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1 -alpha partially and transiently rescued the myeloid and lymphoid abnormalities found in NHD13(+) Tg
2 s are accumulated to the same degree in both myeloid and lymphoid acute leukemia cells, paralleling t
3 ermediates correlated with the levels of the myeloid- and lymphoid-associated transcription factors m
4 giving rise to progenitors that initiate the myeloid and lymphoid branches of hematopoiesis.
5 ies for therapeutic intervention in specific myeloid and lymphoid cancers.
6 igher in treated pups than in controls; both myeloid and lymphoid cell chimerism increased because of
7 evere pulmonary inflammation, with increased myeloid and lymphoid cell infiltration.
8   These results show that FL can affect both myeloid and lymphoid cell lineages in vivo and further d
9 in long-term allogeneic repopulation of both myeloid and lymphoid cell lineages were observed in reci
10 -sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph
11 ly activated in both transiently transfected myeloid and lymphoid cell lines by the 80-bp gene fragme
12  the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell ly
13 ctin ligands on granulocytes, monocytes, and myeloid and lymphoid cell lines, and not on peripheral b
14  levels of adenosine-metabolizing enzymes in myeloid and lymphoid cell lines.
15  HFV productively infects a variety of human myeloid and lymphoid cell lines.
16                                  Circulating myeloid and lymphoid cell populations were increased two
17 tect clonal cytogenetic markers in different myeloid and lymphoid cell types of the peripheral blood
18  autophagy contributes to differentiation of myeloid and lymphoid cell types, coordinates multicellul
19 tile adults with a full immune complement of myeloid and lymphoid cell types.
20 ilure, and to patients with aplastic anemia, myeloid, and lymphoid cell malignancies.
21 ession, thereby providing protection to both myeloid and lymphoid cells against L. monocytogenes-indu
22 es with Imatinib against BCR/ABL-transformed myeloid and lymphoid cells and increases survival in a m
23 ude that CD45 is regulated differentially in myeloid and lymphoid cells and that sequences critical t
24                                       Mature myeloid and lymphoid cells as well as immunoglobulins be
25                                              Myeloid and lymphoid cells as well as intestinal epithel
26 etected constitutively in both primary human myeloid and lymphoid cells by Northern blot hybridizatio
27 ctional data, EMSA demonstrated that in both myeloid and lymphoid cells C/EBPbeta binds specifically
28 monstrated significantly higher infiltrating myeloid and lymphoid cells compared with GBM, MED, or NT
29 lity to shape the transcriptome of activated myeloid and lymphoid cells controlling diverse biologica
30                     Expression signatures in myeloid and lymphoid cells demonstrated that HOXA9 funct
31 to the same cellular chromosomal DNA site in myeloid and lymphoid cells descended from a common HSC p
32 tat5 in maintaining a normal balance between myeloid and lymphoid cells during hematopoiesis, and we
33                                Generation of myeloid and lymphoid cells from progenitors involves dyn
34 gainst wild-type cells in the development of myeloid and lymphoid cells in in vivo reconstitution ass
35 er 21 to 413 days, percentages of donor type myeloid and lymphoid cells in recipient blood were measu
36 reased L. monocytogenes-induced apoptosis of myeloid and lymphoid cells in the spleen that are requir
37 dicating that FcgammaRIIb expression on both myeloid and lymphoid cells is regulated by the naturally
38                                 Furthermore, myeloid and lymphoid cells likely synergize to promote o
39 y, PU.1(-/-) mice that are unable to develop myeloid and lymphoid cells received bone marrow transpla
40 thro-myeloid cells and pre-B cells, and both myeloid and lymphoid cells seem to be derived from the C
41   Transient transfection experiments in both myeloid and lymphoid cells showed an increase in CCR5 pr
42 higher level of chimerism and generated both myeloid and lymphoid cells that contained molecular or c
43  microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeosta
44 ilized CD34(+) cells with Neo(R) gene marked myeloid and lymphoid cells up to 32 months after transpl
45 rd distinct HLA type and donor and recipient myeloid and lymphoid cells were identified after 8 to 10
46 have a potential to differentiate in vivo to myeloid and lymphoid cells, and (4) have a high prolifer
47               CD300a is broadly expressed on myeloid and lymphoid cells, and its expression is differ
48 as been shown in a wide range of circulating myeloid and lymphoid cells, but their role in normal hem
49 lement receptors (CRs), expressed notably on myeloid and lymphoid cells, play an essential function i
50 oduction of TNF-alpha and IFN-gamma by liver myeloid and lymphoid cells, respectively.
