ライフサイエンスコーパス: PLZF

1 n factor promyelocytic leukemia zinc finger (PLZF).

2 IL-4 and promyelocytic leukemia zinc finger (PLZF).

3 promyelocytic leukemia zinc finger protein (PLZF).

4 ly modulate lineage-dependent expressions of PLZF.

5 1 retrotransposons as the primary targets of PLZF.

6 potential role for Ly108 in the induction of PLZF.

7 ike T-cell homeostasis depending on XIAP and PLZF.

8 nduces their signature transcription factor, PLZF.

9 half expressed IL-4 and only half expressed PLZF.

10 anscription factors T-bet, eomesodermin, and PLZF.

11 he NKT lineage-specific transcription factor PLZF.

12 atural spontaneous mutation that inactivates plzf.

13 een shown to be dependent upon expression of PLZF.

14 man T cells marked by intermediate levels of PLZF.

15 an bind to the human BTB-zinc finger protein PLZF.

16 T cells expressing the transcription factor PLZF.

17 enic mouse T cells with forced expression of PLZF.

18 receptor alpha (PLZF-RARalpha) and RARalpha-PLZF.

19 and a region C terminal to the RD2 domain of PLZF.

20 CD4 T cells from mice ectopically expressing PLZF.

21 le CD1d and express the transcription factor PLZF.

22 duced expression of the transcription factor PLZF.

23 in, BRAF/RAF1, APC, beta-catenin, and ZBTB16/PLZF.

24 pressing promyelocytic leukemia zinc finger (PLZF), a broad complex, tramtrack, bric-a-brac, poxvirus

25 However, promyelocytic leukemia zinc-finger (PLZF), a critical transcription factor for iNKT cell dev

26 is promyelocytic leukemia zinc-finger gene (PLZF), a member of the POK (POZ and Kruppel) family of t

27 ssion of promyelocytic leukemia zinc finger (PLZF), a transcription factor specifically expressed in

28 We find that SPCs lacking Plzf, a transcription factor essential for SPC maintenan

29 increase and Sall4 physically interacts with Plzf, a transcription factor exclusively required for ad

30 row that transiently express high amounts of PLZF, a transcription factor previously associated with

31 NKT cells also have increased expression of PLZF, a transcription factor required for alphabeta NKT

32 Xu et al. find that the transcription factor PLZF activates interferon-stimulated genes and facilitat

33 dence for a mechanism through which RARalpha-PLZF acts as a modifier oncogene that subverts different

34 o promote T cell effector functions and that PLZF acts independently of SAP- and Fyn-mediated signali

35 PLZF also activates expression of regulated in developme

36 Here, we demonstrate that PLZF also interacts with Rb in vitro and in vivo.

37 LL4) and promyelocytic leukemia zinc finger (PLZF; also known as ZBTB16) are known to be required for

38 In contrast, PLZF altered the negative selection of thymocytes expres

39 ay also be involved in the oncogenic role of PLZF and BCL6 in leukaemias and lymphomas.

40 and thymocytes lacking Jarid2 show increased PLZF and decreased H3K9me3 levels.

41 KLK4 interacts with PLZF and decreases its stability.

42 f known iNKT differentiation factors such as Plzf and Gata3 was not dramatically altered.

43 factors, including the transcription factor PLZF and microbial colonization.

44 these data suggest that interactions between PLZF and Rb could be important in stem cell biology.

45 Both PLZF and Rb have been shown to function in stem cells an

46 The interaction between PLZF and Rb is mediated through the Rb pocket and the re

47 at higher TCR avidity correlates with higher PLZF and reduced T-bet expression.

48 Motif analyses identified putative PLZF and SALL4 binding sequences, but rarely both at sha

49 PLZF and SALL4 preferentially bound gene promoters and i

50 ether, these data reveal the full profile of PLZF and SALL4 regulatory targets in undifferentiated sp

51 sa and piwil1 and the spermatogonial markers plzf and sox17 for at least six weeks in culture.

52 ption factor motifs to identify and validate PLZF and SRF as regulators of adipogenesis.

53 ntial induction of the transcription factors PLZF and TCF1.

54 uction of the signature transcription factor PLZF and that ID3 was critical for development of TBET-d

55 ddition, Rb can simultaneously interact with PLZF and the E2F1 S phase-inducing transcription factor,

56 (+) nTh17 cells are their high expression of PLZF and their absence from lamina propria; iTh17 cells

57 lls from adipose tissues that do not express PLZF and those from PLZF haplodeficient mice have low RO

58 However, PLZF(+) and NK1.1(+) NKTgammadelta cells express identic

59 These results could suggest that the PLZF(+) and the NK1.1(+) subsets are developmentally unr

60 cells from Valpha19 TCR transgenic mice are PLZF(-) and express a naive CD44(lo) phenotype.

