ライフサイエンスコーパス: pro-B-cell

1 Cd19 and Blnk expression in Pax5(-/-) murine pro B cells.

2 ression of Foxo1 and Irf4 in Fra-2-deficient pro-B cells.

3 e apoptosis-triggering protein Fas ligand in pro-B cells.

4 cells (ESCs), Myod1 in myotubes, and PU.1 in pro-B cells.

5 hoid progenitors and pre-pro-B cells but not pro-B cells.

6 e suppression of death in Apaf-1(fog) mutant pro-B cells.

7 -B cell stage as well as survival of CD19(+) pro-B cells.

8 nferring cytokine-independent growth to BaF3 pro-B cells.

9 role for Shc in IL-7-dependent signaling in pro-B cells.

10 te block in micro0 germline transcription in pro-B cells.

11 cooperatively to induce apoptosis in primary pro-B cells.

12 e cannot functionally complement Emu loss in pro-B cells.

13 lgi network (TGN) in transformed and primary pro-B cells.

14 of IFNbeta to stimulate apoptosis of primary pro-B cells.

15 actors are recruited to HS1 sequence only in pro-B cells.

16 CD22 expression and proliferation in primary pro-B cells.

17 indicating that these mice were able to make pro-B cells.

18 requency, was also observed in RAG-deficient pro-B cells.

19 Met complexes on the surface of CLPs and pre-pro-B cells.

20 o be regulated by interleukin 7 signaling in pro-B cells.

21 er leaflet of the plasma membrane of primary pro-B cells.

22 in the Pax5-deficient state, OCs arise from pro-B cells.

23 nd STAT5b-CA mice exhibit large increases in pro-B cells.

24 sed germline transcription of Ig loci in pre-pro-B cells.

25 rag2 expression and recombinase activity in pro-B cells.

26 riable (V(H)) and diversity gene segments in pro-B cells.

27 D)J recombinase is not diminished in Pax5-/- pro-B cells.

28 s sufficient to induce apoptosis in cultured pro-B cells.

29 d cell death protein 1 (PD-1) found on T and pro-B cells.

30 munoglobulin heavy chain gene (IgH) locus in pro-B cells.

31 by knockdown blocks B-1 development in fetal pro-B cells.

32 ntly spliced BTK in B lymphocytes, including pro-B cells.

33 b treatment led to reduced numbers of CD127+ pro-B cells.

34 unoglobulin heavy-chain gene (Igh) in living pro-B cells.

35 Rag transcription in transformed and primary pro-B cells.

36 UTRs of genes upregulated in Dicer-deficient pro-B cells; a top miR-17 approximately 92 target, the p

37 -7R signaling pathway functionally segregate pro-B cells according to cell cycle status.

38 Spi-B(-/-) pro-B cells relative to wild-type pro-B cells after IL-7 withdrawal.

39 Depletion of SWI/SNF in pro-B cells also inhibits antisense transcription throug

40 ) mice showed no defect in the number of pre-pro-B cells, although IL-7Ralpha(449F/449F) mice had dec

41 of 5'-RACE products of the Igh repertoire in pro-B cells, amplified in an unbiased manner.

42 iption of Rag1 and Rag2 was repressed at the pro-B cell and immature B cell stages by the kinase Akt

43 concentrations (25 or 100 microM for primary pro-B cells and a pro/pre-B cell line, respectively), in

44 15d-PGJ(2) was reduced in APAF1 null primary pro-B cells and accompanied by alteration of mitochondri

45 at the levels of Klf4 expression were low in pro-B cells and continuously increased in pre-B and in m

46 le for less efficient V(D)J recombination in pro-B cells and diminished progression to the pre-B cell

47 nduced STAT5 phosphorylation in CD19+/IL-7R+ pro-B cells and human B-lineage acute lymphoblastic leuk

48 ha(449F/449F) mice had decreased Ebf1 in pre-pro-B cells and impairment in B cell-committed CLPs.

49 B-lymphocyte differentiation: in bone marrow pro-B cells and in CD4(+)CD8(+) double positive thymic T

50 -)) had significantly reduced numbers of pre-pro-B cells and increased numbers of myeloid cells.

