ライフサイエンスコーパス: pre-B-cell

1 the differentiation of large pre-B to small pre-B cells.

2 chain loci normally undergo recombination in pre-B cells.

3 g-range Vkappa gene usage spanning 3.2 Mb in pre-B cells.

4 r to activate RAG1 and RAG2 transcription in pre-B cells.

5 es that are bound and regulated by Ikaros in pre-B cells.

6 t(8;21) myeloid precursor control cells, and pre-B cells.

7 stranded DNA (dsDNA) breaks in cycling large pre-B cells.

8 a dramatic decrease in locus contraction in pre-B cells.

9 program shutting off the c-Myc gene in large pre-B cells.

10 progenitors while inhibiting development of pre-B cells.

11 RAG1 and RAG2 gene transcription in pro- and pre-B cells.

12 nic stem cells, we observed the formation of pre-B cells.

13 tion in the number of pro-B cells as well as pre-B cells.

14 ce of IGH rearrangements and resembled small pre-B cells.

15 for Igkappa in cis and IgH loci in trans in pre-B cells.

16 on murine leukemia virus (Ab-MLV) transforms pre-B cells.

17 d malignant B cells but are not expressed on pre-B cells.

18 angements was detected in E(het) and ER(het) pre-B cells.

19 vo and directly suppress c-Myc expression in pre-B cells.

20 ring MYC-induced transformation of wild-type pre-B cells.

21 induced following pre-BCR signaling in large pre-B cells.

22 ge, with a strong reduction in the number of pre-B cells.

23 transcription is biallelic and occurs in all pre-B cells.

24 transcripts were up-regulated in beta-gal(+) pre-B cells.

25 at both Ig loci were contracted in pro-B and pre-B cells.

26 berrant DSB repair and genome instability in pre-B cells.

27 r functions in transduced murine B and human pre-B cells.

28 complex (pre-BCR) and the differentiation of pre-B cells.

29 L) arises by transformation of a progenitor (pre-B) cell.

30 cells followed by that of IgL in precursor (pre-) B cells.

31 As MPPs commit to pre-B cells, a predominantly demethylating phenotype ens

32 potent effects in relapsed and/or refractory pre-B cell acute lymphoblastic leukemia (B-ALL), but ant

33 Some cases of pre-B cell acute lymphoblastic leukemia (pre-B-ALL) are

34 point and functions as a tumor suppressor in pre-B cell acute lymphocytic leukemia.

35 iption factors occur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL).

36 has demonstrated marked success in relapsed pre-B-cell acute lymphoblastic leukaemia (ALL).

37 (GC) hormones induce apoptosis in T-cell and pre-B-cell acute lymphoblastic leukemia (ALL) cells.

38 and cell death in normal pre-B cells and in pre-B-cell acute lymphoblastic leukemia (ALL) driven by

39 ng of the pathogenesis of CNS involvement in pre-B-cell acute lymphoblastic leukemia (ALL).

40 sponse of patients suffering from T-cell and pre-B-cell acute lymphoblastic leukemia by increasing st

41 A pre-B-cell acute lymphocytic leukemia miR, miR-143-3p, a

42 e of PAX5 alterations in the pathogenesis of pre-B cell ALL and implicate PAX5 in a new syndrome of s

43 Among the 25 patients (median age, 14 years; pre-B cell ALL, 84%; >/= 2 prior regimens: 84%; refracto

44 ssion of the Mer receptor tyrosine kinase in pre-B-cell ALL (B-ALL) cell lines and pediatric patient

45 Two children with relapsed and refractory pre-B-cell ALL received infusions of T cells transduced

46 volved in the pathogenesis of CNS disease in pre-B-cell ALL, support a model in which CNS disease occ

47 g inherent plasticity in genetic subtypes of pre-B-cell ALL.

