ライフサイエンスコーパス: double-negative

1 positive only, 14 EP-I positive only, and 70 double negative.

2 wo stages of intrathymic T cell development (double negative 1 and double negative 2) corresponding t

3 Progression from double negative 1 to double negative 2 stage thymocytes

4 est stages of thymocyte differentiation, the double-negative 1 (DN1) stage, leading to decreased peri

5 ocks the developmental transition of CD4/CD8 double-negative 1 (DN1; CD44(+) CD25(-)) thymocytes to t

6 erate germline messages in murine CD44+CD25- double-negative 1 cells.

7 , IL-21 seems to be involved as early as the double-negative 1 stage, and the cells from the knockout

8 monstrated a block in differentiation at the double-negative 1 stage.

9 E4BP4-deficient CD44(+)CD25(-) double-negative 1 thymocytes efficiently develop in vitr

10 he block of thymocyte differentiation at the double negative 2 stage at which myeloid lineage and T l

11 hat it is expressed in all thymocytes at the double negative 2 stage of thymic development.

12 Progression from double negative 1 to double negative 2 stage thymocytes in NOD mice is ineffi

13 ic T cell development (double negative 1 and double negative 2) corresponding to T lineage specificat

14 cells, early thymic progenitors (ETPs), and double-negative 2 thymocytes and cultured these populati

15 ARID5B expression is down-regulated at the double-negative 2-4 stages in normal thymocytes, while i

16 mocytes and marked down-regulation after the double-negative-2 stage of maturation.

17 ed display of NK cell markers, compared with double-negative 24alphabeta NKT cells.

18 larity, blocked thymocyte development at the double negative 3 (DN3) stage, and resulted in reduced e

19 inactivation completely reverses the severe double negative 3 developmental block that occurs in SLP

20 icient in SLP76 have a complete block at the double negative 3 stage of T cell development.

21 At the double negative 3 thymocyte stage where the pre-TCR is f

22 as developmental blocks at the CD4(-)CD8(-) double-negative 3 (CD25(+)CD44(-)) and CD8-immature CD8(

23 itive stages, but in the apparent absence of double-negative 3 (DN3) cells; however, DN3 cells are pr

24 d accelerated differentiation of ETPs to the double-negative 3 stage, similar in efficiency to IL-7.

25 artial block of thymocyte development at the double-negative 3 stage.

26 ll development was partially arrested at the double-negative 3 stage.

27 Double-negative 3 thymocytes lacking Zfp36l1/l2 share a

28 lockage of thymocytes at the transition from double-negative 3 to 4 stages, and a reduction of all th

29 te development was perturbed with attenuated double-negative 3/double-negative 4 maturation and alter

30 a gene expression profile with postselected double-negative 3b cells despite the absence of intracel

31 o suboptimal signaling, partial CD4(-)CD8(-) double-negative 4 (CD25(-)CD44(-)) proliferation, and CD

32 artial block at the transition stage between double-negative 4 and double-positive cells.

33 orrelated with higher proliferation rates of double-negative 4 cells in hnRNP L(-/-) mice.

34 h)CD25(low) cells, which seem to derive from double-negative 4 gammadelta TCR(+) cells that acquired

35 perturbed with attenuated double-negative 3/double-negative 4 maturation and altered surface-express

36 s also had smaller thymi, with reductions in double-negative 4 T cell precursors, accompanied by redu

37 ymphopoiesis in BM and an increase in thymic double-negative 4 T cells, inverse to that observed upon

38 a partial block in T cell development at the double-negative 4:double-positive transition in the thym

39 We propose that these double-negative alpha/beta T cells that express HIV prot

40 uced thymocyte cellularity and blocks at the double-negative and double-positive stages.

41 9 (hCD19) was selectively suppressed in late double-negative and double-positive thymocytes, coincidi

42 w that Mcl-1 is required for the survival of double-negative and single-positive thymocytes as well a

43 , the target(s) and clinical associations of double-negative antibodies need to be determined.

44 ibodies without LGI1 or CASPR2 reactivities (double-negative) are more common than LGI1 or CASPR2 spe

45 with increased numbers of CD206(-)CD11c(-) (double-negative) ATMs.