51 ool of NF-kappaB transcriptional activity in myeloid and lymphoid cells, which is believed to be seco
52 ion, MN1-TEL expression was detected in both myeloid and lymphoid cells.
53 an essential role in the development of both myeloid and lymphoid cells.
54 lity to chromosomal damage may exist between myeloid and lymphoid cells.
55 Cs that gave rise stably to skewed ratios of myeloid and lymphoid cells.
56 stem and progenitor cells, as well as mature myeloid and lymphoid cells.
57  mouse displays recombinase activity in both myeloid and lymphoid cells.
58 s virtually identical in all types of mature myeloid and lymphoid cells.
59 n, lineage-committed progenitors, and mature myeloid and lymphoid cells.
60 ily of nuclear receptors and is expressed in myeloid and lymphoid cells.
61 t retain the potential to differentiate into myeloid and lymphoid cells.
62 ntiate within teratomas to derive functional myeloid and lymphoid cells.
63  macrophages, with partial deletion in other myeloid and lymphoid cells.
64  that control the production and function of myeloid and lymphoid cells.
65 ration, proliferation and differentiation of myeloid and lymphoid cells.
66  regulation of growth and differentiation of myeloid and lymphoid cells.
67 eptor-SFK-Syk signalling events in mammalian myeloid and lymphoid cells.
68                 The generation of erythroid, myeloid, and lymphoid cells from human fetal liver proge
69 rsors plus a complex mixture of mesenchymal, myeloid, and lymphoid cells in the marrow space.
70 highly proliferating and serially replatable myeloid and lymphoid colony-forming cultures could be es
71 These cells are believed to derive from both myeloid- and lymphoid-committed precursors.
72 tential hematopoietic stem cells into common myeloid- and lymphoid-committed progenitors establishes
73 IFN production develop efficiently from both myeloid- and lymphoid-committed progenitors.
74   In addition, evidence for the existence of myeloid and lymphoid DC lineages and their different fun
75 (i) reduces the numbers of Langerhans cells, myeloid and lymphoid DC, and activated CD4(+) T cells in
76 g the yield of plasmacytoid and conventional myeloid and lymphoid DC.
77 ombinant Adv readily targets transduction of myeloid and lymphoid DCs in the draining popliteal lymph
78 ch resulted in depletion of 88-95% of mature myeloid and lymphoid DCs, with less depletion (75%) of p
79 ription factor binding sites associated with myeloid- and lymphoid-derived cell types.
80 ha transgenic reporter was activated in both myeloid- and lymphoid-derived PDCs at a level comparable
81 s well as RAG transcripts were found in both myeloid- and lymphoid-derived PDCs.
82  is known about the function of FOG-1 during myeloid and lymphoid development or how FOG-1 expression
83 rmal and malignant processes associated with myeloid and lymphoid development.
84 ion factor PU.1, is indispensable for normal myeloid and lymphoid development.
85 (Spi-1) is a well-characterized regulator of myeloid and lymphoid development.
86 factors and signaling components involved in myeloid and lymphoid development.
87 ineage competency factors to facilitate both myeloid and lymphoid developmental programs.
88 controlling hematopoietic stem cell biology, myeloid and lymphoid differentiation and lymphocyte effe
89                           However, long-term myeloid and lymphoid differentiation is compromised beca
90  CD14+ and CD7+ cells, consistent with early myeloid and lymphoid differentiation, respectively.
91 now know that Gfi1 is primarily important in myeloid and lymphoid differentiation, whereas Gfi1b is c
92 eukemia fusion protein CBFbeta-SMMHC impairs myeloid and lymphoid differentiation.
93  haematopoietic stem cells (HSCs) as well as myeloid and lymphoid differentiation.
94  protein CBFbeta-SMMHC (CM) known to disrupt myeloid and lymphoid differentiation.
95  Our data indicate that Cbfb is required for myeloid and lymphoid differentiation; but does not play
96                                              Myeloid and lymphoid diseases arise from transformed mur
97 d infiltrating hematopoietic cells including myeloid and lymphoid elements that impact tumor growth,
98 onal maturation of promyelocytes (erythroid, myeloid, and lymphoid [EML]-derived promyelocytes) deriv
99 tment because recipients displayed increased myeloid and lymphoid engraftment and because sunitinib-t
100 bust (>80% human chimerism) and reproducible myeloid and lymphoid engraftment, with T cells arising 1
101 s, and sunitinib enhanced marrow, peripheral myeloid, and lymphoid engraftment after BMT in Rag1(-/-)
102  well as hematopoietic genes; MPPs coexpress myeloid and lymphoid genes; CMPs coexpress myeloerythroi
103 essor that plays a critical role during both myeloid and lymphoid haematopoietic lineage commitment.