48 IL-7Ralpha(449F/449F) and IL-7Ralpha(-/-) pre-B cells also showed defective cyto-Igmu and CD25 exp

49 patterns was comparable in Wt and Ebf1(+/-) pre-B-cells, although the number of progenitors was redu

50 Mutations in Btk, components of the pre-B cell and B cell receptor (lambda5, Igalpha, Igbeta

51 in genes required for signaling through the pre-B cell and B cell receptors.

52 is in deficient animals was caused by "weak" pre-B cell and BCR expression.

53 regulatory region induced both a decrease of pre-B cell and newly formed B cell compartments and a st

54 ents that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade

55 RAG expression in cycling-transformed mouse pre-B cells and human pre-B B-ALL cells that involves th

56 presence of viral genome in bone marrow pro-pre-B cells and immature B cells during early latency an

57 ces cellular stress and cell death in normal pre-B cells and in pre-B-cell acute lymphoblastic leukem

58 ession required for strong signaling through pre-B cells and newly formed BCRs and thus participates

59 of genotoxic stress on RAG1/2 expression in pre-B cells and show that activation of the DNA damage r

60 omised with transitional block from pro-B to pre-B cells and the inability of thymocytes to develop b

61 esult, Ccnd3 is upregulated in PDK1 knockout pre-B cells and they have an impaired ability to undergo

62 functioned to constrain the proliferation of pre-B cells and trigger their differentiation.

63 icacy of tyrosine kinase inhibitors in mouse pre-B cells and xenografts of human Ph-like ALL.

64 (TSSs) during MYC-induced transformation of pre-B cells and, subsequently, during lymphomagenesis.

65 ate that MOZ localizes to the Meis1 locus in pre-B-cells and maintains Meis1 expression.

66 as gene expression regulatory properties for pre-B cells, and provide a catalog reference for the epi

67 ression of p27 and downregulate cyclin D3 in pre-B cells, and the growth-inhibitory effect of Ikaros

68 Signals through the pre-B cell antigen receptor (pre-BCR) and interleukin 7

69 ion through the pre-B stage triggered by the pre-B-cell antigen receptor (pre-BCR).

70 Our data suggest that pre-B cells are endowed with a protective mechanism that

71 MCPyV infection and transformation of pro-/pre-B cells are likely to induce the expression of simpl

72 B cell receptor (BCR) checkpoint, developing pre-B cells are selected for successful rearrangement of

73 on of the Ikaros DNA-binding domain in early pre-B cells arrested their differentiation at a stage at

74 by a reduction in IL2Ralpha-expressing late pre-B-cells as well as by cell cycle analysis and by the

75 own that Fzd9(-/-) mice have a deficiency in pre-B cells at a stage when self-renewing division is oc

76 ere similar, the NHD13 mice showed decreased pre-B cells (B220(+)/CD43(-)), indicating impaired diffe

77 deletion of Sox4 had little effect on normal pre-B cells but compromised proliferation and viability

78 Finally, we demonstrate that DSBs induced in pre-B cells by etoposide or bleomycin inhibit recombinat

79 on at the fraction C' stage, and Ikaros-null pre-B cells cannot differentiate upon withdrawal of IL-7

80 Btk is required for pre-B cell clonal expansion and B-cell antigen receptor

81 Few surviving pre-B cell clones had acquired permissiveness to oncogen

82 Here we show, using B6/Cast hybrid pre-B-cell clones, that a limited number of V segments o

83 Although our previous studies found Pre-B-cell colony-enhancing factor (PBEF) as a highly up

84 Adipokines such as adiponectin and visfatin/pre-B-cell colony-enhancing factor (PBEF) have been rece

85 Visfatin (also termed pre-B-cell colony-enhancing factor (PBEF) or nicotinamid

86 gh the first discovery of this molecule as a pre-B-cell colony-enhancing factor suggested primarily a

87 Visfatin, also known as pre-B-cell colony-enhancing factor, is secreted from a v

88 n-frame (IF) V(H) usage increased in cycling pre-B cells compared with that in pro-B cells, whereas t

89 Analysis of the pre-B-cell compartment in Ebf1 heterozygote mice reveale

90 analysis suggested that the reduction of the pre-B-cell compartment was a result of impaired pre-B-ce

91 al arrest results from rapid caspase-induced pre-B cell death, and that a Bcl2 transgene reconstitute

92 ltiple replicates of four separate stages of pre-B cells derived from normal human fetal bone marrow

93 as a central regulator of IL-7 signaling and pre-B cell development.