51 a) and J(kappa) loci to V(D)J recombinase in pro-B cells and induces Igk rearrangement in these cells

52 etion disrupts the nonrandom distribution of pro-B cells and induces the mobilization of pro-B cells

53 te that Sox4 is required for the survival of pro-B cells and may functionally interact with c-Kit and

54 cells exhibit a pattern intermediate between pro-B cells and mouse embryonic fibroblasts.

55 dicates that Tcl1 expression is initiated in pro-B cells and persists in splenic marginal zone and fo

56 nlike recombinant (r) IL-7, which stimulated pro-B cells and pre-B cells only, scIL-7/HGFbeta stimula

57 ission electron microscopy on murine primary pro-B cells and pre-B cells to analyze the aggregation s

58 We studied pre-pro-B cells and Rag(-/-) progenitor-B cells to determine

59 both a loss of V(D)J recombinase activity in pro-B cells and reduced numbers of pre-B cells.

60 ely regulates Cdk6 transcription in leukemic pro-B cells and that the v-Abl kinase stimulates Cdk6 ex

61 e view of the conformation of IgH alleles in pro-B cells and the mechanisms by which it is establishe

62 ufficient to induce B-1 development in adult pro-B cells and whose silencing by knockdown blocks B-1

63 sorting-enumerated monocytes, mature and pre/pro-B cells, and functional B-cell progenitors.

64 ntiation of common lymphoid progenitors, pre-pro-B cells, and hematopoietic progenitor cells (day 12

65 totic Bcl2 protein was decreased in residual pro-B cells, and its restoration using a Bcl2 transgene

66 e distinct blood cell lineages: pre-T cells, pro-B cells, and macrophages.

67 horylated in response to IL-7 stimulation in pro-B cells, and pro-B cells from mice with impaired Shc

68 and Rag2 mRNA levels in primary pre-B cells, pro-B cells, and pro-T cells, indicating that inhibition

69 or the function of CLPs, the survival of pre-pro-B cells, and the establishment of a B lineage-specif

70 The tumor cells resembled pro-B cells, and were CD19(+)IgM(-)IgD(-)CD93(+)CD43(+)C

71 nt mice, common lymphoid progenitors and pre-pro-B cells appeared normal, but cells at subsequent sta

72 For most V(H)s, the IF fraction in pro-B cells approximated 33% and then shifted to the nea

73 the activation of Cbfbeta-SMMHC reduces pre-pro-B cells approximately 3-fold and pre-B cells more th

74 YY1(-/-) pro-B cells are greatly impaired in distal V(H) gene rea

75 Although Rpl22-deficient pro-B cells are hyporesponsive to IL-7, a key cytokine r

76 ity and low levels of protein association in pro-B cells are increased substantially as the cells pro

77 We report here that Tyk2-null pro-B cells are markedly deficient in basal oxygen consu

78 Our data, suggesting that pro-B cells are not a single homogeneous population, exp

79 sh that in longitudinal femoral BM sections, pro-B cells are preferentially localized in close proxim

80 Polycomb Group (PcG) protein YY1 results in pro-B cell arrest and reduced immunoglobulin locus contr

81 nditional deletion of Flcn recapitulates the pro-B cell arrest of Fnip1(-/-) mice.

82 s showed a severe reduction in the number of pro-B cells as well as pre-B cells.

83 quired for the intrinsic survival of CD19(+) pro-B cells as well as the proper expression of the alph

84 V(D)J recombination in progenitor B (pro-B) cells assembles Igh variable region exons upstrea

85 gram and are biased toward overproduction of pro-B cells at the expense of T cell progenitors.

86 expression and V(D)J recombinase activity in pro-B cells at the single cell level.

87 Although the pro-B cell (B220(+)/CD43(+)) populations from the NHD13

88 to kidney neoplasia, but display a striking pro-B cell block that is entirely independent of mTOR ac

89 cycle entry and apoptosis of IL-7-dependent pro-B cells, blocking Ig synthesis and B cell maturation

90 In committed pro-B cells, Brg1 regulated contraction of the locus enc

91 In committed pro-B cells, Brg1 suppressed a pre-B lineage-specific pa

92 ation of common lymphoid progenitors and pre-pro-B cells but not pro-B cells.

