ライフサイエンスコーパス: promyelocytic leukemia

1 comprising 280 adults with primary non-acute promyelocytic leukemia.

2 O, As2 O3 ) is currently used to treat acute promyelocytic leukemia.

3 ontinuing problem with early deaths in acute promyelocytic leukemia.

4 ts after chemotherapy in patients with acute promyelocytic leukemia.

5 cute myeloid leukemia (AML), excluding acute promyelocytic leukemia.

6 rapeutic drug used in the treatment of acute promyelocytic leukemia.

7 genic chromatin signature, we analyzed acute promyelocytic leukemia, a subtype of leukemia characteri

8 The gene product of this ORF localizes to promyelocytic leukemia-adjacent nuclear bodies.

9 )) is an effective therapeutic against acute promyelocytic leukemia and certain solid tumors.

10 The interior of the spheres contained promyelocytic leukemia and HSP70 proteins.

11 or suppressor originally identified in acute promyelocytic leukemia and implicated in tumorigenesis i

12 odulatory effects and is used to treat acute promyelocytic leukemia and inflammatory disorders such a

13 tric acute myeloid leukemia (AML), excluding promyelocytic leukemia and myeloid neoplasms of patients

14 translocation (15:17) and expression of the promyelocytic leukemia and the retinoic receptor alpha (

15 phocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and the BH3-mimetic ABT199 in ly

16 successfully used for the treatment of acute promyelocytic leukemia (APL) and has activity in multipl

17 We also observed robust engraftment of acute promyelocytic leukemia (APL) and myelofibrosis (MF) samp

18 lucidated the DNA methylome in primary acute promyelocytic leukemia (APL) and the role of promyelocyt

19 l residual disease (MRD) monitoring in acute promyelocytic leukemia (APL) are available only in the c

20 More effective treatments for acute promyelocytic leukemia (APL) are needed.

21 etinoic acid (ATRA) -based therapy for acute promyelocytic leukemia (APL) averages 70% at 5 years.

22 study, we investigated the dynamics of acute promyelocytic leukemia (APL) before and during therapy w

23 gap in quality of care and outcomes in acute promyelocytic leukemia (APL) between developed and devel

24 rinolysis is an important component of acute promyelocytic leukemia (APL) bleeding diathesis.

25 S) has excellent cytotoxic activity in acute promyelocytic leukemia (APL) but its activity in solid t

26 In most acute promyelocytic leukemia (APL) cases, translocons produce

27 expression was significantly lower in acute promyelocytic leukemia (APL) compared with non-APL patie

28 n successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decade.

29 rans retinoic acid (ATRA) treatment in acute promyelocytic leukemia (APL) has been the paradigm of ta

30 ith the microgranular variant (M3V) of acute promyelocytic leukemia (APL) in the all-trans retinoic a

31 Acute promyelocytic leukemia (APL) is a distinct subtype of ac

32 Acute promyelocytic leukemia (APL) is a hematological malignan

33 Acute promyelocytic leukemia (APL) is a malignancy of the bone

34 Because PML-RARA-induced acute promyelocytic leukemia (APL) is a morphologically differ

35 Acute promyelocytic leukemia (APL) is a subtype of acute myelo

36 A hallmark of acute promyelocytic leukemia (APL) is altered nuclear architec

37 Acute promyelocytic leukemia (APL) is characterized by a block

38 Acute promyelocytic leukemia (APL) is characterized by a block

39 Acute promyelocytic leukemia (APL) is characterized by granulo

40 Acute promyelocytic leukemia (APL) is characterized by the t(1

41 Acute promyelocytic leukemia (APL) is commonly complicated by

42 Acute promyelocytic leukemia (APL) is driven by a chromosomal

43 -trans retinoic acid and chemotherapy, acute promyelocytic leukemia (APL) is now the most curable typ

44 Acute promyelocytic leukemia (APL) is rare in children.

45 onstrated that the immense majority of acute promyelocytic leukemia (APL) patients can be definitivel

46 Up to 15% of acute promyelocytic leukemia (APL) patients fail to achieve or

47 Acute promyelocytic leukemia (APL) remains the best example of

48 population of unselected patients with acute promyelocytic leukemia (APL) remains unknown because of

49 lantation advantage and development of acute promyelocytic leukemia (APL) required DNMT3A.