94 ll mice revealed that Fnip1 is essential for pre-B-cell development.

95 Restoration of Ikaros function rescues pre-B cell differentiation in vitro and in vivo and depe

96 om IL-7-rich environments cooperate to drive pre-B cell differentiation via transcriptional programs

97 Pro-B cell proliferation and small pre-B cell differentiation were fully rescued by express

98 Upon IKAROS loss, expression of pre-B-cell differentiation genes is attenuated, while a

99 IKAROS defines superenhancers at pre-B-cell differentiation genes together with B-cell ma

100 In pre-B cells, DNA double-strand breaks (DSBs) induced at

101 PDK1 arrested at the transition of pro-B to pre-B cells, due to a cell autonomous defect.

102 We found that V(H)4(a)-utilizing pre-B cells exhibit reduced pre-BCR signaling and do not

103 Raptor-deficient pre-B cells exhibited significant decreases in oxidative

104 Nevertheless, addition of IL-7 enhanced pre-B cell expansion and inhibited maturation into IgM(+

105 ining the reduction in pre-BCR signaling and pre-B cell expansion.

106 Pre-B-cell expansion is driven by signals from the inter

107 -B-cell compartment was a result of impaired pre-B-cell expansion.

108 ros and Aiolos, which functions to terminate pre-B-cell expansion.

109 that are induced after oncogene expression, pre-B cells express the tumor suppressor gene at high le

110 their serum and showed evidence of escape of pre-B cells expressing prototypic autoantibody heavy cha

111 genes are then reexpressed in small, resting pre-B cells for immunoglobulin light chain gene rearrang

112 resembling those in GC B cells, and protects pre-B cells from DNA damage-induced apoptosis during imm

113 , which directly corresponded to the loss of pre-B cells from Hdac3(Delta/-) bone marrow.

114 Pre-B cells from IL-7Ralpha(449F/449F) mice also failed

115 Igkappa transcription was impaired in small pre-B cells from PU.1/Spi-B-deficient bone marrow.

116 Rs, beta-gal was preferentially expressed in pre-B cells from the mice with self-specific BCRs.

117 We found that pro-B and pre-B cells generated in vitro can proliferate autonomou

118 ctors Foxo1 and Pax5, which coactivated many pre-B cell genes, including Rag1, Rag2 and Blnk.

119 r tetherin) was initially identified to be a pre-B-cell growth promoter, but it also inhibits the rel

120 rative functions that prevent the transit of pre-B cells harboring RAG DSBs from G1 into S phase, whe

121 a metabolic checkpoint that may ensure that pre-B cells have sufficient metabolic capacity to suppor

122 in hematopoietic stem cells, thymocytes, and pre-B cells, highlighting its essential role in lymphoid

123 omic D-J(H) rearrangements, which supports a pre-B-cell identity.

124 atic hydrocarbon, activates caspase-3 in pro/pre-B cells in a bone marrow stromal cell-dependent mann

125 Pre-B cells in such mice produce approximately 50% wild-

126 chd1, there was an increase in the number of pre-B cells in the periphery, likely accounting for the

127 he CDR-H3 repertoire first expressed by late pre-B cells in the TdT-insufficient perinatal liver.

