ライフサイエンスコーパス: megakaryocytic

1 to mechanisms of normal megakaryopoiesis and megakaryocytic abnormalities that accompany Down syndrom

2 atopoietic cell defects including anemia and megakaryocytic abnormalities, in addition to previously

3 site, mHS-25/6, as having erythroid but not megakaryocytic activity in primary cells.

4 a knockin mouse model of the one twenty-two-megakaryocytic acute leukemia (OTT-MAL) fusion oncogene

5 leukemia (CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic

6 e megakaryocyte-erythroid progenitor between megakaryocytic and erythroid development.

7 EphB4 enforces preferential megakaryocytic and erythroid differentiation and may be

8 miR-125b-2 overexpression did not affect megakaryocytic and erythroid differentiation, but severe

9 Gfi-1b directly regulates a wide spectrum of megakaryocytic and erythroid genes, predominantly repres

10 Megakaryocytic and erythroid lineages derive from a comm

11 oid leukemias (ML-DS) characterized by mixed megakaryocytic and erythroid phenotype and by acquired m

12 granulocyte-macrophage CSF, and expansion of megakaryocytic and erythroid progenitors by thrombopoiet

13 EphB4 resulted in the elevated expression of megakaryocytic and erythroid specific markers, consisten

14 inding at many nonerythroid sites, including megakaryocytic and myeloid target genes, was normal.

15 myeloid (granulocytic/monocytic, erythroid, megakaryocytic) and lymphoid (natural killer and B cell)

16 containing cells belonging to the monocytic, megakaryocytic, and definitive erythroid lineages--when

17 LSD1 perturbs differentiation of erythroid, megakaryocytic, and granulocytic cells as well as primar

18 The transgenic mice showed erythroid, megakaryocytic, and granulocytic hyperplasia in the bone

19 ogenitors redirects them into the erythroid, megakaryocytic, and granulocytic lineages.

20 r, GATA-1, is required for normal erythroid, megakaryocytic, and mast cell development.

21 oiesis, and inhibitory roles in the myeloid, megakaryocytic, and progenitor compartments.

22 the father, and exhibited erythrocytosis and megakaryocytic atypia but normal platelet number.

23 es, which was correlated with an increase in megakaryocytic, but a decrease in erythroid, progenitors

24 suggest previously unknown in vivo roles in megakaryocytic cell differentiation.

25 In this work, we establish a human megakaryocytic cell line (MEG-01) as a model system for

26 m megakaryocytes, mRNA was isolated from the megakaryocytic cell line MEG-01 and the cDNA for CKIIalp

27 a new mouse embryonic stem (ES) cell-derived megakaryocytic cell line, MKD1.

28 bly, when SU6656 (2.5 microM) was added to a megakaryocytic cell line, UT-7/TPO, the cells ceased cel

29 LOH in the CMK megakaryocytic cell line, which has a hypotetraploid kar

30 structurally altered P(2X1)-like receptor in megakaryocytic cell lines (Dami and CMK 11-5) and platel

31 1, which have been reported in platelets and megakaryocytic cell lines, and TRPM1, TRPM2 and TRPM7, w

32 ot PAR1-mediated activation of platelets and megakaryocytic cell lines.

33 s showed reduced capacity to form erythroid/ megakaryocytic cells and exhibited a tendency toward mye

34 Here, we show that human megakaryocytic cells could overexpress the lysosomal enz

35 Genome-wide studies in megakaryocytic cells demonstrate significant chromatin o

36 nhanced apoptosis in myeloid, erythroid, and megakaryocytic cells in the bone marrow leading to ineff

37 n Ca(2+) entry in human platelets and Meg-01 megakaryocytic cells loaded with Fluo-3 was examined by

38 ibition of Fli-1 decreases the production of megakaryocytic cells relative to erythroid cells, wherea

39 Chromatin immunoprecipitation (ChIP) using megakaryocytic cells revealed RUNX1 binding to MYL9 prom

40 hibited enhanced production of erythroid and megakaryocytic cells that proliferated excessively.