46 s, distortion in IgM(+) B cells, increase in double negative B cells, change in B-cell markers, and e

47 abnormal immunophenotype including expanded double-negative, but depleted follicular helper, T-cell

48 filtration of IFN-gamma-producing CD8(+) and double-negative CD3(+)CD4(-)CD8(-) T cells in perivascul

49 of CC chemokine receptor 5 and were commonly double negative (CD3+CD4-CD8-).

50 Previous in vitro studies indicate that double negative (CD4(-)CD8(-), DN) thymocytes can develo

51 Double-negative (CD4(-)8(-)) and double-positive (CD4(+)

52 eficiency, peripheral eosinopenia, increased double-negative (CD4(-)CD8(-)) T cells, and decreased na

53 ive, SLAMF6 single positive, or SLAMF1SLAMF6 double negative cells were found within mature CD24(-)CD

54 n expansion of IFN-gamma(-) and TNF-alpha(-) double-negative cells compared with those within both is

55 Cultured CD4 and CD8 double-negative cells from NOD mice exhibited major defe

56 In most double-negative cells, one Tcrb allele was recruited to

57 lticellular mechanosensory organs requires a double-negative circuit involving miRNA-mediated suppres

58 lonal relationships (among MZ, IgM-only, and double-negative compartments) involved sequences with th

59 th indirect activation of LHY and CCA1, in a double-negative connection via a direct ELF3 target, PRR

60 on condition in preference to "single-" and "double-negative" designations.

61 e expansion or maintenance of gammadelta and double negative (DN) alphabeta T cells.

62 Tcra recombination programs in CD4(-)CD8(-) double negative (DN) and CD4(+)CD8(+) double positive (D

63 sed memory (P=0.02) and CD19+/CD27(-)/IgD(-) double negative (DN) B cells (P=0.02) and decreased naiv

64 IgD(-)CD27(-) double negative (DN) B cells with proinflammatory charac

65 development, for example in CD4((-))CD8((-)) double negative (DN) cells, impact on later fate decisio

66 delta-chains simultaneously rearrange at the double negative (DN) stage of development, the possibili

67 In this study, we show that CD4(-)CD8(-) double negative (DN) T cells are a major responding T ce

68 Mature double negative (DN) T cells are a population of alphabe

69 Double negative (DN) T cells are expanded in patients wi

70 production, whereas T follicular helper and double negative (DN) T cells significantly expanded.

71 The origin and function of human double negative (DN) TCR-alphabeta+ T cells is unknown.

72 Transplantation of CD4-CD8- double negative (DN) thymocytes (which were also negativ

73 ns of earliest thymic progenitors (ETPs) and double negative (DN) thymocytes in the thymus, and recru

74 that WNK1 is required for the transition of double negative (DN) thymocytes through the beta-selecti

75 induced donor antigen-specific CD4(-) CD8(-) double negative (DN) Treg-based therapy, in a fully MHC

76 poietic progenitors led to a small thymus, a double negative (DN)1/DN2 thymocyte transition block, an

77 and a significant fraction are CD4(-)CD8(-) [double negative (DN)].

78 Commitment occurs between the CD4 and CD8 double-negative (DN) 2 and DN3 stages in mouse early T c

79 Double-negative (DN) 3 progenitors from both wild-type a

80 However, a role for GATA-3 before the double-negative (DN) 3 stage of T cell development has t

81 -deficient mice have a complete block at the double-negative (DN) 3 stage.

82 e-TCR signals regulate the transition of the double-negative (DN) 3 thymocytes to the DN4, and subseq

83 in thymic cellularity and limited CD4- CD8- double-negative (DN) 3 to DN4 thymocyte transition, beca

84 CD4(-) CD8(-) double-negative (DN) alphabeta T cells with innate-like

85 development, being repressed in CD4(-)CD8(-) double-negative (DN) and CD8 cells, but expressed in CD4

86 CD27(+) memory and memory-like CD27(-)IgD(-) double-negative (DN) B cells, but not CD27(-)IgD(+) naiv

87 ls stimulate tumor-resident CD11b(-)CD103(-) double-negative (DN) cDCs to proliferate and differentia

88 hymocytes to differentiate from CD4(-)CD8(-) double-negative (DN) cell to CD4(+)CD8(+) double-positiv

89 n CD4(+), CD8alpha(+), and CD4(-)CD8alpha(-) double-negative (DN) iNKT cells with autologous peripher

90 with influenza virus expands a CD4(-)CD8(-) double-negative (DN) natural killer T (NKT) cell subpopu

91 d CD8(+) thymocytes, and a large increase in double-negative (DN) precursors.