128 rleukin 7 (IL-7)-receptor signaling in small pre-B cells induced expression of the bromodomain-family

129 d p185(BCR-ABL)-expressing (p185+) Arf (-/-) pre-B cells into healthy syngeneic mice induces aggressi

130 ed gene knockdowns, and the reprogramming of pre-B cells into macrophages induced by the ectopic expr

131 e that the cessation of the IL-7 response of pre-B cells is controlled via a cell-autonomous mechanis

132 However, the production rate of pro- and pre-B cells is reduced due to a p53-dependent DNA damage

133 hat expression of ETV6-RUNX1 alone in normal pre-B cells is sufficient to activate EPOR transcription

134 d factor 6 or NF-kappaB activator 1 in 70Z/3 pre-B cells led to decreased Rgs16 expression, indicatin

135 Pre-B cell leukemia homeobox 1 (Pbx1)-d is a dominant-ne

136 ic deletion of CDH-implicated genes encoding pre-B cell leukemia transcription factors (Pbx) led to l

137 R (pre-BCR) signaling, spontaneously develop pre-B cell leukemia.

138 e phenotype (35%) or a lethal, short-latency pre-B-cell leukemia (20%).

139 nce for the epigenetic changes that occur in pre-B-cell leukemia and other B-cell-related diseases.

140 Pre-B-cell leukemia homeobox (PBX) and myeloid ecotropic

141 Pre-B-cell leukemia homeobox (PBX) transcription factors

142 Pre-B-cell leukemia homeobox (Pbx)-regulating protein-1

143 g protein (PBXIP1/HPIP) is a co-repressor of pre-B-cell leukemia homeobox 1 (PBX1) and is also known

144 yeloid ecotropic viral integration 1 (Meis1)/pre-B-cell leukemia homeobox 3 (Pbx3) genes.

145 Pre-B-cell leukemia homeobox interacting protein 1 or hu

146 h proteins competitively heterodimerize with pre-B-cell leukemia homeobox-1 (Pbx1).

147 locus modified binding of the proadipogenic pre-B-cell leukemia homeobox-1/homeobox 9 complex.

148 nockout mice for one of the candidate genes, pre-B-cell leukemia transcription factor 1 (Pbx1), and i

149 eloid leukemia, and the t(12;21)(p13;q22) in pre-B-cell leukemia, respectively.

150 ing (earlier) pro-B cells with the increased pre-B-cell levels of just one transcription factor, IRF4

151 with recombination substrates in a cultured pre-B cell line as well as Cre recombinase-mediated Bcl1

152 re, we established a dual-regulatable FL5.12 pre-B cell line in which myristoylated Akt is expressed

153 poly-N-acetyl-lactosamine (SC-PNAL) on human pre-B cell line Nalm-6.

154 Using an inducible pre-B cell line, we demonstrate that active PTM on Jkapp

155 tein complementation assay screen in a mouse pre-B cell line.

156 trate 2 (RAC2), among others, in an invasive pre-B-cell line that produced CNS leukemia in NOD-SCID m

157 troviral transduction of Pax5-deficient pro-/pre-B cell lines with a doxycycline-inducible (TetON) fo

158 Using Abelson transformed pre-B cell lines, we find that H2AX is not required for

159 sed here minichromosomal substrates in human pre-B cell lines.

160 how is crucial for Rag expression in Abelson pre-B cell lines.

161 ol vector (NEO) were stably expressed in two pre-B-cell lines that lack endogenous receptor.

162 strate a striking gradient in VH gene use as pre-B cells mature into follicular and then into margina

163 processes of adhesion and invasion unique to pre-B cells may prevent recurrences within the CNS.

164 PAX5 in a new syndrome of susceptibility to pre-B cell neoplasia.

165 transcriptional regulator Ikaros into mouse pre-B cell nuclei triggered immediate binding to target

166 Pre-B ALL originates from a committed pre-B cell or an earlier progenitor, with potential to r

167 Unlike normal pre-B cells, patient-derived ALL cells express the inhib

168 e-BCR cooperates with IL-7R in expanding the pre-B cell pool, but it is also critical to control the

169 letion by 5-fluorouracil, with the pro-B and pre-B cell pools still markedly decreased 2 wk after a s

170 nd interleukin 7 receptor (IL-7R) coordinate pre-B cell population expansion with subsequent recombin

171 ma characterized by a clonal, transplantable pre-B-cell population of neoplastic lymphocytes.