41 nstrated decreased cortical actin tension in megakaryocytic cells with reduced CIP4 or WASP protein.

42 The yield of megakaryocytic cells, as determined by flow cytometry, w

43 d that Mef2C is directly regulated by Scl in megakaryocytic cells, but not in erythroid cells.

44 rora-B kinase mRNA is decreased in polyploid megakaryocytic cells, suggesting that deficiency of Auro

45 In transfected CHRF-288-11 megakaryocytic cells, the corresponding activity decreas

46 In transfected CHRF-288-11 megakaryocytic cells, the corresponding activity decreas

47 Using Dami megakaryocytic cells, we confirmed that AP-2 is required

48 c, B lymphoid, erythroid, and, unexpectedly, megakaryocytic cells.

49 for normal differentiation of erythroid and megakaryocytic cells.

50 development of granulocytic, monocytic, and megakaryocytic cells.

51 y with transformation of bipotential erythro-megakaryocytic cells.

52 bortezomib dose without negative effects on megakaryocytic cellularity, ploidy, or morphology.

53 emia (HEL) and CHRF 288-11 cells, which have megakaryocytic characteristics, and HL-60 promyelocytic

54 emia (HEL) and CHRF 288-11 cells, which have megakaryocytic characteristics, with promyelocytic HL-60

55 nsplantable leukemia with both erythroid and megakaryocytic characteristics.

56 ytic differentiation and formation of normal megakaryocytic colonies in patients with AML and MDS.

57 , Ifi27l2a, or Hmga2 significantly increased megakaryocytic colonies in the BM of Jak2V617F mice, ind

58 ls from Npm1-TCTG/WT;Cre(+) mice formed more megakaryocytic colonies in vitro.

59 s failed to give rise to either erythroid or megakaryocytic colonies.

60 ALR mutations inhibited cytokine-independent megakaryocytic colony formation.

61 elet count reduction and an expansion of the megakaryocytic compartment in the BM and spleen.

62 a similar miRNA profile and expansion of the megakaryocytic compartment.

63 nd flow cytometry analysis demonstrated that megakaryocytic DAMI cells internalize FV.

64 ng megakaryocytes and platelets, and also in megakaryocytic Dami cells.

65 anscription factor involved in erythroid and megakaryocytic development and suggest that it serves a

66 ressor Gfi-1b is essential for erythroid and megakaryocytic development in the embryo.

67 ovides evidence that the NPM1 mutant affects megakaryocytic development, further expanding our knowle

68 While altered GATA1 inhibits erythro-megakaryocytic development, less is known about how tris

69 hus, whereas mHS-3.5 alone is sufficient for megakaryocytic development, mHS-3.5 and mHS-25/6 collect

70 rains erythroid differentiation and promotes megakaryocytic development, resulting in ET phenotype.

71 G-1) for its essential role in erythroid and megakaryocytic development.

72 development often parallel abnormalities in megakaryocytic development.

73 which has also been implicated in promoting megakaryocytic development.

74 s; miR-10a, miR-10b, and miR-20a) inhibiting megakaryocytic differentiation along with increased expr

75 ces, loss of a uSTAT5 program that restrains megakaryocytic differentiation and activation of a canon

76 inding to the KLF1 locus is increased during megakaryocytic differentiation and counterbalances the a

77 d that Eltrombopag was capable of increasing megakaryocytic differentiation and formation of normal m

78 The NUP98-HOXD13 fusion gene inhibits megakaryocytic differentiation and increases apoptosis i

79 ssion of Cxcl12, Fzd2, or Ifi27l2a increases megakaryocytic differentiation and proliferation in the

80 horbol-12-myristate-13-acetate (PMA) induces megakaryocytic differentiation and Rac2 gene transcripti

81 tially regulated by GATA-2 and GATA-1 during megakaryocytic differentiation and reveal that the combi

82 kl1 expression is up-regulated during murine megakaryocytic differentiation and that enforced overexp

83 the erythroid gene expression program during megakaryocytic differentiation by epigenetic repression

84 GATA1 organizes erythroid and megakaryocytic differentiation by orchestrating the expr

85 influences the balance between erythroid and megakaryocytic differentiation by shifting the balance b

86 This inhibitory effect of stroma on megakaryocytic differentiation correlates with a blockad

87 -145 and RPS14 cooperates to alter erythroid-megakaryocytic differentiation in a manner similar to th

88 adenylyl cyclase agonist forskolin inhibits megakaryocytic differentiation in a protein kinase A-dep

89 rs were subjected to stimuli known to induce megakaryocytic differentiation in erythroleukemic cells.