61 persistently express high levels of Zbtb16 (PLZF) and Il4, genes that are normally downregulated in

62 factors promyelocytic leukemia zinc finger (PLZF) and RAR-related orphan receptor gamma (RORgammat).

63 factors, promyelocytic leukemia zinc finger (PLZF) and Slug were induced more than 15-fold 3 h after

64 egulator promyelocytic leukemia zinc finger (PLZF) and the adaptor molecule signaling lymphocyte acti

65 ly, both promyelocytic leukemia zinc finger (PLZF)(+) and NK1.1(+) NKTgammadelta cells were found in

66 r-2 to the promoter of Zbtb16, which encodes PLZF, and resulted in PLZF levels similar to those seen

67 ion of the transcription factors (TFs) Tbet, Plzf, and Rorgammat, iNKT cells have been classified in

68 sient expression of the transcription factor PLZF, and the lineage relationships of innate lymphoid c

69 id2 binds to the Zbtb16 locus, which encodes PLZF, and thymocytes lacking Jarid2 show increased PLZF

70 ssential role for CUL3 in the development of PLZF- and BCL6-dependent lineages.

71 These data indicate that deletions of PLZF are a common occurrence in MM and that downregulati

72 n factor promyelocytic leukemia zinc finger (PLZF) are valuable new markers to identify the recently

73 phenotype in human cells, expand the role of PLZF as a critical regulator in the human adaptive immun

74 nked to cell cycle regulation, and positions plzf as a key player in controlling HSC homeostasis.

75 These studies demonstrate a role for PLZF as an activator of transcription important both for

76 ave identified the transcriptional repressor PLZF as an interacting protein of LYRIC/AEG through a ye

77 llectively, our results reveal RORgammat and PLZF as characteristic markers for identifying nTh17 cel

78 n factor promyelocytic leukemia zinc finger (PLZF), as well as expression of intracellular signaling

79 promyelocytic leukemia zinc finger protein (PLZF) at the rs12101261 site.

80 tion in PLZF-mediated repression by reducing PLZF binding to promoters.

81 r" RORgammat) cross-regulate each other, and PLZF binds at the RORC promoter in CCR6(+) cells.

82 by using PLZF(-/-) mice and mixed wild-type:PLZF(-/-) bone marrow chimeras.

83 receptor alpha (PLZF-RARalpha) and RARalpha-PLZF, both of which participate in leukemia development.

84 mouse THY1(+) spermatogonia identified 4176 PLZF-bound and 2696 SALL4-bound genes, including 1149 an

85 Unlike other iNKT cells, they lacked PLZF but expressed the transcription factor E4BP4, which

86 ha may act as a dominant-negative version of PLZF by affecting the regulation of shared targets.

87 Whether PLZF can mediate this effector conversion independently

88 Furthermore, PLZF causes the formation of barrier-type boundaries by

89 support the conclusion that itk(-/-) innate PLZF(+)CD4(+) T cells are a novel subset of innate T cel

90 We show that itk(-/-) innate PLZF(+)CD4(+) T cells are not CD1d-dependent NKT cells,

91 Furthermore, although the itk(-/-) innate PLZF(+)CD4(+) T cells express alphabeta TCRs, neither be

92 heral tissues indicates that itk(-/-) innate PLZF(+)CD4(+) T cells preferentially home to spleen and

93 btained upon intrathymic injection of sorted PLZF(+) cells, thus indicating their developmental relat

94 Bioinformatic analysis of the PLZF cistrome shows that PLZF negatively regulates multi

95 n amplified aging phenotype, suggesting that plzf controls age-related pathway.