93 enes encoding RAG-1 and RAG-2 in transformed pro-B cells by a pathway requiring the transcription fac

94 IL-7 stimulation or in IL-7R alpha(-/-) pre-pro-B cells by activation of STAT5, a major signaling mo

95 Second, the possibility exists that pro-B cells can give rise to osteoclast-like cells (OCLs

96 uggests that Spi-C, ectopically expressed in pro-B cells, can bind PU.1 consensus sites in the IgH in

97 However, survival of c-Myb-deficient CD19(+) pro-B cells cannot be rescued by transduction with CD127

98 The reduction of pre-pro-B cells coincided with an increase in apoptosis in t

99 /HGFbeta stimulated the proliferation of pre-pro-B cells, common lymphoid progenitors (CLPs), and col

100 efficient in generating progenitor B cells (pro-B cells) compared with the more common in vitro meth

101 lation of cells within the bone marrow early pro-B cell compartment that possess functional plasticit

102 B cell development by analyzing the CLP and pro-B cell compartments under steady-state conditions an

103 reens in both human AML and engineered mouse pro-B cells converge on a surprisingly small number of g

104 Pax5-/- pro-B cells could be induced to form OCLs by treatment w

105 Herein we provide evidence for innate pro-B cells (CpG-proBs) that emerged within the bone mar

106 nontransformed pro-/pre-B cell line, primary pro-B cells cultured on bone marrow stromal cells underw

107 In addition, IL-7-stimulated pro-B cell cultures revealed a reduced differentiation f

108 IFNbeta-stimulated apoptosis is the same in pro-B cells derived from wild type and Stat1(-/-) mice.

109 uction in recombination activity in cultured pro-B cells despite the fact that its expression and loc

110 Notably, these pro-B cells, despite having normal expression of the tra

111 the KitY719F mutation, blocks pro T cell and pro B cell development in an age-dependent manner.

112 nib (Gleevec) leads to deficits in pro T and pro B cell development, similar to those seen in KitY567

113 r regulators of the G1/S transition restored pro-B cell development from Justy progenitor cells, sugg

114 that EBF1 is required for B cell commitment, pro-B cell development, and subsequent transition to the

115 a pan B-cell surface receptor expressed from pro-B-cell development until its down-regulation during

116 anscription factor shown to be essential for pro-B-cell development.

117 kemias arising from p19(ARF)-null HSC versus pro-B cells differ biologically, including relative resp

118 Rather, Ras promotes STAT5-dependent pro-B cell differentiation by enhancing IL-7Ralpha level

119 arget genes, but only the Pax5(+/-)Ebf1(+/-) pro-B cells down-regulated genes central for the preserv

120 decreased the expression of the IgH chain in pro-B cells due to impaired recombination of the IgH dis

121 Wild-type (WT) pro-B cells ectopically expressing Spi-C (WT-Spi-C) have

122 B-cell progenitors, up to and including the pro-B cell, efficiently initiate Ph(+) B-ALL.

123 ells within the initial 2 wk, CD19+/pre-BCR- pro-B cells emerged, of which 25-50% expressed the IL-7R

124 Finally, Ba/F3 murine pro-B cells, engineered to express mutant ERBB2, became

125 and STAT5 transcription factors bound to its pro-B-cell enhancer (PBE), but is inhibited by HDAC inhi

126 Finally, we divided the pro-B cell epigenome into clusters of loci with occupanc

127 In addition, WT-Spi-C pro-B cells express increased levels of IgH sterile tran

128 IgH V(D)J assembly occurs in progenitor (pro-) B cells followed by that of IgL in precursor (pre-

129 ulates mRNAs that are important for pre- and pro-B cell formation or function, and its ectopic expres

130 ified a progenitor within bone marrow, early pro-B cell/fraction B, that differentiates into tissue M

131 nsgenic mice severely depleted pre-pro-B and pro-B cells from BM, preceding any decline in HSCs.