90 horbol 12-myristate 13-acetate (PMA)-induced megakaryocytic differentiation in human leukemia K562 ce

91 en shown to possess the potential to undergo megakaryocytic differentiation in response to a variety

92 lxL has been reported as up-regulated during megakaryocytic differentiation in vitro, but absent duri

93 found that the FPD iPSCs display defects in megakaryocytic differentiation in vitro.

94 report, we show that GPVI expression during megakaryocytic differentiation is dependent on cytosine-

95 tic progenitor cells, thrombopoietin-induced megakaryocytic differentiation led to a time and dose-de

96 and BACH1, a probable negative regulator of megakaryocytic differentiation located on chromosome 21.

97 tion, as revealed by decreased expression of megakaryocytic differentiation marker CD61 and cell cycl

98 ation in the bone marrow suggests that human megakaryocytic differentiation occurred efficiently in t

99 Induction of megakaryocytic differentiation of human erythroleukemia

100 MKL1 overexpression also promotes megakaryocytic differentiation of primary human CD34(+)

101 mediate TPO-induced proliferation arrest and megakaryocytic differentiation of the human megakaryobla

102 novel precursor population in the erythroid/megakaryocytic differentiation pathway of humans, and im

103 s the evidence supporting these nonclassical megakaryocytic differentiation pathways and consider the

104 ns in Rcor1/3 levels during erythroid versus megakaryocytic differentiation potentiate antagonistic o

105 We show here that the process of megakaryocytic differentiation requires the presence of

106 mechanism for the blockade of erythroid and megakaryocytic differentiation seen in leukemias with t(

107 vidence for P-TEFb cross-talk with GATA-1 in megakaryocytic differentiation, a program with parallels

108 es, RUNX1 and CBFbeta up-regulation preceded megakaryocytic differentiation, and down-regulation of t

109 g of PK (PKM2 and PKR) inhibited PMA-induced megakaryocytic differentiation, as revealed by decreased

110 estricted differentiation potential promoted megakaryocytic differentiation, but not granulocytic or

111 ER by estradiol overrode stromal blockade of megakaryocytic differentiation, implicating the proximal

112 was specifically associated with spontaneous megakaryocytic differentiation, in part, by activating R

113 tion factor, a master regulator of erythroid/megakaryocytic differentiation, is suppressed in the hem

114 (PMA), a PKC activator, cells exhibited full megakaryocytic differentiation, manifested by adhesion,

115 ptional activation at enhancers and promotes megakaryocytic differentiation, providing a relevant int

116 n K562 cells initiates events of spontaneous megakaryocytic differentiation, such as expression of sp

117 mic cell clones exhibited both erythroid and megakaryocytic differentiation, suggesting that transfor

118 Upon megakaryocytic differentiation, the amount of released e

119 To discover novel regulatory pathways during megakaryocytic differentiation, we performed microRNA ex

120 An example of this effect is seen with megakaryocytic differentiation, wherein stromal contact

121 as long been implicated in the repression of megakaryocytic differentiation.

122 hat enforced overexpression of MKL1 enhances megakaryocytic differentiation.

123 h confirmed contribution of Cdk9 activity to megakaryocytic differentiation.

124 n with the expression of Ets family genes in megakaryocytic differentiation.

125 nd cell lines by RNA interference suppresses megakaryocytic differentiation.

126 All of these changes are characteristics of megakaryocytic differentiation.

127 h of which have been implicated in promoting megakaryocytic differentiation.