92 early expression of tg alphabeta-TCRs at the double-negative (DN) stage.

93 We also show that IL-2 can drive double-negative (DN) T cell death through an indirect me

94 uced binding of DLL4 Notch ligand to CD4/CD8 double-negative (DN) T cell progenitors, and reduced exp

95 d mitochondrial mass of CD3(+)/CD4(-)/CD8(-) double-negative (DN) T cells (p = 1.1 x 10(-22)) and FOX

96 apamycin (mTOR) is activated in CD4(-)CD8(-) double-negative (DN) T cells and its blockade is therape

97 Double-negative (DN) T cells are important sources of in

98 r, TCRalphabeta(+)CD3(+)CD4(-)CD8(-)NK1.1(-) double-negative (DN) T cells are increased in the periph

99 ovel subset of TCRalphabeta(+) CD4(-) CD8(-) double-negative (DN) T cells was described to suppress i

100 ts, we identify CD4(-)CD8(-)TCRalphabeta(+), double-negative (DN) T cells, in mouse secondary lymphoi

101 ity, including immunoregulatory CD4(-)CD8(-) double-negative (DN) T cells.

102 Coreceptor CD4 and CD8alphabeta double-negative (DN) TCRalphabeta(+) intraepithelial T c

103 D4/8 coreceptor expression and masquerade as double-negative (DN) TCRalphabeta(hi) thymocytes.

104 activity of the Cd4 silencer in CD4(-)CD8(-) double-negative (DN) thymocytes and CD8(+) cytotoxic lin

105 ndergoes V(D)J recombination in CD4(-)CD8(-) double-negative (DN) thymocytes to assemble Tcrd genes a

106 es (27%) due to the reduced proliferation of double-negative (DN) thymocytes.

107 th an increased percentage of CD4(-)/CD8(-) (double-negative (DN)) cells and a decreased percentage o

108 SP and N-WASP was important for CD4(-)CD8(-) double-negative (DN)-to-CD4(+)CD8(+) double-positive (DP

109 TCR-alphabeta(+) double-negative (DN; CD4(-)CD8(-)) T cells represent a p

110 gence in interest in CD4 - CD8+, CD4 - CD8- (double negative [DN]), and CD4 + Foxp3- type 1 Treg (Tr1

111 CD8alphaalpha(+) TCRalphabeta(+) precursors (double-negative [DN] TCRalphabeta(+) T cells) in the gut

112 TH2(-)IL7Ralpha(+) and CRTH2(-)IL7Ralpha(-) (double-negative [DN]) human blood and lung cells.

113 ll lineage, midway through the CD4(-)CD8(-) (double-negative [DN]) stages 1-3.

114 s contained both CD56(+) and CD16(-)CD56(-) (double-negative [DN]) subsets.

115 thy from aberrant expansion of CD4(-)CD8(-) (double-negative [DN]) T cells.

116 eta alleles are accessible in CD4(-)/CD8(-) (double-negative [DN]) thymocytes, when they recombine, a

117 e neonatal thymus by immature, CD4(-)CD8(-) "double negative" (DN) thymocytes and thymic epithelium.