96 Thus, our findings demonstrate that PLZF controls ROS levels, which in turn governs the infl

97 egulator promyelocytic leukemia zinc finger (PLZF) controls the development of essentially all of the

98 pped extensively, further demonstrating that PLZF could induce the effector program in most CD4 T cel

99 PLZF-cre Runx1 cKO mice lack iNKT17 cells in the thymus,

100 We determined the consequences of PLZF deficiency on ILC2 function in response to innate a

101 PLZF deficiency specifically affected the effector diffe

102 We hypothesized that PLZF-deficient ILC2s have functional defects in the inna

103 PLZF-deficient iNKT cells failed to secrete large amount

104 PLZF-deficient lung ILC2s exhibit a cell-intrinsic defec

105 Ectopic expression of PLZF in PLZF-deficient MM cells resulted in decreased cell viabi

106 For example, PLZF-deficient NKT cells do not acquire an 'activated' p

107 sitive selection of NKT cell precursors, and PLZF-deficient NKT cells failed to undergo the intrathym

108 The impaired effector differentiation of PLZF-deficient Vgamma6(+) gammadelta T cells was not due

109 Repression by PLZF depended on the rs12101261 disease susceptibility a

110 ion factor, and their development is largely PLZF dependent.

111 erse androgen-independent growth mediated by PLZF depletion.

112 Zbtb16-encoded transcription factor PLZF directs the differentiation of multiple innate and

113 PLZF elevation increases FGFR3 expression and STAT3 path

114 factors promyelocytic leukemia zinc finger (PLZF), eomesodermin, and T-bet and enhanced capacity to

115 a novel promyelocytic leukaemia zinc finger (PLZF)-expressing ILC precursor (ILCP) strictly committed

116 uency of promyelocytic leukemia zinc finger (PLZF)-expressing, IL-4-producing thymocytes that promote

117 ce lacking Ly108 showed decreased numbers of PLZF-expressing CD4(+) T cells.

118 Furthermore, IL-4 produced by PLZF-expressing cells causes some CD8 T cells to acquire

119 IL-4- and PLZF-expressing cells were first found at the double-pos

120 ferentiation gene 3 control the frequency of PLZF-expressing gammadelta T cells.

121 ThPOK, is important for the phenotype of the PLZF-expressing gammadelta T cells.

122 Canonical, PLZF-expressing NK cells were retained in asymptomatic c

123 In contrast, TCF1-deficient mice do not have PLZF-expressing thymocytes and eomesodermin-expressing m

124 and beta-catenin regulate the generation of PLZF-expressing thymocytes and thereby facilitate the ge

125 development of NKT thymocytes downregulated PLZF expression and directed their terminal differentiat

126 let-7 miRNAs, NKT thymocytes maintained high PLZF expression and terminally differentiated into inter

127 tor PLZF, to post-transcriptionally regulate PLZF expression and thereby the effector functions of na

128 he induction of PLZF, the factors regulating PLZF expression are incompletely understood.

129 PLZF expression at the innate lymphoid cell precursor st

130 layer in iNKT cell maturation that regulates PLZF expression by modulating H3K9 methylation.

131 cule family receptor Ly108 markedly enhanced PLZF expression compared with that induced by TCR stimul

132 we identify a critical enhancer controlling PLZF expression exclusively in innate lymphoid lineages.

133 TCR cross-linking induced PLZF expression in all polyclonal immature gammadelta th

134 -based approaches to assess the induction of PLZF expression in non-innate T cells by T cell receptor

135 PLZF expression in T-cell allografts attenuates expansio

136 hat, in contrast to multiple recent reports, PLZF expression is highly specific to innate T cells and

137 In this study, we show that PLZF expression is not restricted to NK T cells but is a

138 Reintroduction of PLZF expression is sufficient to reverse androgen-indepe

139 Here, we demonstrate that knockdown of PLZF expression promotes a CRPC and enzalutamide-resista

140 Furthermore, PLZF expression results in selective ubiquitination chan

141 present mouse studies demonstrating a sharp PLZF expression threshold requirement for induction of t

142 Whereas transgene-mediated PLZF expression was not sufficient to rescue NKT cell de

143 PLZF expression was sufficient to provide some memory/ef

144 daptive CD56(dim) NK-cell population lacking PLZF expression.

145 the kinetic rather than the overall level of PLZF expression.

146 ough a limited set of ILC1 genes depended on PLZF for expression, characteristically including Il7r,

147 Others, such as PLZF for NKT cells and Bcl-6 for T follicular helper cel

148 cells in Skint-1 mutant mice, they required PLZF for their effector maturation, similarly to Vgamma6

149 the main population relies on NFIL3, but not PLZF, for development and, therefore, is developmentally

150 Thus, the present study identifies that PLZF function is not restricted to NKT or IL-4(+) T cell

151 Thus, we identify the mTORC1-Plzf functional interaction as a critical rheostat for m

152 that H3K27me3 levels at the bivalent Zbtb16/PLZF gene define a threshold enabling precise coupling o

153 We found that the Zbtb16/PLZF gene promoter that drives iNKT cell differentiation

154 sues that do not express PLZF and those from PLZF haplodeficient mice have low ROS.