128 high levels of hemoglobin manifested partial megakaryocytic differentiation.

129 during PMA induction, which are important in megakaryocytic differentiation.

130 is by ensuring a proper balance of erythroid/megakaryocytic differentiation.

131 macrocytic anemia, erythroid hypoplasia, and megakaryocytic dysplasia with thrombocytosis, and that p

132 further suggest that the pathways leading to megakaryocytic endomitosis and c-Myc-induced tetraploidy

133 ic differentiation and possibly for the poor megakaryocytic engraftment seen after bone marrow transp

134 eficient hematopoietic stem cells (HSCs) and megakaryocytic erythroid progenitors identified highly u

135 c stem cells throughout differentiation into megakaryocytic-erythroid and granulocytic-monocytic line

136 specialized cells that arise from a bipotent megakaryocytic-erythroid progenitor (MEP).

137 ect, restoring common myeloid progenitor and megakaryocytic-erythroid progenitor, granulocyte-monocyt

138 s), granulomonocytic progenitors (GMPs), and megakaryocytic-erythroid progenitors (MEPs).

139 etween PU.1 and GATA1 precedes and initiates megakaryocytic-erythroid versus granulocytic-monocytic l

140 At the megakaryocytic/erythroid bifurcation, the cross-antagoni

141 Megakaryocytic/erythroid progenitor (MEP) reductions in

142 yeloid progenitor (CMP) cells, as well as in megakaryocytic/erythroid progenitor cells (MEPs).

143 d mouse megakaryocytic progenitors (MPs) and megakaryocytic/erythroid progenitors (MEPs).

144 inhibits erythroid differentiation of murine megakaryocytic/erythroid progenitors and primary human C

145 There is myeloid and megakaryocytic expansion in spleen and bone marrow, an i

146 l differentiation and to inhibit myeloid and megakaryocytic expansion, it is not clear what the norma

147 oter, mHS-3.5, can direct both erythroid and megakaryocytic expression.

148 many of the transcription factors that drive megakaryocytic fate determination have been identified a

149 re-Meg/Es display dysregulated erythroid and megakaryocytic fate-determining factors including increa

150 on of blasts with biphenotypic erythroid and megakaryocytic features and contain somatic GATA1 mutati

151 bocytopenia is due to a reversible effect on megakaryocytic function rather than a direct cytotoxic e

152 In mice with megakaryocytic GATA-1 deficiency, Cdk9 inhibition produc

153 MG-GFP BAC fully recapitulated the erythroid-megakaryocytic Gata1 expression.

154 Cs: pan-myeloid (ETV2 and GATA2) and erythro-megakaryocytic (GATA2 and TAL1).

155 2 is an important regulator of erythroid and megakaryocytic gene expression.

156 the ability of glycoprotein (GP) Ibalpha, a megakaryocytic gene product, to sequester the signal tra

157 Here, the megakaryocytic gene promoter group, which consists of bo

158 The expression of megakaryocytic genes during megakaryopoiesis is controll

159 ication, and represses expression of several megakaryocytic genes including GATA-1 to block different

160 Transcription of all three megakaryocytic genes is correlated with the presence of

161 l binding sites for these factors in several megakaryocytic genes, including GPIIb, GPIX, and C-MPL.

162 stically regulate the expression of multiple megakaryocytic genes, the level of GATA-1 present on a s

163 sufficient to promote transcription of some megakaryocytic genes.

164 educed pathogenic Jak/STAT signaling by 53%, megakaryocytic hyperplasia by 70%, and the Jak2 mutant b

165 cell rimming around lymphoid aggregates, and megakaryocytic hyperplasia in a bone marrow is highly su

166 characterized by features of AMKL, including megakaryocytic hyperplasia in the spleen; impaired megak

167 processes underlying and resulting from the megakaryocytic hyperplasia that characterizes idiopathic

168 Megakaryocytic hyperplasia with abnormal features are ch

169 phenotype was characterized by splenomegaly, megakaryocytic hyperplasia, and marked thrombocythemia,

170 ive acute megakaryoblastic leukemia, confers megakaryocytic identity via the GLIS2 moiety while both

171 of two related blood lineages, erythroid and megakaryocytic, in mice.