172 the differentiation of highly proliferative pre-B-cell precursors, and loss of IKAROS function indic

173 uppress Rag1 and Rag2 mRNA levels in primary pre-B cells, pro-B cells, and pro-T cells, indicating th

174 BCR-ABL-expressing pro/pre-B cells producing smArf alone are as oncogenic as th

175 receptor-mediated activation of BCL6 limits pre-B cell proliferation and induces cellular quiescence

176 e context-dependent activities in regulating pre-B cell proliferation and survival.

177 55 transgenic mice) has been shown to induce pre-B-cell proliferation followed by high-grade lymphoma

178 They are preceded by a polyclonal pre-B-cell proliferation, have variable clinical present

179 expression of Ikaros and Aiolos to suppress pre-B-cell proliferation.

180 in the Vkappa-Jkappa intervening sequence in pre-B cells, proteins believed to be responsible for dam

181 the cell of origin of MCCs is a pro/pre- or pre-B cell rather than the postmitotic Merkel cells.

182 At the pre-B cell receptor (BCR) checkpoint, developing pre-B c

183 Checkpoints at the stage of pre-B cell receptor (pre-BCR) and BCR expression can eli

184 marrow, the expression and activation of the pre-B cell receptor (pre-BCR) constitute crucial checkpo

185 Besides binding glycans, GAL1 is also a pre-B cell receptor (pre-BCR) ligand that induces recept

186 Pre-B cell receptor (pre-BCR) signaling and migration fr

187 bitor dasatinib due to its inhibition of the pre-B cell receptor (pre-BCR) signaling complex.

188 In developing B cells, pre-B cell receptor (pre-BCR) signals initiate immunoglo

189 B cell precursor ALLs that differed by their pre-B cell receptor (pre-BCR) status were induced and di

190 ific epigenetic landscape at Igk dictated by pre-B cell receptor (pre-BCR)-dependent Erk activation.

191 eagues surveyed the activation status of the pre-B cell receptor and comprehensively investigated dow

192 rucial mediator of negative selection at the pre-B cell receptor checkpoint and a safeguard against l

193 dly, that Bach2 also plays a key role in the pre-B cell receptor checkpoint and functions as a tumor

194 o apoptosis in response to metabolic stress (pre-B cell receptor crosslinking, oncogene activation).

195 Here, we demonstrate that the pre-B cell receptor functions as a tumor suppressor upst

196 Initial cell surface expression of the pre-B cell receptor induces proliferation.

197 signaling pathway, even if expression of the pre-B cell receptor itself is compromised.

198 ducible activation of BCL6 downstream of the pre-B cell receptor results in transcriptional repressio

199 After productive VH-DJH gene rearrangement, pre-B cell receptor signaling ends BACH2-mediated negati

200 we demonstrate that inducible activation of pre-B cell receptor signaling induces cell-cycle exit th

201 cooperation with downstream molecules of the pre-B cell receptor signaling pathway, even if expressio

202 of a mu heavy chain, however, activation of pre-B cell receptor signaling strongly induces BCL6 expr

203 uivalent to acute activation of autoreactive pre-B cell receptor signaling, which engaged a deletiona

204 from B cell precursors that are arrested at pre-B cell receptor-dependent stages.

205 Hence, pre-B cell receptor-mediated activation of BCL6 limits p

206 Pre-B cell receptor-mediated cell cycle arrest in Ph(+)

207 it as the endpoint of an emerging pathway of pre-B cell receptor-mediated tumor suppression.

208 critical tumor suppressor downstream of the pre-B cell receptor.

209 n these B-ALLs encode proteins implicated in pre-B-cell receptor (BCR) signaling and migration/adhesi

210 With expression of a functional pre-B-cell receptor (BCR), cytokine signaling is attenua

211 Expression of the pre-B-cell receptor (pre-BCR) by pre-BII cells constitut

212 The pre-B-cell receptor (pre-BCR) is an important checkpoint

213 unique type of binding protein based on the pre-B-cell receptor (pre-BCR).