155 Therefore, it is becoming clear that PLZF has a broad impact on the immune response.

156 Overexpression of PLZF has been shown to induce cell cycle arrest at the G

157 tant (luxoid.Zbtb16(LU)/J) mice deficient in PLZF have hearing and responses to acoustic trauma simil

158 roducing promyelocytic leukemia zinc finger (PLZF)(hi) immature invariant natural killer T (iNKT) cel

159 PLZF(high) cells were committed ILC progenitors with mul

160 Id3 was expressed in PLZF(high) NKT2 cells and loss of Id3 allowed for increa

161 PLZF(high) precursors also expressed high amounts of ID2

162 PLZF immunoreactivity is present in the spiral ganglion,

163 m transcription start site of CCR6 that bind PLZF in CCR6(+) cells.

164 tion of memory/effector functions induced by PLZF in conventional T cells was independent of Fyn and

165 iated signaling was not sufficient to induce PLZF in conventional T cells.

166 actors that control the normal expression of PLZF in lymphocytes are unknown.

167 Ectopic expression of PLZF in PLZF-deficient MM cells resulted in decreased ce

168 Our study reveals a new role for plzf in regulating HSC function that is linked to cell c

169 They also reveal the broad, defining role of PLZF in the differentiation of innate lymphocytes.

170 ycle analyses revealed an important role for plzf in the regulation of the G1-S transition of HSCs.

171 Plzf in turn antagonizes Sall4 function by displacing Sa

172 PLZF in turn interacts with AR and inhibits its function

173 n factor promyelocytic leukemia zinc finger (plzf) in HSC fate using the Zbtb16(lu/lu)mouse model, wh

174 providing a signal that links Egr2 to induce PLZF, in part by regulating signaling lymphocyte activat

175 e finding of genetic loss in CRPC implicates PLZF inactivation as a mechanism promoting ADT resistanc

176 ge-specific zinc-finger transcription factor PLZF, inadequate proliferation of iNKT cell precursors,

177 Thus, our study reveals the PLZF-independent mechanisms of the development and funct

178 GATA3, as well as TOX, a known regulator of PLZF-independent NK and LTi lineages.

179 cription promyelocytic leukemia zinc finger (PLZF), indicating a developmental relationship with NKT

180 that agonist selection might be required for PLZF induction.

181 her supporting the importance of the TCR for PLZF induction.

182 We show that RARalpha-PLZF inhibits myeloid cell differentiation through inter

183 se possibilities, we characterized the CD4(+)PLZF(+) innate T cells in itk(-/-) mice.

184 LK4) and promyelocytic leukemia zinc finger (PLZF), integrate optimal functioning of AR and mTOR sign

185 have confirmed that nuclear LYRIC/AEG-1 and PLZF interact in mammalian cells via the N- and C termin

186 PLZF is a canonical androgen-regulated putative tumor su

187 Zbtb16-encoded PLZF is a signature transcription factor (TF) that direc

188 PLZF is also essential in osteoblast and spermatogonial

189 PLZF is also present in the brain and PLZF mRNA in brain

190 In this study, we show that PLZF is also required for the development and function o

191 We observed that PLZF is expressed in fetal-derived invariant Vgamma5(+)

192 RT-PCR and immunoblot analysis revealed that PLZF is greatly downregulated in MM cell lines compared

193 Although PLZF is known to direct the effector program of NKT cell

194 This report shows that PLZF is likewise responsible for the innate, NKT-like ph

195 PLZF is necessary and sufficient to induce a multipotent

196 Thus, PLZF is remarkable in that it is a transcription factor

197 These data show that PLZF is sufficient to promote T cell effector functions

198 n factor promyelocytic leukemia zinc finger (PLZF) is required for development of the characteristic

199 myelocytic zinc finger transcription factor (PLZF) is required for the development of activated pheno

200 n factor promyelocytic leukemia zinc finger (PLZF) is transiently expressed during development of typ

201 entiation were suppressed following SALL4 or PLZF knockdown.