50 ns retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the firs

51 31 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III historicall

52 Acute promyelocytic leukemia (APL), a cytogenetically distinct

53 In acute promyelocytic leukemia (APL), all-trans retinoic acid (A

54 In acute promyelocytic leukemia (APL), both isoforms are expresse

55 In acute promyelocytic leukemia (APL), repression by the PML-RARa

56 emotherapy is the standard of care for acute promyelocytic leukemia (APL), resulting in cure rates ex

57 In PML/RARA-driven acute promyelocytic leukemia (APL), retinoic acid (RA) induces

58 In acute promyelocytic leukemia (APL), the promyelocytic leukemia

59 s performed, yielding the diagnosis of acute promyelocytic leukemia (APL), with t(15;17)(q23;q21.1) i

60 nd PMLRARalpha interaction with Fas in acute promyelocytic leukemia (APL)-derived cells and APL prima

61 ceptor-alpha (PML-RARalpha)-associated acute promyelocytic leukemia (APL).

62 y diagnosed, low- or intermediate-risk acute promyelocytic leukemia (APL).

63 e experience as many surprises as with acute promyelocytic leukemia (APL).

64 RAR is involved in the pathogenesis of acute promyelocytic leukemia (APL).

65 h distinct outcomes in newly diagnosed acute promyelocytic leukemia (APL).

66 as a therapeutic drug for treatment of acute promyelocytic leukemia (APL).

67 -RARalpha fusion protein causative for acute promyelocytic leukemia (APL).

68 e therapy of low- or intermediate-risk acute promyelocytic leukemia (APL).

69 te PML and the PML-RARA oncoprotein of acute promyelocytic leukemia (APL).

70 tanding of the coagulopathy present in acute promyelocytic leukemia (APL).

71 guide molecularly targeted therapy in acute promyelocytic leukemia (APL).

72 that contributes to the development of acute promyelocytic leukemia (APL).

73 ha oncogene is the central effector of acute promyelocytic leukemia (APL).

74 of t(15;17)(q22;q21) translocations in acute promyelocytic leukemia (APL).

75 PR), the fusion protein that initiates acute promyelocytic leukemia (APL).

76 1980s and only in one subtype of AML, acute promyelocytic leukemia (APL).

77 ard-risk patients with newly diagnosed acute promyelocytic leukemia (APL).

78 eloid differentiation genes and drives acute promyelocytic leukemia (APL).

79 y effective agent for the treatment of acute promyelocytic leukemia (APL).

80 , a curative agent in clinical use for acute promyelocytic leukemia (APL); in our studies, ATO inhibi

81 e treatment for patients with relapsed acute promyelocytic leukemia (APL); its role as consolidation

82 es (IRR = 2.20) to nearly equal IRs of acute promyelocytic leukemia (APL; IRR = 1.08).

83 comes in patients with newly diagnosed acute promyelocytic leukemia (APL; see figure).

84 mias (MLL-AF9;Nras(G12D); PML-RARalpha acute promyelocytic leukemia [APL] cells) and Emicro-Myc lymph

85 onic myeloblastic leukemia and ATRA in acute promyelocytic leukemia [APL]).

86 ast-phase chronic myeloid leukemia and acute promyelocytic leukemia arguing against this strategy.

87 for corepressor release and operate in acute promyelocytic leukemia as dominant-negative inhibitors o

88 acid decreased plasminogen binding to acute promyelocytic leukemia blasts.

89 hsaki et al. show that the nuclear membrane, promyelocytic leukemia bodies, and the protein PML-II pl

90 nd telomeric association of TRF1, preventing promyelocytic leukemia body recruitment of telomere-boun

91 ozogamicin is efficacious not only for acute promyelocytic leukemia but, in combination with conventi

92 ul strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans retin

93 pendent and -independent manner in the human promyelocytic leukemia cell line HL-60.