132 Enriched pro-B cells from CD19-CreDeltaPB mice induced disease up

133 combination may be significantly impaired in pro-B cells from enhancer-deficient mice.

134 In compensation, early pro-B cells from FLT3/ITD cells mice show increased leve

135 Early pro-B cells from FLT3/ITD mice were found to have a lowe

136 These data suggest that, in early pro-B cells from FLT3/ITD mice, impairment of classic NH

137 ppressed the generation of early B cells and pro-B cells from hematopoietic stem/progenitor cells, in

138 actor EBF restored the generation of CD19(+) pro-B cells from Ikaros-deficient hematopoietic progenit

139 onse to IL-7 stimulation in pro-B cells, and pro-B cells from mice with impaired Shc signaling displa

140 Indeed, we found in freshly isolated pro-B cells from muMT mice a positive correlation betwee

141 F expression facilitates rapid generation of pro-B cells from PU.1-/- progenitors.

142 However, in pro-B cells from Tyk2(-/-) mice, where there is normal a

143 al organization map of the G1-arrested mouse pro-B cell genome and used high-throughput genome-wide t

144 WT-Spi-C pro-B cells have reduced levels of dimethylation on lysi

145 l events underlying myeloma may arise at the pro-B-cell hematological progenitor cell level, much ear

146 Furthermore, in Pax5-/- pro-B cells, higher EBF expression repressed alternative

147 suggest the importance of FAK in regulating pro-B cell homeostasis and maintenance of their spatial

148 In pro-B cells, hs4 to -7 are associated with marks of acti

149 RR has revealed a similar modular pattern in pro-B cells; hs4 to -7 sites are unmethylated, while the

150 In pro-B cells, IL-7/IL-7R signaling induces histone hypera

151 SOCS3 overexpression in pro-B cells impaired CXCL12-induced FAK phosphorylation

152 oietic stem cells almost entirely eliminated pro-B cells in both fetal livers and adult bone marrow,

153 ace expression of BP-1 was increased on late pro-B cells in ER(het) mice.

154 Importantly, thymic pro-B cells in STAT5b-CA mice are derived from early T c

155 Notably, the expansion of pro-B cells in STAT5b-CA mice correlated with an increas

156 Thymic pro-B cells in STAT5b-CA mice show a modest increase in

157 We observed that the proliferation of pro-B cells in stromal cocultures was impaired by interr

158 STAT5b-CA mice exhibit a 40-fold increase in pro-B cells in the thymus.

159 years old), the incidence of E47-expressing pro-B cells in vivo and E47 protein steady state levels

160 yeast Saccharomyces cerevisiae , and murine pro B cells, including how these electrical properties v

161 cRS signal ends are abundant in pro-B cells, including those recovered from microMT mice

162 iferation and differentiation of progenitor (pro-) B cells into pre-B cells.

163 the ability of CLP to differentiate into pre-pro-B cells is also compromised by senescence.

164 Proliferative expansion of pro-B cells is an IL-7-dependent process that allows for

165 Ig heavy chain locus (IgH), a nucleosome in pro-B cells is generally positioned over each IgH variab

166 First, modulation of Let-7 in fetal pro-B cells is sufficient to alter fetal B-1 development

167 on of DNA damage by UV light, confirmed that pro-B cells lacking 1 functional allele of Ebf1 display

168 Using pro-B cells lacking the phosphatase Pten (phosphatase an

169 ice, a dramatic increase in the frequency of pro-B cell leukemia was observed in mice with combined h

170 in innate immunity to virally induced acute pro-B cell leukemia.

171 tion of Ig gene segments in a Rag2-deficient pro-B cell line and that this correlated with decreased

172 nction approach using a PU.1/Spi-B-deficient pro-B cell line in which PU.1 can be induced by doxycycl

173 Ba/F3, a murine interleukin-3 dependent pro-B cell line is increasingly popular as a model syste

174 eased Flt3 transcription and expression in a Pro-B cell line that expressed low levels of Flt3.

175 nized pools of Ba/F3 cells, an IL3-dependent pro-B-cell line, which acquired cytokine independence an

176 in peripheral organs, while also leading to pro-B cell lineage promiscuity.