202 Coexpression of LYRIC/AEG-1 with PLZF leads to a reduction in PLZF-mediated repression by

203 Zbtb16, which encodes PLZF, and resulted in PLZF levels similar to those seen in NKT cells.

204 PLZF loss enhances CRPC tumor growth in a xenograft mode

205 In contrast, PLZF loss reduces FGFR3 levels, leading to premature neu

206 Deletion of PLZF markedly altered the development of several ILC sub

207 occurrence in MM and that downregulation of PLZF may contribute to MM pathogenesis by promoting cell

208 PLZF-mediated DNA methylation induces silencing of the f

209 YRIC/AEG-1 with PLZF leads to a reduction in PLZF-mediated repression by reducing PLZF binding to pro

210 ins to induce expression of Kit, a target of Plzf-mediated repression required for differentiation.

211 Cell stress releases PLZF-mediated repression, resulting in L1 activation/ret

212 pping a functional PLZF site and antagonizes PLZF-mediated repression, suggesting that PLZF-RARalpha

213 one deacetylases, which are known to promote PLZF-mediated repression.

214 innate and adaptive immune stimuli by using PLZF(-/-) mice and mixed wild-type:PLZF(-/-) bone marrow

215 PLZF(-/-) mice, wild-type littermates, or mixed bone mar

216 ty of PLZF/SALL4 shared sites contained only PLZF motifs.

217 PLZF is also present in the brain and PLZF mRNA in brain is elevated following conditioning st

218 PLZF mRNA levels in the cochlea are increased following

219 tic analysis of the PLZF cistrome shows that PLZF negatively regulates multiple pathways, including t

220 mic iNKT cell expansion and abundance of the PLZF(+) NKT2 sublineage.

221 Plzf opposes mTORC1 activity by inducing expression of t

222 PLZF or Slug stimulated productive infection 20- or 5-fo

223 with the promyelocytic leukemia zinc-finger (PLZF) or PML genes lead to expression of oncogenic PLZF-

224 Our findings suggest that therapy with PLZF-overexpressing T cells would result in overall impr

225 Interferon-induced PLZF phosphorylation and histone deacetylase 1 recruitme

226 n factor Promyelocytic Leukemia Zinc Finger (PLZF) plays a critical role shaping patterns of neuronal

227 Depletion of H3K27me3 at the Zbtb16/PLZF promoter leads to uncoupling of iNKT cell developme

228 ound the promyelocytic leukemia zinc finger (PLZF) promoter and were required for expression of this

229 PLZF (Promyelocytic Leukemia Zinc Finger protein), a mem

230 ticosteroid-responsive transcription factor, PLZF (promyelocytic leukemia zinc finger protein), which

231 LRF was originally identified as a PLZF (promyelocytic leukemia zinc finger) homolog that p

232 We report that PLZF (promyelocytic leukemia zinc finger, Zbtb16), a mem

233 The transcription factor PLZF (promyelocytic leukemia zinc finger; zbtb16) is ess

234 ssion of promyelocytic leukemia zinc finger (PLZF) protein directs the effector differentiation of in

235 s harbor promyelocytic leukemia zinc finger (PLZF) protein homozygous deletions.

236 er myeloid leukemias, supporting the role of PLZF-RARalpha as an aberrant repressor in APL.

237 PLZF-RARalpha binds to a region of the c-MYC promoter ov

238 es PLZF-mediated repression, suggesting that PLZF-RARalpha may act as a dominant-negative version of

239 or PML genes lead to expression of oncogenic PLZF-RARalpha or PML-RARalpha fusion proteins, respectiv

240 In primary murine hematopoietic progenitors, PLZF-RARalpha promotes cell growth, and represses Dusp6

241 g, we identify novel, direct target genes of PLZF-RARalpha that tend to be repressed in APL compared

242 ia zinc finger-retinoic acid receptor alpha (PLZF-RARalpha) and RARalpha-PLZF, both of which particip

243 ia zinc finger-retinoic acid receptor alpha (PLZF-RARalpha) and RARalpha-PLZF.

244 common x-RARalpha fusions, PML-RARalpha and PLZF-RARalpha, have gained the ability to recognize spec

245 RA induced the differentiation of PLZF-RARalpha-transformed murine hematopoietic cells and

246 ntaining a self-renewal pathway triggered by PLZF-RARalpha.

247 Furthermore, RARalpha-PLZF recruits HDAC1 and causes histone H3 deacetylation

248 PLZF regulates the expression of genes involved in cell

249 ting an important growth inhibitory role for PLZF, relatively little is known regarding regulation of

250 Using NFIL3-deficient mice, PLZF reporter/fate mapping mice, and mixed bone marrow c

251 Here, using PLZF-reporter mice and cell transfer assays, we studied

252 reveal a novel mechanism of action by which, PLZF represses retrotransposons, safeguarding normal pro

253 ing tumourigenesis through the regulation of PLZF repression.

