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1 G-actin-associated transcriptional cofactor, megakaryoblastic acute leukemia factor-1 (MKL).
2 , initiation of differentiation of the human megakaryoblastic cell line CHRF-288-11 with phorbol 12-m
3 acetate (PMA)-mediated maturation of a human megakaryoblastic cell line CMK.
4                            We used the human megakaryoblastic cell line MEG-01 as an in vitro model f
5 telet-like particles (PLPs) derived from the megakaryoblastic cell line MEG-01 stimulate proliferatio
6                Restoring NF-E2 activity in a megakaryoblastic cell line or in NF-E2-deficient primary
7 ively activated Mek or Erk cDNA into a human megakaryoblastic cell line, CMK, by electroporation.
8                           In the SET-2 human megakaryoblastic cell line, heterozygous for the JAK2 V6
9 sufficient to induce differentiation in this megakaryoblastic cell line.
10       Expression of GPVI is increased in the megakaryoblastic cell lines HEL and CMK on differentiati
11 ses in human platelets as well as in several megakaryoblastic cell lines.
12                                     In human megakaryoblastic cells (MEG-01), transfection with const
13 exes from phorbol ester-induced L8057 murine megakaryoblastic cells and identified the ets transcript
14 croscopy to determine that platelets, MEG-01 megakaryoblastic cells, and bone marrow megakaryocytes c
15 row, human megakaryocytes, and MEG-01 clonal megakaryoblastic cells.
16 ate acetate (PMA)-induced differentiation of megakaryoblastic cells; NMDA receptor blockade by specif
17                                          The megakaryoblastic CHRF-288 cell line was used to investig
18 d MWNPs incorporating membranes derived from megakaryoblastic CHRF-288-11 cells, which can accumulate
19 rly changes in gene expression necessary for megakaryoblastic commitment and differentiation.
20 a cell line is bipotential for erythroid and megakaryoblastic differentiation.
21 hibition produced a fulminant but reversible megakaryoblastic disorder reminiscent of the transient m
22 sorder (age 0-24 days) and in all with acute megakaryoblastic leukaemia (age 14-38 months).
23 r transient myeloid disorder (n=10) or acute megakaryoblastic leukaemia (n=6).
24 of the mechanosensitive transcription factor megakaryoblastic leukaemia 1 (MKL1), a myocardin family
25 tations in GATA1 have been reported in acute megakaryoblastic leukaemia in Down's syndrome.
26 tions do not necessarily predict later acute megakaryoblastic leukaemia.
27  markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic
28  (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic
29 cal and biologic features of pediatric acute megakaryoblastic leukemia (AMKL) and to identify prognos
30 cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leukemia
31                              Pediatric acute megakaryoblastic leukemia (AMKL) associated with the CBF
32 actor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1.
33                                        Acute megakaryoblastic leukemia (AMKL) comprises between 4% an
34 The recurrent t(1;22) translocation in acute megakaryoblastic leukemia (AMKL) encodes the RBM15-MKL1
35 ly death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported.
36                                        Acute megakaryoblastic leukemia (AMKL) is a form of acute myel
37                                        Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise
38                                        Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise
39                                        Acute megakaryoblastic leukemia (AMKL) is a rare subtype of AM
40                                        Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m
41                                        Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m
42                                        Acute megakaryoblastic leukemia (AMKL) is more frequently obse
43 of pediatric non-Down's syndrome (DS), acute megakaryoblastic leukemia (AMKL), a malignancy with poor
44 ndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expre
45 eukemia that closely phenocopied human acute megakaryoblastic leukemia (AMKL), reflected by flow cyto
46              TMD may be a precursor to acute megakaryoblastic leukemia (AMKL), with an estimated 30%
47  is a key event in the pathogenesis of acute megakaryoblastic leukemia (AMKL).
48 ), and 20% to 30% of those progress to acute megakaryoblastic leukemia (AMKL).
49 clonal preleukemia, and/or who develop acute megakaryoblastic leukemia (AMKL).
50 trisomic for Hsa21, are predisposed to acute megakaryoblastic leukemia (AMKL).
51  myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL).
52 myeloproliferative disorder (TMD), and acute megakaryoblastic leukemia (AMKL).
53 k of developing leukemia, particularly acute megakaryoblastic leukemia (AMKL).
54 es of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns present wi
55  in the vast majority of patients with acute megakaryoblastic leukemia (DS-AMKL) and in nearly every
56 drome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the related tran
57 striction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized by th
58  of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL).
59 ative disorder (TMD) and Down syndrome-acute megakaryoblastic leukemia (DS-AMKL).
60 ttention as a candidate oncogene in DS-acute megakaryoblastic leukemia (DS-AMKL).
61 ed transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M
62  syndrome with erythroid features, and acute megakaryoblastic leukemia (FAB M7) and are characterized
63                                              Megakaryoblastic leukemia (MKL)/serum-response factor (S
64 mutation spectrum in non-Down syndrome acute megakaryoblastic leukemia (non-DS-AMKL), we performed tr
65 um response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased express
66                                              Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate
67                                              Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate
68 utrophil immunodeficiency disorder caused by megakaryoblastic leukemia 1 (MKL1) mutation.