94 Cells of human promyelocytic leukemia cell line-60 were differentiated

95 toxicity (IC50) of the prodrugs toward human promyelocytic leukemia cells (HL-60) from 52 to 12 muM.

96 anspeptidase (gamma-GT) protects human acute promyelocytic leukemia cells (NB4) from Dar, but not fro

97 th the accumulation of Hsp70 protein in HL60 promyelocytic leukemia cells recovering from acute therm

98 ted chemotaxis of differentiated HL-60 human promyelocytic leukemia cells was blocked by PPTN with a

99 the combination of the two methods on human promyelocytic leukemia cells, our results surprisingly r

100 d in breast and prostate cancer cells and in promyelocytic leukemia cells.

101 gulated Oct4 during differentiation of HL-60 promyelocytic leukemia cells.

102 he passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease relapse

103 If one excludes acute promyelocytic leukemia, current AML management still rel

104 tarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, thrombo

105 ominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is gen

106 In acute promyelocytic leukemia, granulocytic differentiation is

107 The treatment of acute promyelocytic leukemia has improved considerably after r

108 trioxide is an effective treatment for acute promyelocytic leukemia has renewed interest in the pharm

109 cancer), MCF-7 (breast cancer), HL-60 (Human promyelocytic leukemia), HepG2 (Hepatocellular carcinoma

110 fite in a pure enzymatic system and in human promyelocytic leukemia HL-60 clone 15 cells, maturated t

111 n assayed for cytotoxicity against the human promyelocytic leukemia (HL-60) cell line.

112 To validate our method, we mechanotype human promyelocytic leukemia (HL-60) cells and thereby confirm

113 We used human promyelocytic leukemia (HL-60) cells as a model system t

114 bed here is toxic toward cancer cells (human promyelocytic leukemia (HL-60), IC(50) = 9 muM, and huma

115 us cell cancer FaDu (intermediate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative) xenografts.

116 f our method not only by screening two acute promyelocytic leukemia human cells lines (NB4 and AP-106

117 ing to the International Consortium on Acute Promyelocytic Leukemia (IC-APL) study.

118 The International Consortium on Acute Promyelocytic Leukemia (IC-APL) was established to creat

119 nts of the International Consortium on Acute Promyelocytic Leukemia (IC-APL), an initiative of the In

120 iated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may possess t

121 on therapy in the setting of high-risk acute promyelocytic leukemia in first remission.

122 In a mouse model of promyelocytic leukemia in which the MRP8 promoter drives

123 were excluded, including patients with acute promyelocytic leukemia, incorrect diagnosis, or no adequ

124 rsenic trioxide, a frontline agent for acute promyelocytic leukemia, inhibits DeltaNp63 but not TAp63

125 drug FDA approved for the treatment of acute promyelocytic leukemia, inhibits the growth of Ewing sar

126 lpha) oncofusion protein, which causes acute promyelocytic leukemia, inhibits TNFalpha induced gene e

127 Human acute promyelocytic leukemia is causally linked to chromosomal

128 Acute promyelocytic leukemia is one of the few hematologic dis

129 nic trioxide, a drug for patients with acute promyelocytic leukemia, is found to target and degrade a

130 oplastic compound for the treatment of acute promyelocytic leukemia, is proarrhythmic via two separat

131 ndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated thromb

132 rkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-trans reti

133 ere further tested in vivo in a murine acute promyelocytic leukemia model, resulting 14d the most eff

134 scitation (n=116) and to patients with acute promyelocytic leukemia (n=83).

135 ct nuclear bodies, including nucleoli (148), promyelocytic leukemia nuclear bodies (38), nuclear spec

136 Using promyelocytic leukemia nuclear bodies (PML NBs) as a mod

137 ported that MORC3, a protein associated with promyelocytic leukemia nuclear bodies (PML NBs), is a ta

138 irus 1 (HSV-1) is conferred by components of promyelocytic leukemia nuclear bodies (PML NBs), which r

139 ates caspase-6 mediated cleavage of SATB1 at promyelocytic leukemia nuclear bodies (PML NBs).