254 Finally, we found that PLZF(+)RORgammat(+) nTh17 cells represent one of the pri

255 Indeed, the majority of PLZF/SALL4 shared sites contained only PLZF motifs.

256 n factor promyelocytic leukemia zinc finger (PLZF) seemed to control the ROS levels.

257 Thus, the expression of IL-4 and PLZF seems to be determined by an unidentified event tha

258 the c-MYC promoter overlapping a functional PLZF site and antagonizes PLZF-mediated repression, sugg

259 Aberrant mTORC1 activation in Plzf(-/-) SPCs inhibits their response to GDNF, a growth

260 onventional T cells that ectopically express PLZF spontaneously acquire an activated, effector phenot

261 However, the PLZF(+) subset, but not the NK1.1(+) subset, also expres

262 In these mice, IL-4 produced by the CD4(+)PLZF(+) T cell population leads to the conversion of con

263 CD8(+) T cells via the production of IL-4 by PLZF(+) T cells.

264 support the development of large numbers of PLZF+ T cells, further supporting the importance of the

265 We examined tissue homing, expression of PLZF, T-bet, and RORgammat, and cytokine profiles and fo

266 sociated TCRalpha sequences in wild-type and PLZF-Tg mice overlapped extensively, further demonstrati

267 ated through the Rb pocket and the region of PLZF that lies between its transcriptional repression (p

268 rt that promyelocytic leukaemia zinc finger (PLZF), the BTB-zinc finger (BTB-ZF) transcription factor

269 tion has been implicated in the induction of PLZF, the factors regulating PLZF expression are incompl

270 e current understanding of how expression of PLZF, the innate T cell determinant, is initiated during

271 The expression of PLZF, the signature invariant NKT cell transcription fac

272 PLZF, therefore, is an iNKT cell-specific transcription

273 Mechanistically, Sall4 sequesters Plzf to noncognate chromatin domains to induce expressio

274 es the lineage-specific transcription factor PLZF, to post-transcriptionally regulate PLZF expression

275 ssed between ILC1s and cNKs, indicating that PLZF together with other, yet to be defined, factors con

276 y the gradual post-thymic acquisition of the PLZF transcription factor and the ability to produce IFN

277 The PLZF transcription factor is essential for the innate ph

278 es lifespan via the Ras-MAPK pathway and the PLZF transcription factors EOR-1 and EOR-2.

279 ress the promyelocytic leukemia zinc finger (PLZF) transcription factor, and their development is lar

280 ubsequent degradation of PLZF, which impairs PLZF transcriptional repression ability and antagonizes

281 Functionally, PLZF transgenic CD4 and CD8 lymphocytes were similar to

282 Furthermore, PLZF transgenic cells maintained a diverse TCR repertoir

283 PLZF transports CUL3 to the nucleus, where the two prote

284 Egr2 and promyelocytic leukemia zinc finger (PLZF), two key transcription factors for acquiring the N

285 onstrated that transgenic (Tg) expression of PLZF under the CD4 promoter induced the innate effector

286 PLZF was induced immediately after positive selection of

287 Furthermore, cellular localization of PLZF was not altered in the absence of mTOR2 signaling.

288 Although PLZF was not required for Vgamma5(+) gammadelta T cells

289 Interestingly, the ectopic expression of PLZF was shown to push conventional T cells into an acti

290 The inactivated state of PLZF was stably maintained in mature T cells, even under

291 Surprisingly, we found that PLZF was stably repressed in non-innate T cells and that

292 nd the iNKT cell master transcription factor PLZF was UTX dependent.

293 BTB-ZF), promyelocytic leukemia zinc finger (PLZF), was recently shown to control the development of

294 ecipitation for modified histones, p300, and PLZF, we identified enhancer-like sites at -9/-10 and -1

295 Diminished expression of Egr2 and PLZF were not caused by aberrant TCR signaling, as deter

296 n factor promyelocytic leukemia zinc finger (PLZF), which confers effector properties resembling inva

297 sor gene promyelocytic leukemia zinc finger (PLZF), which was validated by analysis of genomic DNA us

298 ubiquitination and subsequent degradation of PLZF, which impairs PLZF transcriptional repression abil

299 Conversely, overexpression of PLZF/ZBTB-16 in conventional T cells leads to a proapopt

300 Knockdown of the transcription factor PLZF/ZBTB-16, which is involved in the effector program