172 During megakaryocytic induction in this system, the myeloid tra

173 Megakaryocytic induction was associated with dynamic cha

174 nderwent sustained activation as a result of megakaryocytic induction, as previously described.

175 is shown to render K562 cells refractory to megakaryocytic induction.

176 stromal blockade of ERK/MAPK signaling or of megakaryocytic induction.

177 support these observations and suggest that megakaryocytic inhibition is achieved, at least in part,

178 in K562 cells enhanced the induction of the megakaryocytic integrin proteins alphaIIb and alpha2.

179 7.5 years, respectively; P <.001), with more megakaryocytic leukemia (70% v 6%; P <.001).

180 ty to develop leukemia, in particular, acute megakaryocytic leukemia (AMkL) associated with somatic G

181 ion of mature megakaryocyte markers in acute megakaryocytic leukemia (AMKL) blasts and displayed pote

182 ptional regulation of the CBS gene in the DS megakaryocytic leukemia (AMkL) cell line, CMK, character

183 Children with Down syndrome (DS) with acute megakaryocytic leukemia (AMkL) have very high survival r

184 ts in Down syndrome (DS) children with acute megakaryocytic leukemia (AMkL) were 4.4-fold (P < .001)

185 ient myeloproliferative disease (TMD), acute megakaryocytic leukemia (AMKL), and acute lymphoid leuke

186 To characterize acute megakaryocytic leukemia (FAB M7 AML), we identified 37 p

187 esin mutations are highly prevalent in acute megakaryocytic leukemia associated with Down syndrome (D

188 We used a bcr-abl-deficient human megakaryocytic leukemia cell line MO7E and an isogenic M

189 ecule probes that induce polyploidization of megakaryocytic leukemia cells and serve as perturbagens

190 nsient myeloproliferative disorder and acute megakaryocytic leukemia in children with Down syndrome a

191 ormalities and underlies the pathogenesis of megakaryocytic leukemia in Down syndrome.

192 elp elucidate the mechanism of t(1,22) acute megakaryocytic leukemia pathogenesis, a conditional alle

193 e uniform detection of GATA1 mutations in DS megakaryocytic leukemia suggested the potential role of

194 restricted to newborns with trisomy 21, is a megakaryocytic leukemia that although lethal in some is

195 ose being the rare but uniformly fatal acute megakaryocytic leukemia type 7.

196 nique occurrence of myelodysplasia and acute megakaryocytic leukemia type 7.

197 a fusion partner in t(1;22)-associated acute megakaryocytic leukemia, is also essential for maintaini

198 ted in Mks lacking Mkl1, which is mutated in megakaryocytic leukemia, is via elevated GEF-H1 expressi

199 re congenital malformations, including acute megakaryocytic leukemia, transient myeloproliferative di

200 not only lymphoid leukemia but also erythro-megakaryocytic leukemia.

201 nsient myeloproliferative disorder and acute megakaryocytic leukemia.

202 e A (AURKA) is a therapeutic target in acute megakaryocytic leukemia.

203 and a 500-fold increased risk of developing megakaryocytic leukemia; however, the specific effects o

204 ncreased in ML-DS compared with non-DS acute megakaryocytic leukemias (AMKLs).

205 and the aberrant erythroid phenotype of the megakaryocytic leukemias of DS.

206 In a subset of human megakaryocytic leukemias, the transcription factor GATA1

207 n to the presence of few mutations was acute megakaryocytic leukemias, with the majority of these leu

208 ngs provide proof of concept that cells from megakaryocytic lineage and platelets are capable of gene

209 (cytokine signaling) transforms cells of the megakaryocytic lineage and suggest that specific targeti

210 outcome is also specific: only cells of the megakaryocytic lineage are generated.

211 phomyeloid grafts, they exhibit an intrinsic megakaryocytic lineage bias.