140 ral cellular proteins that are components of promyelocytic leukemia nuclear bodies (PML NBs, also kno

141 Promyelocytic leukemia nuclear bodies (PML-NB) are sub-n

142 ge-limited human fibroblasts by dissociating promyelocytic leukemia nuclear bodies (PML-NBs).

143 Promyelocytic leukemia nuclear bodies (PML-NBs)/nuclear

144 A component of promyelocytic leukemia nuclear bodies, Daxx is a transcr

145 , ErbB4 colocalized with PIAS3 and SUMO-1 in promyelocytic leukemia nuclear bodies, nuclear domains i

146 tivity-induced increase in the expression of promyelocytic leukemia nuclear bodies, which decreases G

147 assays, and enhances c-Maf localization into promyelocytic leukemia nuclear bodies.

148 intrinsic antiviral immunity are mediated by promyelocytic leukemia nuclear body (PML-NB) constituent

149 ellular intrinsic immune defense mediated by promyelocytic leukemia nuclear body (PML-NB) proteins su

150 in E1A/E1B-55K-mediated tumorigenesis, other promyelocytic leukemia nuclear body (PML-NB)/PML oncogen

151 EBNA2 that works though interaction with the promyelocytic leukemia nuclear-body-associated protein S

152 We show that Nrf2 traffics, in part, to promyelocytic leukemia-nuclear bodies (PML-NBs).

153 ated intravascular coagulation scores, acute promyelocytic leukemia patients had higher fibrinogen bu

154 fferentiation will be useful for identifying promyelocytic leukemia patients who are eligible for new

155 an both nondrowning cardiac arrest and acute promyelocytic leukemia patients.

156 s human Ms differentiated from monocytes and promyelocytic leukemia PLB-985 cells (with and without m

157 ssociation of the major organizer of ND10, a promyelocytic leukemia (PML) and ND10 constituent, Sp100

158 egradation of both sumoylated and unmodified promyelocytic leukemia (PML) and other sumoylated cellul

159 however, partially defective for disrupting promyelocytic leukemia (PML) bodies compared to the abil

160 The effective BGLF4-mediated dispersion of promyelocytic leukemia (PML) bodies was dependent on SUM

161 We identified a metabolic function for the promyelocytic leukemia (PML) gene, uncovering an unexpec

162 Promyelocytic Leukemia (PML) is a nuclear protein that f

163 Promyelocytic leukemia (PML) is a pleiotropic tumor supp

164 The tumor-suppressor protein promyelocytic leukemia (PML) is aberrantly degraded in m

165 red nuclear architecture, with disruption of promyelocytic leukemia (PML) nuclear bodies (NBs) mediat

166 Promyelocytic leukemia (PML) nuclear bodies (NBs) recrui

167 at K120 and K382 and colocalizes with p53 in promyelocytic leukemia (PML) nuclear bodies following ce

168 Promyelocytic leukemia (PML) nuclear bodies selectively

169 the proviral chromatin in close proximity to promyelocytic leukemia (PML) nuclear bodies, a reversibl

170 iction mediated by one or more components of promyelocytic leukemia (PML) nuclear bodies, and IE1 and

171 d on IFN-induced gene products associated to promyelocytic leukemia (PML) nuclear bodies, and we show

172 ns, causes p53 to colocalize with E1B-55K in promyelocytic leukemia (PML) nuclear bodies, nuclear dom

173 atin remodeling complexes and associate with promyelocytic leukemia (PML) nuclear bodies.

174 from the nucleolus, but it also disorganizes promyelocytic leukemia (PML) nuclear bodies.

