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 y T-lineage progenitors within the CD4- CD8- double-negative 1 and downstream double-negative 2 thymo

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

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 e CD4- CD8- double-negative 1 and downstream double-negative 2 thymocyte subsets.

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

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

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

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

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

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

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

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

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

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

25 development, including T-cell arrest at the double-negative 3 stage (CD4(-) CD8(-) CD25(+) CD44(-)),

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

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

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

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

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

31 proliferation, and impaired progression from double-negative 3 to double-negative 4.

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

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

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

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

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

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

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

39 by wt cells and failed to develop beyond the double-negative 4 stage.

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

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

42 paired progression from double-negative 3 to double-negative 4.

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

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

45 the two galectins: whereas galectin-1 kills double-negative and double-positive human thymocytes wit

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

47 9 (hCD19) was selectively suppressed in late double-negative and double-positive thymocytes, coincidi

48 erwent long-range interactions by looping in double-negative and double-positive thymocytes, respecti

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

50 d TCRalphabeta(+) thymocytes are CD4 and CD8 double-negative, and their final maturation, including t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 habetaT lymphocyte development occurs at the double negative (DN) 3 (CD4(-)CD8(-)CD25(+)c-kit(-)) sta

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

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

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

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

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

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

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

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

74 /c corneal endothelial cells was mediated by double negative (DN) T cells, as treatment of CD8 cells

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

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

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

78 a-chain genes are assembled in CD4(-)CD8(-) (double negative (DN)) thymocytes and TCRalpha-chain gene

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

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

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

82 impaired in initial pre-TCR signaling at the double-negative (DN) 3 beta selection stage and show red

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

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

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

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

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

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

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

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

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

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

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

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

104 sponsible for up to 70% of ERK activation in double-negative (DN) thymocytes in vivo and ex vivo.

105 TCRbeta expression in CD4(-)CD8(-) double-negative (DN) thymocytes induces signaling pathwa

106 on of a functional rearrangement in CD4-CD8- double-negative (DN) thymocytes leads to the assembly of

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

108 ctivation of Notch signaling in CD4(-)CD8(-) double-negative (DN) thymocytes was previously shown to

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

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

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

112 suggested that cell numbers starting at the double-negative (DN)4 stage are significantly reduced in

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

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

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

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

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

118 -positive (TCR(+)) T cells are CD4(-)CD8(-) (double-negative [DN]) T cells, capable of down-regulatin

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

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

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

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

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

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

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

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

127 ich alterations in T-cell development at the double-negative/double-positive (DN/DP) stages cooperate

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

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

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

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

132 A double negative feedback loop between the Warts kinase o

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

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

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

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

137 We propose that this double-negative feedback circuit shapes the output profi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 markers on iNKT cells, selectively enhanced double-negative iNKT cell survival, but did not induce t

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

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

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

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

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

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

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

191 Double-negative patients were evaluated for mutations of

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

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

194 crease in the percentage of the CD4(-)CD8(-) double-negative population, and are partially blocked in

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

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

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

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

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

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

201 50 neutralization titer increases in 2 of 70 double-negative samples (2.9%; P > 0.5).

202 they are unlikely to face the aforementioned double-negative selection.

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

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

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

206 The double-negative specification gate was logically require

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

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

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

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

211 3 is required for the efficient transit from double-negative stage 4 through positive selection.

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

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

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

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

216 n an inhibition of T-cell development at the double-negative stage within the thymus.

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

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

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

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

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

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

223 Double negative T cells have been claimed to derive from

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

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

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

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

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

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

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

231 22 institutions, measuring peripheral blood double-negative T cells (DNTs) and Fas-mediated apoptosi

232 patosplenomegaly, and an increased number of double-negative T cells (DNTs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 determine whether gld-induced tolerance and double-negative T-cell lymphoproliferation can be uncoup

258 autoimmune diabetes but also causes massive double-negative T-cell lymphoproliferation.

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

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

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

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

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

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

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

266 Furthermore, double-negative thymocyte development was perturbed with

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

268 elete CBP and p300 starting at the CD4- CD8- double-negative thymocyte stage of T-cell development.

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

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

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

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

273 1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripher

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 efficiency, galectin-3 preferentially kills double-negative thymocytes.

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 ological levels can rescue the transition of double-negative to double-positive thymocytes in RAG-nul

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

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

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

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

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

300 Double-negative VGKC complex antibodies are often direct