104  are involved in the pathogenesis of several myeloid and lymphoid hematological malignancies.
105 ry progenitors that can reinitiate long-term myeloid and lymphoid hematopoiesis in vitro.
106 econdary and tertiary recipients, as well as myeloid and lymphoid hematopoietic progenitor subsets an
107  proinflammatory cytokine that interconnects myeloid and lymphoid host defense.
108 d temporal and spatial relationships between myeloid and lymphoid immune responses in wild-type C57BL
109 ng via the G protein-coupled receptor G2A on myeloid and lymphoid inflammatory cells.
110 umor antigen that is aberrantly expressed in myeloid and lymphoid leukemia and in this issue of Blood
111 granulate when challenged with primary acute myeloid and lymphoid leukemia blasts; and (5) Vdelta2 ce
112 ng the equivalent cytotoxicity found between myeloid and lymphoid leukemia cell lines.
113 hnique to compare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at l
114 echanism by which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate t
115 mosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner gen
116 mosomal translocations associated with acute myeloid and lymphoid leukemia.
117 contribute to a selective GVL effect against myeloid and lymphoid leukemias after F-->M HSCT.
118 paB to the pathogenesis of BCR-ABL1-positive myeloid and lymphoid leukemias are unknown.
119  plays distinct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, vali
120  rapid death of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytot
121 r proliferation of malignant clones in acute myeloid and lymphoid leukemias.
122  a rational combination for the treatment of myeloid and lymphoid leukemias.
123  epitope is presented on the surface of both myeloid and lymphoid leukemic cells from male HLA-B*2705
124       Expression of DDX3Y is detected in all myeloid and lymphoid leukemic cells that carry an intact
125 ALL, we show here that GAB2 is essential for myeloid and lymphoid leukemogenesis by BCR-ABL1.
126 mportance of the Bcr/Abl-Grb2 interaction to myeloid and lymphoid leukemogenesis in vivo is unclear.
127  opposing functions of CEBP dysregulation in myeloid and lymphoid leukemogenesis.
128 ich P2X(7)R signaling occurs differs between myeloid and lymphoid leukocytes.
129 quent genetic changes in infant leukemias of myeloid and lymphoid lineage and in treatment-induced se
130 ith the capacity to produce normal levels of myeloid and lymphoid lineage cells.
131 PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutel
132 miR-17-92-overexpressing mice are capable of myeloid and lymphoid lineage differentiation, and recapi
133  with diverse potencies and can give rise to myeloid and lymphoid lineage progenitors.
134 tern in that it is expressed on cells of the myeloid and lymphoid lineage, suggesting that it plays a
135 lineage short-term progenitors reconstituted myeloid and lymphoid lineages at 1 month but were suppla
136 he hematopoietic flow from stem cells toward myeloid and lymphoid lineages during development and adu
137  of cytokines to induce differentiation into myeloid and lymphoid lineages following AAV infection, t
138 ematopoietic development with segregation of myeloid and lymphoid lineages from multipotent progenito
139 ent), compared with negligible expression in myeloid and lymphoid lineages in blood, BM, spleen, and
140 lta/Delta) HSCs contributed normally to both myeloid and lymphoid lineages in both primary and second
141 ells and are able to differentiate into both myeloid and lymphoid lineages in vitro.
142        Multipotential clones contributing to myeloid and lymphoid lineages were identified.
143 tained these high transduction levels in all myeloid and lymphoid lineages, including early progenito
144  characterized by a maturation arrest in the myeloid and lymphoid lineages, leading to early onset, r
145 of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone m
146 ntiate into more specific progenitors of the myeloid and lymphoid lineages, ultimately leading to dif
147 plasma cells), and that tumors arise in both myeloid and lymphoid lineages.
148 tion (CD) antigens are expressed on cells of myeloid and lymphoid lineages.
149 ewal as well as commitment and maturation of myeloid and lymphoid lineages.
150 enitor cells (HPCs) and fully differentiated myeloid and lymphoid lineages.
151 velopment of XSCID CD34(+) cells into mature myeloid and lymphoid lineages.
152  establishes an early separation between the myeloid and lymphoid lineages.
153 arranged in acute human leukemia of both the myeloid and lymphoid lineages.
154 has only been previously demonstrated in the myeloid and lymphoid lineages.
155 on of hematopoietic stem cells (HSCs) to the myeloid and lymphoid lineages.
156 ting primarily to myeloid, lymphoid, or both myeloid and lymphoid lineages.
