ライフサイエンスコーパス: promyelocytic leukemia

1 MDA-MB-231 breast adenocarcinoma, and HL-60 promyelocytic leukemia).

2 comprising 280 adults with primary non-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 O, As2 O3 ) is currently used to treat acute promyelocytic leukemia.

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

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

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

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

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

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

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

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

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

17 ly related to poorer prognosis in both acute promyelocytic leukemia (APL) and acute myeloid leukemia,

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

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

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

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

31 Acute promyelocytic leukemia (APL) is a hematological malignan

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

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

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

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

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

37 Acute promyelocytic leukemia (APL) is characterized by granulo

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

39 Acute promyelocytic leukemia (APL) is commonly complicated by

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

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

42 Acute promyelocytic leukemia (APL) is often associated with ac

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

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

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

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

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

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

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

50 31 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III historicall

51 Acute promyelocytic leukemia (APL), a cytogenetically distinct

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

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

54 In acute promyelocytic leukemia (APL), NTAL depletion from lipid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds t

83 acid decreased plasminogen binding to acute promyelocytic leukemia blasts.

84 y all-trans RA, an anticancer drug for acute promyelocytic leukemia, blocked SMC transition to SEM ce

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

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

87 g-G) as a tumor suppressor in not only acute promyelocytic leukemia, but also in other solid tumors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 In acute promyelocytic leukemia, granulocytic differentiation is

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

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

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

106 Next, neutrophil-differentiated human promyelocytic leukemia HL-60 cells (HL60D) were treated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 Human acute promyelocytic leukemia is causally linked to chromosomal

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

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

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

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

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

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

128 (ALT) pathway that depends on ALT-associated promyelocytic leukemia nuclear bodies (APBs), whose func

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

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

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

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

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

134 mponents involved in this innate process are promyelocytic leukemia nuclear bodies (PML-NBs), which a

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

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

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

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

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

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

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

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

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

144 All registered non-acute promyelocytic leukemia patients with intensive induction

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

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

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

148 LT-like phenotypes, including ALT-associated promyelocytic leukemia (PML) bodies (APBs), telomere sis

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

150 er is the excessively clustered telomeres in promyelocytic leukemia (PML) bodies, represented as larg

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

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

153 Promyelocytic leukemia (PML) is a pleiotropic tumor supp

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

155 reported that ICP0 differentially recognizes promyelocytic leukemia (PML) isoforms.

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

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

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

159 Upregulated Mad1 localizes to ProMyelocytic Leukemia (PML) nuclear bodies in breast ca

160 Promyelocytic leukemia (PML) nuclear bodies selectively

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

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

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

164 RL4-mediated degradation by associating with promyelocytic leukemia (PML) nuclear bodies, ensuring it

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

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

167 structurally organized, containing canonical promyelocytic leukemia (PML) nuclear body protein SP100

168 Promyelocytic leukemia (PML) plays a tumor suppressive r

169 In hBMECs, NBs formed by STAT2 and promyelocytic leukemia (PML) protein are present constit

170 The promyelocytic leukemia (PML) protein has been implicated

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

172 xible hinge domain containing 1 (SMCHD1), or promyelocytic leukemia (PML) protein increased basal lev

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

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

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

176 The promyelocytic leukemia (PML) protein organizes PML nucle

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

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

179 singly, mTRF1 suppresses the accumulation of promyelocytic leukemia (PML) protein, BRCA1 and the SMC5

180 The promyelocytic leukemia (PML) protein, initially discover

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

182 suppresses intrinsic immunity driven by the promyelocytic leukemia (PML) protein, which limits ZIKV

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

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

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

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

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

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

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

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

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

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

193 ier (SUMO)-conjugating enzyme, UBC9, and the promyelocytic leukemia protein (PML) and thus was not du

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

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

196 o makes Aire susceptible to interaction with promyelocytic leukemia protein (PML) bodies, sites of ma

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

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

199 Promyelocytic leukemia protein (PML) has been implicated

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

201 Promyelocytic leukemia protein (PML) is a tumor suppress

202 Promyelocytic leukemia protein (PML) is an essential org

203 Promyelocytic leukemia protein (PML) modulates the p53 t

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

205 Promyelocytic leukemia protein (PML) nuclear bodies (NBs

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

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

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

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

210 3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and forma

211 Promyelocytic leukemia protein (PML) was originally iden

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

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

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

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

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

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

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

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

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

221 The promyelocytic leukemia protein is a well known tumor sup

222 se changes are associated with remodeling of promyelocytic leukemia protein nuclear bodies (PML NBs),

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

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

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

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

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

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

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

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

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

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

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

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

235 TRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 ess NK-inhibitory receptors, and express the promyelocytic leukemia zinc finger (PLZF) transcription

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

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

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

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

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

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

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

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

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

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

272 1 and beta-catenin regulate the frequency of promyelocytic leukemia zinc finger (PLZF)-expressing, IL

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

274 ed by expression of the transcription factor Promyelocytic Leukemia Zinc Finger (PLZF).

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

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

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

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

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

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

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

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

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

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

285 We also found that promyelocytic leukemia zinc finger seemed to play a role

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

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

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

289 ption factors (KLF), i.e., KLF4, KLF6, PLZF (promyelocytic leukemia zinc finger), and KLF15, are indu

290 (IFN-gamma)-producing PLZF(lo)RORgammat(lo) (promyelocytic leukemia zinc finger, retinoic acid-relate

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

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

293 tes expressing the transcriptional regulator promyelocytic leukemia zinc finger.

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

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

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

299 The promyelocytic leukemia zinc-finger transcription factor

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