118 Recently, IgD(-)CD27(-) (double negative, DN) and CD21(-)CD11c(+) (CD21(low)) B c

119 ted cell sorting-enriched CD133(-)/EpCAM(-) (double negative, DN), Huh-7 cells underwent a transwell

120 D56-CD146+ and CD45-CD271+CD56-CD146-(termed double-negative, DN) subsets, and CD45+CD271-hematopoiet

121 We recently identified CD4(-)CD8(-) (double-negative; DN) T cells as an important subset of a

122 IL-17A-producing cells are found in the double negative DN1 compartment of the Rag1(-/-) thymus

123 massive apoptotic depletion of beta-selected double-negative DN3 cells and premitotic arrest of CD4/C

124 AL restored development of thymocytes at the double-negative DN3 stage.

125 trates that two proteolytic pathways work in double-negative fashion - one targeting the other - to p

126 ck between Cdk1 and Cdc25(string) and of the double negative feedback between Cdk1 and Wee1.

127 ision, a mechanism that is likely due to the double negative feedback loop between Clp1/Cdc14 and Cdc

128 These data provide evidence for a double negative feedback loop between the REST silencing

129 A double negative feedback loop between the Warts kinase o

130 on of frq and qrf transcription thus forms a double negative feedback loop that is interlocked with t

131 SNAI2 and miR-203 formed a double negative feedback loop to inhibit each other's ex

132 ss miR-200 expression via a self-reinforcing double negative feedback loop to promote the mesenchymal

133 ot controlled by the mitotic switch but by a double-negative feedback between Cdk1 and Chk1.

134 In essence, these results suggest a double-negative feedback loop between a tumor suppressor

135 Here, we identify a novel double-negative feedback loop between APC and a translat

136 in the regulation of ERK and define a novel double-negative feedback loop between EpCAM and ERK that

137 In addition, we found that there is a double-negative feedback loop between LIN28 and let-7 in

138 Our results describe a double-negative feedback loop between MIR100HG and the t

139 Our results reveal a previously undescribed double-negative feedback loop between sponge lncRNA and

140 y various transcription factors, including a double-negative feedback loop between the microRNA-200 (

141 The double-negative feedback loop between the microRNA-200 f

142 Here we identified a double-negative feedback loop between the transcription

143 tic stemness-regulatory mechanism in which a double-negative feedback loop consisting of PRMT7 and mi

144 A double-negative feedback loop formed by the morning gene

145 DUX4 protein stabilizes DUX4 mRNA through a double-negative feedback loop in FSHD muscle cells.

146 also report that SinR and SlrR constitute a double-negative feedback loop in which SinR represses th

147 R complex is governed by a self-reinforcing, double-negative feedback loop in which SinR represses th

148 Here, we report the definition of a double-negative feedback loop involving AP4 and miR-15a/

149 In summary, our results define a double-negative feedback loop involving miR-15a/16-1 and

150 ogramming factors and miR-145 and uncovers a double-negative feedback loop involving OCT4, SOX2, KLF4

151 oncomitantly induce miR-132 expression via a double-negative feedback loop involving Rest inhibition.

152 cyclin degradation, owing to activation of a double-negative feedback loop involving the Cdk inhibito

153 This double-negative feedback loop is part of a bistable trig

154 The SNAIL1/miR-34 double-negative feedback loop is responsible for the rev

155 ate a bistable response, some component of a double-negative feedback loop must exhibit an ultrasensi

156 he miR-200 family and ZEB1, which exist in a double-negative feedback loop regulated by TGF-beta, ser

157 states of B. subtilis, and show a role for a double-negative feedback loop that locks the system into

158 nt (with CAL-101 [idelalisib]), interrupts a double-negative feedback loop, enhancing GC-regulated tr

159 rols the speed of Sic1 destruction through a double-negative feedback loop, ensuring a robust all-or-

160 We propose a model based on a double-negative feedback loop, vertically transmitted vi

161 ate MYCN, AURKB, and LIN28, the latter via a double-negative feedback loop.

162 eracts with the growth regulator melted in a double-negative feedback loop.

163 and miR-200, independent of Zeb1, to form a double-negative feedback loop.