214 is present in 5%-7% of pediatric and 50% of pre-B-cell receptor (preBCR(+)) acute lymphocytic leukem

215 -kinase delta (PI3Kdelta), a linchpin in the pre-B-cell receptor and interleukin 7 receptor signaling

216 nals from the interleukin-7 receptor and the pre-B-cell receptor and is dependent on cyclin D3 and c-

217 We show that FOXM1 levels peak at the pre-B-cell receptor checkpoint but are dispensable for n

218 at their expression transiently peaks at the pre-B-cell receptor checkpoint.

219 Defects in pre-B-cell receptor components or in downstream signalin

220 Mutations that affect the pre-B-cell receptor result in early B-cell differentiati

221 BLNK adaptor protein has a key role in the pre-B-cell receptor signaling cascade, as illustrated by

222 Collectively, our studies identify a pre-B-cell receptor signaling induced inhibitory network

223 multiple targets in key pathways, including pre-B-cell receptor signaling, cell cycle progression, a

224 Loss of Mef2c in pre-B cells reduces chromatin accessibility in multiple

225 tly less BLIMP1 and XBP1 mRNA and, for human pre-B cells, remained CD138 negative.

226 n this study, we demonstrate that Bach2(+/+) pre-B cells resist leukemic transformation by Myc throug

227 Transplantation of polyclonal Ikaros-mutant pre-B cells resulted in long-latency oligoclonal pre-B-A

228 Inhibition of NF-kappaB in cycling pre-B cells resulted in upregulation of RAG expression a

229 ve regulation of Arf by BCL6 is required for pre-B cell self-renewal and the formation of a diverse p

230 Mice deleted for Ikaros in pro/pre-B cells show a complete block of differentiation at

231 Sorted beta-gal(+) pre-B cells showed increased levels of various markers o

232 DSBs induced in pre-B cells signal rapid transcriptional repression of R

233 uced during Igkappa recombination in primary pre-B cells signal through ATM, but not DNA-PK, to suppr

234 elf-renewal and attenuated signaling via the pre-B cell signaling complex (pre-BCR) and the different

235 Whereas essential pre-B cell signaling molecules were activated normally i

236 Compared with normal pre-B cells, SOX4 promoter regions in Ph(+) ALL cells ar

237 signaling and loss of activated STAT5 at the pre-B cell stage corresponds with Igkappa locus accessib

238 ifferentiation, without the requirement of a pre-B cell stage in zebrafish.

239 d sequestered at the lamina, and only at the pre-B cell stage located to central nuclear domains.

240 uted to a partial developmental block at the pre-B cell stage of development.

241 complete block in B cell development at the pre-B cell stage resulting from a deletion in the Fnip1

242 es not go through a Rag(hi) CD79(+)IgH-mu(+) pre-B cell stage, different from mammals.

243 cells have a developmental block at the pro/pre-B cell stage, whereas a B cell-specific Shp-1 defici

244 lls resulted in a developmental block at the pre-B cell stage, with a corresponding lack of periphera

245 evelopment, and subsequent transition to the pre-B cell stage.

246 as the L chain loci become accessible at the pre-B cell stage.

247 y final (mature) B cell value by the cycling pre-B cell stage.

248 sults in a severe developmental block at the pre-B cell stage.

249 development in the bone marrow at the small pre-B cell stage.

250 te that B-cell development is blocked at the pre-B-cell stage in mice deficient for Mef2c and Mef2d T

251 However, cells at the pre-B-cell stage of development did not initiate disease

252 ll linker protein, arrest development at the pre-B-cell stage.

253 implies that proliferation during pro-B and pre-B cell stages plays an important role in the homeost

254 cks B cell development between the pro-B and pre-B cell stages.