157 inhibits activation signals on cells of both myeloid and lymphoid lineages.
158 itor cells (HSPCs) and mature cells from the myeloid and lymphoid lineages.
159 ould have to arise before the bifurcation to myeloid and lymphoid lineages.
160  into the erythroid lineage but not into the myeloid and lymphoid lineages.
161 tment, self-renewal and differentiation into myeloid and lymphoid lineages; however, the proper diffe
162 gests that the segregation of the erythroid, myeloid, and lymphoid lineages may not always be an earl
163 s confer a graft-versus-malignancy effect in myeloid and lymphoid malignancies and in metastatic rena
164 elapse rates, whereas patients with advanced myeloid and lymphoid malignancies had high relapse rates
165          In contrast, patients with advanced myeloid and lymphoid malignancies had rates of more than
166 igning improved strategies for treating both myeloid and lymphoid malignancies in this high-risk popu
167 neral terms, we review specific use cases in myeloid and lymphoid malignancies to highlight the utili
168 , we review recent major genetic advances in myeloid and lymphoid malignancies, the impact of these f
169 ked to plasma cell abnormalities, as well as myeloid and lymphoid malignancies.
170 es inactivating mutations in a wide range of myeloid and lymphoid malignancies.
171 rtilization, as well as normal expression of myeloid and lymphoid markers.
172  These data suggest that Delta-1 can enhance myeloid and lymphoid marrow-repopulating ability and pro
173 ors induce differentiation and cell death in myeloid and lymphoid model systems.
174                                              Myeloid and lymphoid neoplasm associated with FGFR1 is a
175 cation recognizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abn
176 sive molecular disease detection in selected myeloid and lymphoid neoplasms, with a focus on the curr
177 y developed hematologic malignancies of both myeloid and lymphoid origin with myeloid malignancies di
178 uently rearranged in human leukemias of both myeloid and lymphoid origin, encodes a member of the Ets
179  mononuclear cells (PBMCs) and cell lines of myeloid and lymphoid origin.
180 1a regulates hematopoietic stem cells (HSC), myeloid and lymphoid populations, while its paralog, Gfi
181 tentiality is conserved until segregation of myeloid and lymphoid potential has recently been challen
182 bone marrow progenitor cells with a combined myeloid and lymphoid potential.
183                                              Myeloid and lymphoid potentials are present at the clona
184 gen expression leads to reduced apoptosis of myeloid and lymphoid progenitor cells, and a propensity
185 gand to primitive hematopoietic cells and to myeloid and lymphoid progenitor cells, in contrast to th
186 ar result was obtained with specified common myeloid and lymphoid progenitor cells.
187 h the MegE potential of downstream committed myeloid and lymphoid progenitors and with their ability
188 ndritic cells (DCs) can be derived from both myeloid and lymphoid progenitors in vivo.
189 asts alters the differentiation potential of myeloid and lymphoid progenitors leading to development
190 NA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-X(L) and Bcl-2
191  differential capacity to generate committed myeloid and lymphoid progenitors, and diminished lymphoi
192 ved lineage-specific DNA methylation between myeloid and lymphoid progenitors, characterized immature
193 nt HSCs also failed to generate the earliest myeloid and lymphoid progenitors.
194                     DC can develop from both myeloid and lymphoid progenitors.
195  required for the proper development of both myeloid and lymphoid progenitors.
196 ineage precursors were bipotential, yielding myeloid and lymphoid progeny, whereas most that were c-k
197 ings implicate MyD88 as the key initiator of myeloid and lymphoid proliferation in HLH, and suggest t
198 JL/J) and recipients (BALB/c) contributed to myeloid and lymphoid reconstitution.
199                          To directly compare myeloid and lymphoid recovery using an animal model of b
200 f cord blood transplantation is the delay in myeloid and lymphoid recovery.
201 plasmacytoid DC was similar to that of liver myeloid and lymphoid-related DC.
202 s a heterogeneous population containing both myeloid- and lymphoid-related DC.
203 n of CD11b, which may represent the putative myeloid- and lymphoid-related subsets.
204 rn blood, liver, and spleen, were assayed as myeloid and lymphoid repopulating abilities relative to
205                  (4) Mutual exclusiveness of myeloid and lymphoid support in that a given stromal cel
206 s support a role for relative proportions of myeloid and lymphoid transcripts in tuberculosis outcome
207 fectors that propagate the signal to promote myeloid and lymphoid transformation.
208 we focus on the role of such lesions in both myeloid and lymphoid tumors.
209 ore can cooperate in the development of both myeloid and lymphoid tumors.

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