177 Detection of one site, HS1, is restricted to pro-B cell lines and HS1 is accessible to restriction en

178 l maturation was tested in RAG2(-/-) primary pro-B cell lines and in gene transfer experiments in the

179 BCR-ABL-dependent pre/pro-B cell lines could be established at low frequency f

180 PU.1 expression in cultured CD19-CreDeltaPB pro-B cell lines induced Btk expression, followed by red

181 ells, STAT5 and PU.1 retrovirally transduced pro-B cell lines, or embryonic stem cells induced to dif

182 essed in fetal liver-derived, IL-7-dependent pro-B cell lines.

183 (D)J recombination DSBs in G1-arrested mouse pro-B-cell lines, dispensable for joining CSR-associated

184 EJ of I-SceI-induced DSBs in XRCC4-deficient pro-B-cell lines.

185 absence of XLF and vice versa in G1-arrested pro-B-cell lines.

186 formed murine lymphocytic leukemia and mouse pro-B cell lymphoid cell lines, mitotic cells reversibly

187 h of growth data from mouse lymphoblast and pro-B-cell lymphoid cell lines.

188 We find that deleting Rag-1 prevents pro-B cell lymphoma confirming Rag-induced DSBs induce t

189 and amplifications in the Lig4/p53-deficient pro-B cell lymphoma model.

190 the tumor suppressor, p53 greatly increases pro-B-cell lymphoma in ku80(-/-) mice due to IgH/c-Myc t

191 As pro-B-cell lymphoma is caused by a translocation between

192 former cohort displays much lower levels of pro-B-cell lymphoma than the latter two cohorts.

193 GFR3 TDII transgenic mouse lines developed a pro-B-cell lymphoma, and PLCgamma was highly activated i

194 Like suppression of pro-B-cell lymphoma, neuronal apoptosis requires p53 pre

195 p53, dramatically increases the incidence of pro-B-cell lymphoma.

196 mor suppressor routinely develop progenitor (pro)-B cell lymphomas that harbor translocations leading

197 c) XLF(-/-) p53(-/-) mice develop aggressive pro-B cell lymphomas bearing complex chromosomal translo

198 S18/23A mice fail to develop tumors like the pro-B cell lymphomas uniformly developed in Xrcc4(-/-) p

199 ndogenous N-myc locus, in Lig4/p53-deficient pro-B cell lymphomas.

200 We show that the Igh3'RR is dispensable for pro-B-cell lymphomas with V(D)J recombination-initiated

201 nduced RAG-1 and -2 along with certain other pro-B cell makers, and then redifferentiated after trigg

202 on in all cell lines tested, including Ba/F3 pro-B cells, MC/9 mast cells, M1 leukemia cells, U3A hum

203 These effects of Fak deletion on pro-B cell mobilization and localization in BM are ampli

204 gulated in parallel with IgD, with little in pro-B cells, moderate amounts in immature B cells, and h

205 ct-2, and Oca-B recruitment is negligible in pro-B cells, moderate in pre-B cells, and maximal in ger

206 lopment, we studied VDJ recombination in the pro-B cells of FLT3/ITD mice and discovered an increased

207 t were coisolated from purified CLPs and pre-pro-B cells on scIL-7/HGFbeta affinity gels, indicating

208 eration and differentiation of progenitor B (pro-B) cells or macrophages relative to PU.1 or Spi-B.

209 Sox4-deficient pro-B cells, particularly those expressing the stem cell

210 ature B cells, consistent involvement at the pro-B-cell progenitor stage was established, providing d

211 id progenitors (CLP) and their pre-pro-B and pro-B cell progeny is reduced in old mice, but the age-r

212 Pro-B cell proliferation and small pre-B cell differenti

213 sion, suggesting that STAT5 directly affects pro-B cell proliferation and survival.