175 Promyelocytic leukemia (PML) plays a tumor suppressive r

176 The promyelocytic leukemia (PML) protein has been implicated

177 etreated with siX3, but not siUL54, retained promyelocytic leukemia (PML) protein in cellular PML bod

178 The promyelocytic leukemia (PML) protein is a tumor suppress

179 The promyelocytic leukemia (PML) protein is a tumor suppress

180 The promyelocytic leukemia (PML) protein is an essential com

181 In acute promyelocytic leukemia (APL), the promyelocytic leukemia (PML) protein is fused to the ret

182 The promyelocytic leukemia (PML) protein organizes PML nucle

183 is found in punctate domains associated with promyelocytic leukemia (PML) protein within the nucleus.

184 n 10 (ND10) components, including hDaxx, the promyelocytic leukemia (PML) protein, and Sp100.

185 The promyelocytic leukemia (PML) protein, initially discover

186 CV LTA as well as an increased expression of promyelocytic leukemia (PML) protein, which is known to

187 8) promotes the degradation of the antiviral promyelocytic leukemia (PML) protein.

188 X5 was reported to fuse with the sequence of promyelocytic leukemia (PML) to produce PAX5-PML chimeri

189 tein mediates functional inactivation of the promyelocytic leukemia (PML) tumor suppressor pathway.

190 Here we identify a previously unknown promyelocytic leukemia (PML)-peroxisome proliferator-act

191 us arsenic trioxide (ATO), which degrade the promyelocytic leukemia (PML)-retinoic acid receptor fusi

192 s expression of the tumor suppressor protein promyelocytic leukemia (PML).

193 We report here an interaction between promyelocytic leukemia protein (PML) and ASC.

194 dation during lytic infection, including the promyelocytic leukemia protein (PML) and its small ubiqu

195 e residues and vicinal thiol groups, such as promyelocytic leukemia protein (PML) and PML-retinoic ac

196 P0, via degradation of the ND10 constituents promyelocytic leukemia protein (PML) and Sp100 and the s

197 ontains an E3 ubiquitin ligase that degrades promyelocytic leukemia protein (PML) and Sp100, two majo

198 unctional activities of the tumor suppressor promyelocytic leukemia protein (PML) are mostly associat

199 We identified promyelocytic leukemia protein (PML) as a Fas-interactin

200 and it directly targets the tumor-suppressor promyelocytic leukemia protein (PML) for proteasomal deg

201 The tumor suppressor promyelocytic leukemia protein (PML) functions as a stre

202 Promyelocytic leukemia protein (PML) has been implicated

203 PK2 in nuclear speckles and association with promyelocytic leukemia protein (PML) in response to DNA

204 Promyelocytic leukemia protein (PML) is a tumor suppress

205 Promyelocytic leukemia protein (PML) is an essential org

206 Promyelocytic leukemia protein (PML) modulates the p53 t

207 infection, the virus genome is localized to promyelocytic leukemia protein (PML) nuclear bodies (NB)

208 moylation pathway, and both proteins disrupt promyelocytic leukemia protein (PML) nuclear bodies (NBs

209 Promyelocytic leukemia protein (PML) nuclear bodies (NBs

210 P0 localizes to cellular structures known as promyelocytic leukemia protein (PML) nuclear bodies or N

211 The latter enforces promyelocytic leukemia protein (PML) nuclear body (NB) f

212 ed to HSV-1 genomes but had no effect on the promyelocytic leukemia protein (PML) or Sp100.

213 3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and forma

214 Promyelocytic leukemia protein (PML) was originally iden

215 feron, as they fail to direct degradation of promyelocytic leukemia protein (PML), a component of hos

216 ization with ICP0 are distinct from those of promyelocytic leukemia protein (PML), a well-characteriz

217 olve direct interactions between ATO and the promyelocytic leukemia protein (PML), as well as acceler

218 r structures containing both constant [e.g., promyelocytic leukemia protein (PML), SP100, death domai

219 lear structures contain both constant [e.g., promyelocytic leukemia protein (PML), Sp100, death-domai

220 used to an N-terminal partner, most commonly promyelocytic leukemia protein (PML).

