

291 Whereas AID levels were not altered in Id3-depleted activated B

292 SR) and somatic hypermutation (SHM), whereas AID targeting of non-Ig loci can generate oncogenic DNA

293 (SHM) in B cells, but the mechanism by which AID prevents the accumulation of autoreactive B cells in

294 nd SHM, and had broad defects in genome-wide AID(G133V) chromatin localization.

295 Consistent with AID, comparable somatic hypermutation frequencies and cl

296 erfered with the association of CTNNBL1 with AID, resulting in decreased AID in the nuclei of patient

297 ammalian genes, suggesting co-evolution with AID / APOBECs may have had an impact on the genomes of t

298 In plants, ARF directly interacts with AID in the absence of auxin, and we found that expressio

299 munomodulating agents to treat patients with AID with the risk for developing myeloid neoplasm.

300 therapeutic interventions for patients with AIDs.