214 immunoglobulin heavy chain (IgH) protein in pro-B cells provides feedback to terminate further V(H)

215 Ighc locus rearrangements in mouse Rag1(-/-) pro-B cells reconstituted with wild-type or mutant human

216 nscription is reduced in PU.1(-/-)Spi-B(-/-) pro-B cells relative to wild-type pro-B cells after IL-7

217 ns that promoted B lymphopoiesis, mutant pre-pro-B cells remained alive and began expressing the B ce

218 Pax5 and Bcl2A1 together into PDK1 knockout pro-B cells restored their ability to differentiate in v

219 Foxo1 inactivation in late pro-B cells resulted in an arrest at the pre-B cell stag

220 form of c-Abl, v-Abl, that transforms murine pro-B cells, resulting in acute leukemia and providing a

221 ons in Dclre1c(-/-) v-abl kinase-transformed pro-B cells retrovirally engineered with a construct tha

222 ChIP sequencing was performed on pro-B cells, revealing colocalization of CTCF and Rad21

223 that the extent of histone modifications in pro-B cells should be considered as a mechanism by which

224 L-7 in in vitro stromal cell cocultures, but pro-B cells show defective expansion.

225 C-Kit-expressing pro-B cells showed decreased activation of the c-Kit dow

226 a candidate Igh regulatory region defined by pro-B cell-specific hypersensitivity and interaction wit

227 In spite of a severe block at the pro-B cell stage and profound B cell lymphopenia, signif

228 e blocks early B cell development at the pre-pro-B cell stage and renders B cell progenitors unrespon

229 al for B cell differentiation to the CD19(+) pro-B cell stage as well as survival of CD19(+) pro-B ce

230 n of Foxo1 caused a substantial block at the pro-B cell stage due to a failure to express interleukin

231 IL-7R alpha(2/-) mice is arrested at the pre-pro-B cell stage due to insufficient expression of the B

232 mice and showed that deletion of FADD at the pro-B cell stage had minor effects on B cell development

233 and TdT RNA is expressed exclusively at the pro-B cell stage in B6.56R.

234 B cell development past the pro-B cell stage in mice requires the Cul4-Roc1-DDB1 E3

235 tiation is profoundly blocked beyond the pre-pro-B cell stage in Myb(f/f) Mb1-cre mice.

236 tion marks and germline transcription at the pro-B cell stage in Rag1-deficient mice.

237 1) transgene during the CD43(+)/CD25(-) late pro-B cell stage of B cell development demonstrate marke

238 oxa9, coincides with induction of EBF at the Pro-B cell stage of B cell differentiation.

239 spite intact IL-7 signaling, GON4L-deficient pro-B cell stage precursors failed to undergo a characte

240 What minor differences were detected in the pro-B cell stage tended to diminish with B cell maturati

241 After development into the pro-B cell stage, Ebf1 and other genes switched compartm

242 J recombination with partial blockade at the pro-B cell stage, Emu deletion (core or full length) did

243 Apart from a profound arrest before the pro-B cell stage, other downstream lymphoid progeny of C

244 , but the H chain locus is accessible at the pro-B cell stage, whereas the L chain loci become access

245 uclear lamina to central domains only at the pro-B cell stage, whereas, Igkappa remained sequestered

246 opmental arrest of the B cell lineage at the pro-B cell stage.

247 genitors in the bone marrow beginning at the pro-B cell stage.

248 P and p300 are partially limiting beyond the pro-B-cell stage and that other coactivators in B cells

249 y occur earlier in B-cell development at the pro-B-cell stage in the bone marrow.

250 )CD23(-)VpreB(+)CXCR4(+) Consistent with the pro-B-cell stage of B-cell development, microarray analy

251 From the pro-B-cell stage onward, the approximately 11-kb region

252 y for B-cell development to proceed from the pro-B-cell stage.

253 t initiates floxed gene recombination at the pro-B-cell stage.

254 ut B-cell development was blocked at the pre-pro-B-cell stage.

255 opmental arrest of the B-cell lineage at the pro-B-cell stage.

256 rrow further developed to the B220(+)CD19(+) pro-B-cell stage.

257 B cells were arrested at the B220(+)CD19(-) pro-B-cell stage.

258 ase proliferation at the CD34(+) and CD34(-) pro-B cell stages.

