ライフサイエンスコーパス: PLZF

1 promyelocytic leukemia zinc finger protein (PLZF).

2 n factor promyelocytic leukemia zinc finger (PLZF).

3 n factor Promyelocytic Leukemia Zinc Finger (PLZF).

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

5 le CD1d and express the transcription factor PLZF.

6 duced expression of the transcription factor PLZF.

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

8 y the expression of the transcription factor PLZF.

9 1 retrotransposons as the primary targets of PLZF.

10 potential role for Ly108 in the induction of PLZF.

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

12 nduces their signature transcription factor, PLZF.

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

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

15 he NKT lineage-specific transcription factor PLZF.

16 een shown to be dependent upon expression of PLZF.

17 man T cells marked by intermediate levels of PLZF.

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

19 T cells expressing the transcription factor PLZF.

20 enic mouse T cells with forced expression of PLZF.

21 and H3K27ac resulting in high expression of PLZF.

22 ell-specific "master regulator" functions of PLZF.

23 ly modulate lineage-dependent expressions of PLZF.

24 CD4 T cells from mice ectopically expressing PLZF.

25 atural spontaneous mutation that inactivates plzf.

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

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

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

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

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

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

32 and we demonstrate that DDX5 interacts with PLZF, a transcription factor required for germline maint

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

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

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

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

40 KLK4 interacts with PLZF and decreases its stability.

41 defined by the loss of transcription factor PLZF and Fc receptor gamma-chain.

42 decline in SAM levels, which is dependent on PLZF and is required for osteogenic differentiation.

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

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

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

46 PLZF and SALL4 preferentially bound gene promoters and i

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

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

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

50 ntial induction of the transcription factors PLZF and TCF1.

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

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

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

54 gle cell RNA sequencing of EOMES+ cells from Plzf (+/+) and Plzf (lu/lu) mice support the conclusion

55 ol of undifferentiated spermatogonia between Plzf (+/+) and Plzf (lu/lu) mice, we used RNAseq to iden

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

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

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

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

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

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

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

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

64 efficiently than GR and KL4: however, KLF6, PLZF, and GR had little effect on the bICP0 E promoter.

65 ell lineage, including Zbtb16, which encodes PLZF, and PLZF-targeted genes.

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

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

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

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

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

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

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

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

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

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

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

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

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

84 use NKT cells expressing wild-type levels of PLZF, but deficient for YY1, had developmental defects,

85 Whether PLZF can mediate this effector conversion independently

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

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

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

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

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

91 IFNgamma-producing PLZF+ CD4+ T cells were enriched in the cord blood of in

92 PLZF+ CD4+ T cells were specifically enriched in the fet

93 olon to the thymus in early life to regulate PLZF(+) cell homeostasis.

94 Importantly, perturbations in thymic PLZF(+) cells brought about by alterations in early gut

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

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

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

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

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

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

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

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

103 PLZF deficiency specifically affected the effector diffe

104 Additionally, PLZF-deficient basophils had reduced expression of the I

105 Functionally, PLZF-deficient basophils were less responsive to IgE act

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

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

108 PLZF-deficient mice had decreased numbers of basophil pr

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

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

111 Repression by PLZF depended on the rs12101261 disease susceptibility a

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

113 erse androgen-independent growth mediated by PLZF depletion.

114 egulation of the master transcription factor PLZF did not require CD28-costimulation in either of the

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

116 PLZF elevation increases FGFR3 expression and STAT3 path

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

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

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

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

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

122 microbes influence the thymic homeostasis of PLZF-expressing cells in early life.

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

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

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

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

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

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

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

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

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

132 PLZF expression at the innate lymphoid cell precursor st

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

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

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

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

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

138 PLZF expression in T-cell allografts attenuates expansio

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

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

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

142 Furthermore, PLZF expression results in selective ubiquitination chan

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

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

145 PLZF expression was sufficient to provide some memory/ef

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

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

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

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

150 dependent upon IL-15/IL-2Rbeta signaling and PLZF for their development and/or survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

164 PLZF immunoreactivity is present in the spiral ganglion,

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

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

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

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

182 presence of particular RORgammat(+)T-bet(lo)PLZF(-) iNKT and gammadelta-hi T cell subsets in healthy

183 Impaired thymic development of PLZF(+) innate lymphocytes in germ-free (GF) neonatal mi

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

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

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 n this article, we show that the function of PLZF is completely dependent on the transcription factor

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

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

194 PLZF is necessary and sufficient to induce a multipotent

195 It is not known, however, if the activity of PLZF is regulated by other factors.

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 c leukemia zinc-finger transcription factor (PLZF) is essential for nearly all of the unique, innate-

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

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

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

202 , we revealed that the ZBTB16 locus encoding PLZF, is repressed by Polycomb (PcG) and H3K27me3 in nai

203 entiation were suppressed following SALL4 or PLZF knockdown.

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

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

206 , the gamma interferon (IFN-gamma)-producing PLZF(lo)RORgammat(lo) (promyelocytic leukemia zinc finge

207 ur findings suggest that IFN-gamma-producing PLZF(lo)RORgammat(lo) iNKT1 cells play a role in the pro

208 fection, cornea-resident IFN-gamma-producing PLZF(lo)RORgammat(lo) iNKT1 cells provide protection fro

209 on day 2 postinfection), IFN-gamma-producing PLZF(lo)RORgammat(lo) iNKT1 cells were the predominant i

210 entified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300

211 PLZF loss enhances CRPC tumor growth in a xenograft mode

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

213 quencing of EOMES+ cells from Plzf (+/+) and Plzf (lu/lu) mice support the conclusion that SSCs are h

214 wer proliferation index in wild-type than in Plzf (lu/lu) mice, suggesting that PLZF regulates their

215 ntiated spermatogonia between Plzf (+/+) and Plzf (lu/lu) mice, we used RNAseq to identify a rare sub

216 are lost through proliferative exhaustion in Plzf (lu/lu) mice.

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

218 PLZF-mediated DNA methylation induces silencing of the f

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

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

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

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

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

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

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

226 PLZF mRNA levels in the cochlea are increased following

227 ptible subjects with the largest increase in PLZF-negative NK cells during the transmission season ha

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

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

230 al deletion of Gata3 resulted in the loss of PLZF(+) non-LTi progenitors but not the LTi progenitors

231 Consistently, PLZF(+) non-LTi progenitors expressed high amounts of GA

232 Plzf opposes mTORC1 activity by inducing expression of t

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

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

235 PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promot

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

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

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

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

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

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

242 anscription factors (KLF), i.e., KLF4, KLF6, PLZF (promyelocytic leukemia zinc finger), and KLF15, ar

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

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

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

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

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

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

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

250 e than in Plzf (lu/lu) mice, suggesting that PLZF regulates their proliferative activity and that EOM

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

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

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

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

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

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

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

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

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

264 We examined expression of PLZF, T-bet, and RORgammat, as well as cytokine/chemokin

265 e, including Zbtb16, which encodes PLZF, and PLZF-targeted genes.

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

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

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

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

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

271 PLZF, therefore, is a major player in controlling type 2

272 Discordant expression of YY1 and PLZF, therefore, might define NKT cell subsets with dist

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 osteogenic di

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 that distinguishes them from

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

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

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

288 Subsequently, PLZF was recruited to osteogenic enhancers, influencing

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

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

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

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

293 recipitation experiments showed that YY1 and PLZF were coassociated.

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

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

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

297 e full function of the transcription factor, PLZF, which is essential for the development of natural

298 study, we show that the transcription factor PLZF, which is known for its essential role in the funct

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