164 engages the meiotic kinase network through a double-negative feedback loop; this specific feedback ar

165 s a system of three interlinked positive and double-negative feedback loops (CDK1 -> Cdc25 -> CDK1; C

166 al component of the interlinked positive and double-negative feedback loops that constitute the bista

167 dent heterogeneity in cell cycle activity to double-negative feedback regulation involving CDK2, p21,

168 These properties comprise a double-negative feedback relationship that sustains food

169 Stochastic modeling suggested that the double-negative feedback was sufficient to initiate bifu

170 SK; however, a proportion of MG patients are double-negative for anti-AChR and anti-MuSK antibodies.

171 These two mechanisms (double negative gate and feed-forward loop) are classic

172 The results entirely confirm the double negative gate control system at the cis-regulator

173 or control of alx1 spatial expression by the double negative gate GRN architecture, and explain the r

174 ion of specific regulatory genes by use of a double negative gate; (iii) dynamic stabilization of the

175 tructions, we have determined the age of the double-negative gate (DNG), the subcircuit which specifi

176 miR-142-3p forms a double-negative gate unlocking entry into the hemangiobl

177 e initial tier of control genes depends on a double-negative gate.

178 nce, TCR signals and/or traversal of the DN (double negative) > DP (double positive) checkpoint are r

179 Moreover, both IgA(+) and IgG(+) double negative (IgD(-) CD27(-)) CD11c(+) B cells were i

180 , Ucp1(-/-) and interleukin-4 receptor-alpha double-negative (Il4ra(-/-)) mice.

181 s that promote mucosal NKp44(+) and suppress double-negative ILCs are likely desirable.

182 rotective effect, whereas, NKG2A(-) NKp44(-) double-negative ILCs positively correlated with viral lo

183 d enhancer in CD4-negative thymoma cells and double-negative immature thymocytes.

184 ly"], IgG and IgA) and IgD(-)CD27(-) cells ("double-negative," including IgM, IgG, and IgA).

185 Taken together, our results have identified double-negative iNKT cells as promising cellular targets

186 Double-negative iNKT cells from Valpha14(Tg) NC mice sho

187 iNKT cells such as a biased expansion of the double-negative iNKT subset.

188 data to develop a mathematical model of the double-negative interaction between Hes1 and a microRNA,

189 gulated as thymocytes differentiate from the double-negative into the metabolically quiescent, small,

190 Our data suggest the presence of a double negative loop between PP2A(Cdc55) and APC/C(Cdc20

191 that CD11c/CD206 (M2-type) and CD11c/CD206 (double negative) macrophages, in addition to T cells, ar

192 ells and the generation of a large number of double negative mature T cells.

193 V infection resulted in NK cell dysfunction, double-negative NK cells and those expressing CXCR3, NKG

194 alphabeta type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregula

195 Here we demonstrate that BACH1 acts in a double-negative (overall positive) feedback loop to inhi

196 Double-negative patients were evaluated for mutations of

197 tors of MAPK or FGFR repressed the growth of double-negative PCs in vitro and in vivo.

198 These "double-negative" PCs are notable for elevated FGF and MA

199 ents with AD (P < .05), with lower values of double-negative populations (4% for patients with AD vs.

200 coincident with DJ rearrangement in CD4/CD8 double-negative pro-T cells.

201 nization of the bones and visceral organs in double-negative prostate cancer (DNPC).

202 In HNF4G/HNF1A-double-negative prostate cancer, exogenous expression of

203 transcription factors GRHL2 and ZEB1 form a double negative regulatory feedback loop in breast cance

204 stricted to the large micromere lineage by a double negative regulatory gate.

205 ires the transcriptional activator HrpL, the double negative regulatory loop established by HrpV and

206 50 neutralization titer increases in 2 of 70 double-negative samples (2.9%; P > 0.5).

207 Of the remaining 72 double-negative sera, 10 (14%) immunoprecipitated (125)I

208 shold in correspondence with the strength of double-negative signaling.

209 BAT was double positive/double negative/single positive in 6/2/14 patients.

210 The double-negative specification gate was logically require

211 Pro-T cell progenitors at double-negative stage 1 (DN1) and DN2 maintained nuocyte

212 T cell development did not progress beyond double-negative stage 1 thymocytes, resulting in a hypoc

213 (beta-selection) of TCRbeta(+) CD4(-)CD8(-) double-negative stage 3 (DN3) and DN4 progenitor cells t

214 in thymocytes causes a partial block at the double-negative stage 3 and also a partial block in posi

215 3 is required for the efficient transit from double-negative stage 4 through positive selection.