255 ture with a reduction in the fraction of pro/pre-B cells, suggesting an inhibition in early B cell de

256 Interleukin 7 (IL-7) promotes pre-B cell survival and proliferation by activating the

257 Pre-B cell survival and proliferation were significantly

258 As lost IL-7 signals would limit pre-B cell survival, how cells survive during IgL chain

259 gL chain gene assembly paradoxically promote pre-B cell survival.

260 ated genes selectively expressed in the pro-/pre-B cells that can develop under myeloid/lymphoid cond

261 tic leukemia (ALL) typically originates from pre-B cells that critically depend on survival signals e

262 on supported development of large- and small pre-B cells that expressed the chimeric human/mouse Igmu

263 p53 is required for stringent elimination of pre-B cells that failed to productively rearrange immuno

264 ional pre-BCR mediates positive selection of pre-B cells that have passed the checkpoint.

265 nsformation is largely limited to particular pre-B cells that originate from pro-B cells that had res

266 in vitro Using genetically engineered murine pre-B cells that secrete different forms of sgp130, we f

267 Here we demonstrate that in pre-B cells, the IL-7R but not the pre-BCR was coupled t

268 We also found that in DKO pre-B cells, the kinase Zap70 is associated with the pre

269 ecules were activated normally in Fnip1-null pre-B cells, the metabolic regulators AMPK and mTOR were

270 int for allelic exclusion that occurs at the pre-B cell to immature B cell transition and is dependen

271 show that Emu's effect on IgH levels at the pre-B cell to immature B cell transition strongly influe

272 of B-cell development and is essential for a pre-B cell to traverse into an immature B cell.

273 as oncogenic mimicries and allow transformed pre-B cells to bypass checkpoint control.

274 Bcl11a(lox/lox) deletion in explanted murine pre-B cells to demonstrate direct consequences of BCL11A

275 ecificities would predispose Slp65-deficient pre-B cells to malignant transformation.

276 evealed a reduced differentiation from large pre-B cells to small B cells and immature B cells.

277 Our data show how pre-BCR signaling poises pre-B cells to undergo differentiation after escape from

278 We propose that pre-B cells toggle between pre-BCR signals and a RAG DSB

279 Although murine cells and pre-B cells transduced with the long TACI isoform retain

280 ull-length SHIP significantly reduces Ab-MLV pre-B-cell transformation.

281 Our results explain how normal pre-B cells transit from a highly proliferative and stro

282 n arrests B-cell development at the pro-B-to-pre-B cell transition, but this block is bypassed by exp

283 APE2 and find an inhibition of the pro-B to pre-B cell transition.

284 ins arrested B-lymphopoiesis at the pro-B to pre-B-cell transition and, contrary to their proposed do

285 k in B cell development at the pro-B-cell-to-pre-B-cell transition, leading to a reduction in mature

286 ke previously identified CpG breaks in pro-B/pre-B-cell translocations, the BCL6 breaks do not show e

287 155 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promising therap

288 that DNA damage caused by RAG1/2 activity in pre-B cells was able to downmodulate RAG1/2 expression a

289 The expression of Pax5 in pre-B cells was decreased in PDK1 knockouts, which corre

290 A significant loss of pro-B and pre-B cells was observed when the wild-type allele was r

291 ably, inducible Ikaros expression in cycling pre-B cells was sufficient to drive transcriptional chan

292 circumstances is restricted to pro/pre- and pre-B cells we propose, on the basis of our results, tha

293 By using Irf4-/-Irf8-/- pre-B cells, we demonstrated that two pathways converge

294 hanisms of malignant transformation of human pre-B cells, we found that acute activation of oncogenes

295 in expression was decreased in Emu-deficient pre-B cells, we propose that modification of B cell home

296 ndicated that CD127(+) cells resembled large pre-B cells, which is consistent with their low level of

297 majority of observed germline transcript in pre-B cells while the activity of the proximal promoter

298 Transduction of murine 38B9 pre-B cells with chimeric rabbit-VDJ mouse-Cmu encoding

299 al Igl chain gene rearrangements and driving pre-B cells with RAG DSBs into cycle.

300 Pre-B cells within the bone marrow represent the normal