259 p-dioxin-elicited suppression of early B and pro-B cells, suggesting a role of AHR in regulating B ly

260 ne phosphorylation is defective in Tyk2(-/-) pro-B cells, suggesting that this Stat family member is

261 d rag2) gene expression, leading to enhanced pro-B cell survival and augmented V(D)J recombinase acti

262 transgene allowed not only partial rescue of pro-B cell survival but also B cell maturation in the ab

263 t IRF8 was expressed at higher levels in pre-pro-B cells than more mature B cells in wild-type mice.

264 cells were less contracted than pediatric BM pro-B cells that actively rearrange the IGH locus.

265 To understand changes in pro-B cells that could diminish production of pre-B cell

266 The percentage of pro-B cells that express rag2 is reduced in aged mice an

267 o particular pre-B cells that originate from pro-B cells that had restricted IgH V(H) region accessib

268 ha-/-) HSCs can proliferate and give rise to pro-B cells that home to bone marrow.

269 ings derived from human ALCL cells in murine pro-B cells that were transformed to cytokine independen

270 In pro-B cells, the entire repertoire of V(H) regions (2 Mb

271 Chromatin studies reveal that in pro-B cells, the spatial organization of the Igh locus m

272 ction enzyme digestion exclusively in normal pro-B cells, the stage defined by actively rearranging I

273 well as with a block in the transition from pro-B cell to pre-B cell involving diminished expression

274 In this study, we use chromatin profiling of pro-B cells to define 38 epigenetic states in mouse Ag r

275 , all B cell progenitors-from pre-pro-/early pro-B cells to immature B cells-were dramatically reduce

276 cyte lineage cells extending from early B220 pro-B cells to mature B cells.

277 ession on B-lineage cells is maintained from pro-B cells to plasma cells, SGN-40 may be applicable to

278 pro-B cells and induces the mobilization of pro-B cells to the periphery in vivo.

279 led to a block in B cell development at the pro-B-cell-to-pre-B-cell transition, leading to a reduct

280 ng sites and traced their 3D trajectories in pro-B cells transduced with a retrovirus encoding Tet-re

281 on, we used 3D-FISH to measure compaction in pro-B cells transduced with CTCF shRNA retroviruses.

282 y B cell development at the prepro-B cell to pro-B cell transition and induces apoptosis in primary b

283 We found that the prepro-B to the pro-B-cell transition was associated with a global excha

284 We show that pro-B cells undergo robust switching to a subset of immu

285 s, progresses, and terminates in bone marrow pro-B cells undergoing B cell commitment.

286 EBF expression is restored in IL-7(-/-) pre-pro-B cells upon IL-7 stimulation or in IL-7R alpha(-/-)

287 In adult pro-B cells, V(H) gene segments are acetylated prior to

288 U.1 regulates IL-7Ralpha expression in mouse pro-B cells via a GGAA motif, we demonstrate here that G

289 Although the defect in IL-7Ralpha(449F/449F) pro-B cells was associated with loss of STAT5 activation

290 In pro-B cells we demonstrate four distinct nuclear D-type

291 Although numbers of "committed" pro-B cells were maintained in Ebf1(+/-)Runx1(+/-) (ER(h

292 Notch signaling in Wt and Pax5(+/-)Ebf1(+/-) pro-B cells were reflected in the transcriptional respon

293 interleukin-7-dependent bone marrow-derived pro-B cells, where IFNbeta, but not IFNalpha, induces pr

294 and CD25 were reduced and delayed in ER(het) pro-B cells, whereas surface expression of BP-1 was incr

295 in cycling pre-B cells compared with that in pro-B cells, whereas this did not occur for low IF V(H)s

296 ity of CXCL12 to human CXCR4(+)/C3aR(-), REH pro-B cells, which is compatible with a direct interacti

297 We observed an absence of H3K27me3 in fetal pro-B cells, which predominantly rearrange proximal V(H)

298 Reconstitution of Tyk2-null pro-B cells with either the wild type or a kinase-inacti

299 We show here that equipping (earlier) pro-B cells with the increased pre-B-cell levels of just

300 lcellulose with IL-7 +/- CXCL12, Fak-deleted pro-B cells yield significantly fewer cells and colonies