221 Specifically, the promyelocytic leukemia protein (TRIM19; also called PML)

222 mutations of which lead to BS, localizes to promyelocytic leukemia protein bodies and to the nucleol

223 zed by multitelomere clusters and associated promyelocytic leukemia protein bodies.

224 by translocating to the nucleus, increasing promyelocytic leukemia protein expression and decreasing

225 The promyelocytic leukemia protein is a well known tumor sup

226 n size and ultimately became juxtaposed with promyelocytic leukemia protein nuclear bodies.

227 a characterized intrinsic antiviral factor, promyelocytic leukemia protein, and are antagonized by I

228 bination with the intrinsic antiviral factor promyelocytic leukemia protein, significantly impairs th

229 leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor al

230 isruption and colocalize with Mdm2, p53, and promyelocytic leukemia protein.

231 INs abrogated arsenic-induced degradation of promyelocytic leukemia protein.

232 sed Rara(+/-) mice with mice expressing PML (promyelocytic leukemia)-RARA from the cathepsin G locus

233 le protease neutrophil elastase (NE) cleaves promyelocytic leukemia-retinoic acid receptor (PML-RAR)a

234 promyelocytic leukemia (APL) and the role of promyelocytic leukemia-retinoic acid receptor alpha (PML

235 ) chromosomal translocation that creates the promyelocytic leukemia-retinoic acid receptor alpha (PML

236 emia that results from the expression of the promyelocytic leukemia-retinoic acid receptor alpha (PML

237 nslocation that generates the fusion protein promyelocytic leukemia-retinoic acid receptor alpha (PML

238 n oncoproteins, as recently demonstrated for promyelocytic leukemia-retinoic acid receptor alpha and

239 ion characterize the epigenetic landscape of promyelocytic leukemia/retinoic acid receptor-alpha (PML

240 scence by activating the histone repressor A/promyelocytic leukemia senescence pathway.

241 additional cases of t(15;17)-negative acute promyelocytic leukemia that had cytogenetically invisibl

242 arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with arsen

243 ere complication seen in patients with acute promyelocytic leukemia treated with all-trans retinoic a

244 n 1333 young adult patients, excluding acute promyelocytic leukemia, treated in the United Kingdom MR

245 ung adult patients with AML, excluding acute promyelocytic leukemia, using denaturing high-performanc

246 Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation p

247 those with core binding factor AML and acute promyelocytic leukemia, were randomly assigned to treatm

248 ing subclones) has been exemplified by acute promyelocytic leukemia, where successful targeting of th

249 eferred a difficult diagnostic case of acute promyelocytic leukemia with no pathogenic X-RARA fusion

250 Seven were acute myeloid leukemia (2 acute promyelocytic leukemia with t(15;17), 2 with confirmed p

251 and IL-12Rbeta and the transcription factors promyelocytic leukemia zinc finger (PLZF) and RAR-relate

252 Two transcription factors, promyelocytic leukemia zinc finger (PLZF) and Slug were

253 e dependent on the transcriptional regulator promyelocytic leukemia zinc finger (PLZF) and the adapto

254 that RORgammat and the transcription factor promyelocytic leukemia zinc finger (PLZF) are valuable n

255 ave shown that the transcriptional regulator promyelocytic leukemia zinc finger (PLZF) controls the d

256 tigated the role of the transcription factor promyelocytic leukemia zinc finger (plzf) in HSC fate us

257 ac-zinc finger (BTB-ZF) transcription factor promyelocytic leukemia zinc finger (PLZF) is required fo