212 RUNX1 may participate in the programming of megakaryocytic lineage commitment through functional and

213 In contrast, the megakaryocytic lineage developed beyond the progenitor s

214 o target Piga recombination to the erythroid/megakaryocytic lineage in mice, the Cre/loxP system was

215 a myeloproliferative disorder affecting the megakaryocytic lineage observed in some patients with th

216 LOX is elevated in the megakaryocytic lineage of mouse models of MPNs and in pa

217 wn about transcription factors unique to the megakaryocytic lineage that might program divergence fro

218 In the megakaryocytic lineage, no one single unique transcripti

219 ss Cre recombinase in cells committed to the megakaryocytic lineage, to Srf(F/F) mice in which functi

220 y miR-150 as preferentially expressed in the megakaryocytic lineage.

221 nces in cell-specific gene expression in the megakaryocytic lineage.

222 llagens that is exclusively expressed in the megakaryocytic lineage.

223 previously described for HSCs extends to the megakaryocytic lineage.

224 c stem cell differentiation into the erythro-megakaryocytic lineages remain controversial.

225 ultipotent progenitors, and in erythroid and megakaryocytic lineages, consistent with roles for this

226 cells differentiated into both erythroid and megakaryocytic lineages, suggesting that they represent

227 early precursors of erythroid, myeloid, and megakaryocytic lineages, which were isolated after induc

228 distinct from that seen in the erythroid and megakaryocytic lineages.

229 on of the JAK/STAT pathway, commonly seen in megakaryocytic malignancies.

230 cell adhesion molecules, including the known megakaryocytic markers integrinbeta3 and CD44, upon diff

231 transcription factor expressed in erythroid, megakaryocytic, mast cell and eosinophil lineages.

232 in the conditional adult Runx1 null models, megakaryocytic maturation is not affected in the P1 knoc

233 based on its ability to rescue erythroid and megakaryocytic maturation of a genetically engineered FO

234 precursors with characteristics of increased megakaryocytic maturation, and the CD150(+)CD9(lo)endogl

235 on factor GATA-1 to facilitate erythroid and megakaryocytic maturation.

236 n factor required for terminal erythroid and megakaryocytic maturation.

237 can substitute for GATA1 in many aspects of megakaryocytic maturation.

238 factor GATA-1 is essential for erythroid and megakaryocytic maturation.

239 megakaryocyte progenitors as well as induces megakaryocytic maturation.

240 omponent in the highly coordinated system of megakaryocytic membrane and cytoskeletal remodeling affe

241 Megakaryocytic microparticles (MkMPs), the most abundant

242 KDAC) activities in cell lysates of the CHRF megakaryocytic (Mk) cell line.

243 shown that p53 is activated during terminal megakaryocytic (Mk) differentiation of the CHRF-288-11 (

244 to resolve myeloid (My), erythroid (Er), and megakaryocytic (Mk) fates from single CD34(+) cells and

245 tational modeling was highly suggestive of a megakaryocytic niche capable of independently influencin

246 mic fraction of differentiated granulocytic, megakaryocytic, or erythroid cells obtained from all pat

247 xpressed full-length filamin A, indicating a megakaryocytic origin.

248 SK, a process normally associated with adult megakaryocytic P-TEFb activation.

249 regulators exerts executive control over the megakaryocytic plan.

250 date have not been demonstrated in cells of megakaryocytic/platelet lineage.

251 Analysis of the mouse erythro-megakaryocytic polyadenylated lncRNA transcriptome indic

252 ryonic yolk sac (YS), which are endowed with megakaryocytic potential, differentiate into the first p

253 into blood cells with pan-myeloid or erythro-megakaryocytic potential.

254 al directional cue guiding the elongation of megakaryocytic PP extensions from the interstitium into

255 modulate the fate of a bipotential erythroid/megakaryocytic precursor cell.

256 liver of mutant mice contains erythroid and megakaryocytic precursors arrested in their development.

257 f erythroid differentiation and expansion of megakaryocytic precursors in Ezh2-deficient Jak2V617F mi

258 the proper differentiation of erythroid and megakaryocytic precursors is dependent on SCL/tal-1.