216 o a developmental block of thymocytes at the double-negative stage and a progressive depletion of thy

217 Upon commitment to the double-negative stage of T cell development, Tcrb adopts

218 CRalpha rearrangements are restricted to the double-negative stage of thymocyte development.

219 developing thymocytes from the CD4(-)CD8(-) double-negative stage to the CD4(+)CD8(+) double-positiv

220 This strategy inactivated Hdac3 in the double-negative stages of thymocyte development and caus

221 nt have problems transitioning to subsequent double-negative stages.

222 s and concomitant transitional blocks in the double-negative stages.

223 Accumulation of these cells before their double-negative state appears to be an important early e

224 Mature peripheral double negative T (DNT) cells expressing alphabeta TCR b

225 g characteristic of ALPS is the expansion of double negative T cells (DNTC).

226 typical peripheral T-cell population, termed double negative T cells (DNTs).

227 Double negative T cells have been claimed to derive from

228 This, along with the fact that double negative T cells have been documented in inflamed

229 CREMalpha is essential for the expansion of double negative T cells in SLE.

230 expansion of mature CD4 and CD8 negative or double negative T-cell receptor alphabeta(+) T lymphocyt

231 , autoimmune cytopenias, elevated numbers of double-negative T (DNT) cells, and increased risk of lym

232 ccumulation of TCRalphabeta(+) CD4(-) CD8(-) double-negative T (DNT) cells.

233 -cell receptor (TCR)alphabeta(+)CD4(-)CD8(-) double-negative T cells (DNT) is a hallmark of autoimmun

234 Double-negative T cells (DNTCs; ie, CD3(+)CD4(-)CD8(-) T

235 22 institutions, measuring peripheral blood double-negative T cells (DNTs) and Fas-mediated apoptosi

236 e to an increase in the levels of CD4(+) and double-negative T cells (not CD8(+) cells) and that CD4(

237 th a reduced frequency of CD3(+)CD4(-)CD8(-) double-negative T cells and an expansion of CD4(+) regul

238 crease of IL-17-producing CD3(+)CD4(-)CD8(-) double-negative T cells and an increase in CD4(+)CD25(+)

239 c autoimmunity with accumulation of abnormal double-negative T cells and autoantibodies to a number o

240 a significant increase in the number of both double-negative T cells and naive CD4(+) T cells, and a

241 nal CD27(-)gammadeltaTCR(+) and CD4(-)CD8(-) double-negative T cells are the major RORgammat-expressi

242 +) T cells to maintain immunity and identify double-negative T cells as a potential subset of cells c

243 of CD27(-)gammadeltaTCR(+) and CD4(-)CD8(-) double-negative T cells as the major source of IL-17A vi

244 animals were associated with the presence of double-negative T cells capable of producing Th1, Th2, a

245 s and treatment options in diseases in which double-negative T cells contribute to the pathogenesis.

246 Double-negative T cells derive from CD8(+) T cells throu

247 In this study, we show that double-negative T cells from MRL/lpr mice express high a

248 In both disorders, double-negative T cells infiltrate tissues, induce immun

249 Double-negative T cells were no longer detectable in mos

250 a population of CD3(+)CD4(-)CD8(-) T cells (double-negative T cells) partially compensates for CD4(+

251 sion of T-cell receptor alphabeta(+) CD4/CD8 double-negative T cells, and frequent development of hem

252 lignant lymphoproliferation, accumulation of double-negative T cells, hypergammaglobulinemia G and A,

253 SHP2 inhibition also reduced numbers of double-negative T cells, normalized ERK/MAPK signaling,

254 similar phenotype but lacks the expansion of double-negative T cells.

255 as primarily expressed by CD3(+)CD4(-)CD8(-) double-negative T cells.

256 that express only the alpha-chain of CD8 and double-negative T cells.

257 ortion of these cells are CD3(+)CD4(-)CD8(-) double-negative T cells.