258 The transcription factor promyelocytic leukemia zinc finger (PLZF) is transiently

259 Here, we show that the transcription factor Promyelocytic Leukemia Zinc Finger (PLZF) plays a critic

260 We found that E proteins directly bound the promyelocytic leukemia zinc finger (PLZF) promoter and w

261 Expression of promyelocytic leukemia zinc finger (PLZF) protein direct

262 CRPC) reveals that 5% to 7% of tumors harbor promyelocytic leukemia zinc finger (PLZF) protein homozy

263 The transcription factor promyelocytic leukemia zinc finger (PLZF) seemed to cont

264 Most MAIT cells express the promyelocytic leukemia zinc finger (PLZF) transcription

265 Surprisingly, both promyelocytic leukemia zinc finger (PLZF)(+) and NK1.1(+

266 increase in the frequency of IL-4-producing promyelocytic leukemia zinc finger (PLZF)(hi) immature i

267 ctions with CD1d ligands prior to expressing promyelocytic leukemia zinc finger (PLZF), a broad compl

268 tional CD4 T cells by the sole expression of promyelocytic leukemia zinc finger (PLZF), a transcripti

269 acked expression of the transcription factor promyelocytic leukemia zinc finger (PLZF), as well as ex

270 gher expression of the transcription factors promyelocytic leukemia zinc finger (PLZF), eomesodermin,

271 essed the NKT lineage-specific transcription promyelocytic leukemia zinc finger (PLZF), indicating a

272 s, kallikrein related peptidase 4 (KLK4) and promyelocytic leukemia zinc finger (PLZF), integrate opt

273 Mechanistically, expression of Egr2 and promyelocytic leukemia zinc finger (PLZF), two key trans

274 T cells expressing the transcription factor promyelocytic leukemia zinc finger (PLZF), which confers

275 compassed the transcriptional repressor gene promyelocytic leukemia zinc finger (PLZF), which was val

276 1 and beta-catenin regulate the frequency of promyelocytic leukemia zinc finger (PLZF)-expressing, IL

277 aling, and the cells expressed both IL-4 and promyelocytic leukemia zinc finger (PLZF).

278 ce IL-4 and express the transcription factor promyelocytic leukemia zinc finger (PLZF).

279 transcription factors Sal-like 4 (SALL4) and promyelocytic leukemia zinc finger (PLZF; also known as

280 Moreover, we show that promyelocytic leukemia zinc finger and IL-4 are also req

281 her analyses reveal that Hox5 interacts with promyelocytic leukemia zinc finger biochemically and gen

282 nip1(-/-) iNKT cells failed to down-regulate Promyelocytic leukemia zinc finger compared with their W

283 ugh binding of the transcriptional repressor promyelocytic leukemia zinc finger protein (PLZF) at the

284 bric-a-brac-zinc finger transcription factor promyelocytic leukemia zinc finger protein (PLZF).

285 PLZF (Promyelocytic Leukemia Zinc Finger protein), a member of

286 eroid-responsive transcription factor, PLZF (promyelocytic leukemia zinc finger protein), which media

287 h the expression of the transcription factor promyelocytic leukemia zinc finger protein.

288 xpression of the early growth response 2 and promyelocytic leukemia zinc finger transcription factors

289 yelocytic leukemia zinc finger; however, the promyelocytic leukemia zinc finger transgene does not re

290 nsion of a usually rare population of CD4(+) promyelocytic leukemia zinc finger(+) "gammadelta NKT" c

291 LRF was originally identified as a PLZF (promyelocytic leukemia zinc finger) homolog that physica

292 -/-) T cells require the presence of a novel promyelocytic leukemia zinc finger-expressing, SLAM fami

293 translocation produces two fusion proteins, promyelocytic leukemia zinc finger-retinoic acid recepto

294 howed a significant upregulation of IL-4 and promyelocytic leukemia zinc finger.

295 dependent on the BTB-ZF transcription factor promyelocytic leukemia zinc finger.

296 tes expressing the transcriptional regulator promyelocytic leukemia zinc finger.

297 pment is rescued by transgenic expression of promyelocytic leukemia zinc finger; however, the promyel

298 The transcription factor PLZF (promyelocytic leukemia zinc finger; zbtb16) is essential

299 However, promyelocytic leukemia zinc-finger (PLZF), a critical tr

300 ar localization and functional impairment of promyelocytic leukemia zinc-finger, a transcription fact