259 in hematopoietic tissues, but the numbers of megakaryocytic precursors were unchanged.

260 an T21 fetal livers contain expanded erythro-megakaryocytic precursors with enhanced proliferative ca

261 of erythroid precursors, but not myeloid or megakaryocytic precursors, and suppressed cell growth by

262 is essential for maturation of erythroid and megakaryocytic precursors, as revealed by gene targeting

263 in enhancing the expansion of fetal MEPs and megakaryocytic precursors, resulting in hepatic fibrosis

264 xed lineage colonies with both erythroid and megakaryocytic precursors.

265 ed to exclusively produce GATA1s have marked megakaryocytic progenitor (MkP) hyperproliferation durin

266 cells, we show that VEGFR-3 is expressed on megakaryocytic progenitor cells through to the promegaka

267 he origin of blood platelets; marrow-derived megakaryocytic progenitor cells were functionally define

268 directing the expression of the oncogene to megakaryocytic progenitor cells within the murine bone m

269 K-floxed mice, with significant increases in megakaryocytic progenitors (CFU-MK), mature megakaryocyt

270 feration and self-renewal of human and mouse megakaryocytic progenitors (MPs) and megakaryocytic/eryt

271 the emergence of haematopoietic and erythro-megakaryocytic progenitors and accelerated erythroid dif

272 we found significantly increased numbers of megakaryocytic progenitors and mature megakaryocytes in

273 Fetal but not adult megakaryocytic progenitors are dependent on this pathway

274 ly, knocking down either MPL/TpoR or JAK2 in megakaryocytic progenitors from patients carrying CALR m

275 rizer dependent, and myeloid, erythroid, and megakaryocytic progenitors were generated.

276 ctivity in erythroid but not granulocytic or megakaryocytic progenitors.

277 ulating the differentiation of erythroid and megakaryocytic progenitors.

278 ed with cell-autonomous expansion of erythro-megakaryocytic progenitors.

279 CD45(-) cells represent precommitted erythro-megakaryocytic progenitors.

280 nd lineage-committed myeloid, erythroid, and megakaryocytic progenitors; (2) primes SDF-1-dependent t

281 lls that are bipotent but primarily generate megakaryocytic progeny.

282 Erythropoietic and megakaryocytic programs are directed by the transcriptio

283 Erythropoietic and megakaryocytic programs are specified from multipotentia

284 brosis, and is characterized by granulocytic/megakaryocytic proliferation and lack of reticulin fibro

285 syndrome develop a unique congenital clonal megakaryocytic proliferation disorder (transient myelopr

286 It has been shown to inhibit megakaryocytic proliferation in vitro in cells obtained

287 that JAK2 and MPL expression levels regulate megakaryocytic proliferation vs differentiation in both

288 Thrombocytosis, bone marrow megakaryocytic proliferation, and presence of JAK2, CALR

289 PMF is characterized by bone marrow megakaryocytic proliferation, reticulin and/or collagen

290 , CBFbeta, and GATA-1 in the activation of a megakaryocytic promoter.

291 itment of CBP by NF-E2 to specific erythroid/megakaryocytic promoters might regulate transcription by

292 karos overexpression decreases NOTCH-induced megakaryocytic specification, and represses expression o

293 ed DAMI cells, which represent a more mature megakaryocytic state, not only lose the capacity to expr

294 by uSTAT5 reflects restricted access of the megakaryocytic transcription factor ERG to target genes.

295 eins interact with LSD1 and with the erythro-megakaryocytic transcription factor growth factor indepe

296 ded by studies of mice with mutations in key megakaryocytic transcription factors.

297 tors and ongoing mediation of common erythro-megakaryocytic transcription factors.

298 le of microRNAs in this process by targeting megakaryocytic transcription factors.

299 ere it colocalizes with CTCF and represses a megakaryocytic transcriptional program.

300 we linked the GATA1s mutation to defects in megakaryocytic upregulation of calpain 2 and of P-TEFb-d