258 pleen sections from 9 ALPS patients revealed double-negative T-cell (DN-T) infiltration of the MZ, wh

259 Double-negative T-cell (DNT) percentage and in vitro apo

260 Double-negative T-cell counts and plasma IL-10 and FAS l

261 TCR-alphabeta(+)CD3(+)CD4(-)CD8(-) "double negative" T cells are expanded in the peripheral

262 ll receptor-alphabeta(+) CD3(+)CD4(-)CD8(-) "double-negative" T cells are expanded in the peripheral

263 rmal FAS allele in an unusual population of "double-negative" T cells found in ALPS.

264 ased frequency of IL-17-producing CD3CD4CD8 (double negative) T cells in the peripheral blood and kid

265 higher numbers of host-derived CD4(-)CD8(-) (double negative) T cells in the spleens of recipients of

266 evelopment and contributes to progression of double-negative thymic precursors to single-positive thy

267 mic studies reveal expansion of Notch-active double-negative thymic progenitors, and we find the leuk

268 Furthermore, double-negative thymocyte development was perturbed with

269 d1 and Trdd2) rearrangements in CD4(-)CD8(-) double-negative thymocyte progenitors differentiated in

270 NFATc1 plays a critical role in double-negative thymocyte survival and differentiation.

271 cifically stabilize beta-catenin in CD4-CD8- double negative thymocytes during beta-selection.

272 ption and histone modifications to TRAV12 in double-negative thymocytes and caused a substantial incr

273 ity-joining (V(D)J) segments in CD4(-)CD8(-) double-negative thymocytes and CD4(+)CD8(+) double-posit

274 1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripher

275 ecombines Tcrd gene segments in CD4(-)CD8(-) double-negative thymocytes and Tcra gene segments in CD4

276 hat Tcrb alleles recombine asynchronously in double-negative thymocytes and that V(D)J recombination

277 eta join signals for robust proliferation of double-negative thymocytes and their differentiation int

278 iency of NIR and p53 provided rescue of DN3L double-negative thymocytes and their further differentia

279 remodeled in C57BL/6 and B6/J Rag1(-/-) MOM double-negative thymocytes as indicated by DNaseI hypers

280 kemic mice, we observed increased cycling of double-negative thymocytes expressing the Sur-TCR and in

281 ly V gene segments for Tcrd recombination in double-negative thymocytes is regulated, at least in par

282 ne expression is not observed in Ikaros null double-negative thymocytes or lineage-depleted bone marr

283 es differentiating into anergic CD4(-)CD8(-) double-negative thymocytes positive for the T cell antig

284 nteraction network in the Tcra-Tcrd locus in double-negative thymocytes that was formed by interactio

285 When YY1 was depleted in CD4(-)CD8(-) double-negative thymocytes, development to the CD4(+)CD8

286 tions of CD4(+),CD8(+) or double-positive or double-negative thymocytes, except that the T cell-speci

287 The CD8 gene is silent in CD4(-)CD8(-) double-negative thymocytes, expressed in CD4(+)CD8(+) do

288 In double-negative thymocytes, Ikaros binding to the Cd4 si

289 mbination was preserved in NIR-deficient DN3 double-negative thymocytes, suggesting that NIR does not

290 In CD4(-)CD8(-) double-negative thymocytes, the murine Tcrb locus is com

291 B cells in the bone marrow and from CD4-CD8- double-negative to CD4+CD8+ double-positive T cells in t

292 The transition from CD4/CD8 double-negative to double-positive cells was blocked, an

293 essed an LRRC8A ligand that was critical for double-negative to double-positive thymocyte differentia

294 , accompanied by developmental arrest at the double-negative to double-positive transition.

295 n lymphoid progenitors and thymocytes at the double-negative to double-positive transition.

296 in Hem1-deficient mice at the CD4(-)CD8(-) (double negative) to CD4(+)CD8(+) (double positive) cell

297 thymic cellularity and limited CD4(-)CD8(-) (double-negative) to CD4(+)CD8(+) (double-positive) matur

298 rlier in other parts of the GRN, including a double negative transcriptional regulatory gate, and dyn

299 s co-expressing AR and NE genes (AMPC), (iv) double-negative tumors (i.e. AR-/NE-; DNPC) and (v) tumo

300 Double-negative VGKC complex antibodies are often direct