69                                              Megakaryoblastic leukemia 1 (MKL1) promotes the regulati
70 ocytosis of ACs by splenic MZMs required the megakaryoblastic leukemia 1 (MKL1) transcriptional coact
71                                    Moreover, megakaryoblastic leukemia 1 (MKL1), a well-known actor i
72                                              Megakaryoblastic leukemia 1 (MKL1), also known as MAL or
73                                              Megakaryoblastic leukemia 1 (MKL1), identified as part o
74 and a mechanosensitive transcription factor, megakaryoblastic leukemia 1 (MKL1), that coordinately re
75 ctivation of the transcriptional coactivator megakaryoblastic leukemia 1 (MKL1), which targets the se
76 regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocard
77 in-related protein 2/3 complex subunit 1B or megakaryoblastic leukemia 1 deficiency also failed to sh
78  protein 15 (RBM15) is involved in the RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryobla
79 long noncoding RNA called inflammatory MKL1 (megakaryoblastic leukemia 1) interacting long noncoding
80 Z macrophages (MZMs), which in turn disrupts megakaryoblastic leukemia 1-mediated (MKL1-mediated) mec
81 in)-box transcriptional co-regulator, Mkl-1 (megakaryoblastic leukemia [translocation] 1).
82 ignificant proportion of children with acute megakaryoblastic leukemia acquire a translocation that c
83 of hematologic malignancies, including acute megakaryoblastic leukemia and a subset of myeloprolifera
84 wn syndrome (DS) have had significantly more megakaryoblastic leukemia and have experienced better ou
85       JAK inhibitors are selective for acute megakaryoblastic leukemia and significantly prolong surv
86                          MEG-01 is the human megakaryoblastic leukemia cell line that can be differen
87  megakaryocytic differentiation of the human megakaryoblastic leukemia cell line UT7-MPL.
88 of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leukemia cell line, led to an induction
89  BCL2 or MCL1, for the survival of erythroid/megakaryoblastic leukemia cell lines.
90 toclax as highly effective against erythroid/megakaryoblastic leukemia cell lines.
91 ty of myocardin to physically associate with megakaryoblastic leukemia factor-1 (MKL1) and characteri
92 d possibly increasing ability to distinguish megakaryoblastic leukemia from lymphoid leukemia.
93 formed by the t(1;22) translocation of acute megakaryoblastic leukemia had a markedly increased abili
94 hildren with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that
95 proliferative disease (MPD) with features of megakaryoblastic leukemia in a murine transplant model.
96 sregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down syndrome
97 to identify chromosome 21 genes that promote megakaryoblastic leukemia in children with DS.
98 ons in which several members developed acute megakaryoblastic leukemia in early childhood.
99 o cooperate with GATA1 mutations to initiate megakaryoblastic leukemia in vivo.
100                                        Acute megakaryoblastic leukemia of Down syndrome (DS-AMKL) is
101  platelet counts, more antecedent MDS, acute megakaryoblastic leukemia or undifferentiated AML, and a
102 ranscription factor A (Mrtfa), also known as megakaryoblastic leukemia protein (Mkl1/MAL), associates
103 ethod to gene expression profiling for acute megakaryoblastic leukemia shows that our method detects
104 ablish a model of CBFA2T3-GLIS2 driven acute megakaryoblastic leukemia that allows the distinction of
105 s a fusion oncogene found in pediatric acute megakaryoblastic leukemia that is associated with a poor
106                                              Megakaryoblastic leukemia was unfavorable in others but
107 ies that human GATA1 mutations promote acute megakaryoblastic leukemia, a clonal malignancy with feat
108 s part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in
109 nuclear abundance of transcription cofactor, megakaryoblastic leukemia, and protein levels of its tar
110 oprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic identi
111  the t(1;22) translocation specific to acute megakaryoblastic leukemia, is highly expressed in differ
112 cation involving 14 cases of pediatric acute megakaryoblastic leukemia, MIST more robustly identified
113 ing pediatric Down syndrome-associated acute megakaryoblastic leukemia, myelodysplastic syndromes, ch
114 t t(1;22) chromosomal translocation in acute megakaryoblastic leukemia, the mechanisms by which MRTFA
115 contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative
116 er preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or quali
117 g gene with homology to Drosophila spen, and Megakaryoblastic Leukemia-1 (MKL1), a gene encoding an S
118 ogic disruption of the transcription factors megakaryoblastic leukemia-1 (MKL1)/serum response factor
119 ocardin and the related transcription factor megakaryoblastic leukemia-1 (MKL1/MAL/MRTF-A) can strong
120 n the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1 and MKL2) and t
121 ctin polymerization, nuclear accumulation of megakaryoblastic leukemia-1 protein, and SRF activation.
122 ansient myeloproliferative disease and acute megakaryoblastic leukemia.
123 nsient myeloproliferative disorder and acute megakaryoblastic leukemia.
124 e disorder, and increased incidence of acute megakaryoblastic leukemia.
125 in the pathogenesis of trisomy 21-associated megakaryoblastic leukemia.
126 -megakaryoblastic leukemia 1 fusion in acute megakaryoblastic leukemia.
127 th MKL in the t(1;22) translocation of acute megakaryoblastic leukemia.
128 L as a potential therapy option in erythroid/megakaryoblastic leukemias and highlight an AML subgroup
129 tomics of patient samples with erythroid and megakaryoblastic leukemias identified high BCL2L1 expres
130 ;22) is the principal translocation of acute megakaryoblastic leukemias.
131 ally, we compared the microRNA expression of megakaryoblastic leukemic cell lines with that of in vit
132 Genetic and pharmacological studies in human megakaryoblastic MEG-01 cells showed that DREAM is impor
133 horylation-regulated kinase 1A, was a potent megakaryoblastic tumor-promoting gene that contributed t
134             In contrast, tie-1 expression on megakaryoblastic UT-7 cells was unaffected by PMA or TNF

 
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