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1 vents the expansion of Nras(G12D/+) HSCs and myeloid progenitors.
2 rentiation skewing of multipotent and common myeloid progenitors.
3 gh estrogen receptor (ER) alpha signaling in myeloid progenitors.
4 PU.1 and induces malignant reprogramming of myeloid progenitors.
5 gulatory factor (IRF)-4 in GM-CSF-stimulated myeloid progenitors.
6 ctor signaling or increased proliferation in myeloid progenitors.
7 ost related to haematopoietic stem cells and myeloid progenitors.
8 cell virus vectors and assayed the growth of myeloid progenitors.
9 f monocytes over neutrophils at the level of myeloid progenitors.
10 cell progeny concomitant with an increase in myeloid progenitors.
11 d shortly after Setbp1 expression in primary myeloid progenitors.
12 n granulocyte-monocyte progenitors or common myeloid progenitors.
13 d expansion of undifferentiated cells in 32D myeloid progenitors.
14 ation of hematopoietic stem cells (HSCs) and myeloid progenitors.
15 d myeloid-related genes could be detected in myeloid progenitors.
16 d of culture and an additional 2 d to expand myeloid progenitors.
17 not required for the proliferation of early myeloid progenitors.
18 ssential for neutrophil differentiation from myeloid progenitors.
19 confer aberrant self-renewing properties to myeloid progenitors.
20 nditionally deleted Nemo from osteoclast and myeloid progenitors.
21 ocyte precursors and results in depletion of myeloid progenitors.
22 suppressor cells (mMDSC) from human or mouse myeloid progenitors.
23 enitors settling the thymus include lymphoid-myeloid progenitors.
24 escence with concomitant expansion of murine myeloid progenitors.
25 sed sensitivity to DNA damage in bone marrow myeloid progenitors.
26 egulation of PtdIns(3,4,5)P3 signaling in BM myeloid progenitors.
27 matopoietic function of ICL-repair deficient myeloid progenitors.
28 of the entire hematopoietic tree, including myeloid progenitors.
29 yeloid-derived suppressor cells (MDSCs) from myeloid progenitors.
30 row by inducing differentiation of committed myeloid progenitors.
31 ortality, self-renewal, and tumorigenesis in myeloid progenitors.
33 sult from the endothelial differentiation of myeloid progenitors, a process regulated by tumor necros
34 ependent-1 (Gfi1) loss of function, arrested myeloid progenitors accumulate, whereas terminal granulo
36 PA re-activated replating activity of common myeloid progenitor and granulocyte macrophage progenitor
37 the progenitor cell defect, restoring common myeloid progenitor and megakaryocytic-erythroid progenit
39 xhibit a decrease in myeloid-biased HSCs and myeloid progenitors and an increase in T cells and lymph
40 of the haematopoietic system, such as common myeloid progenitors and common lymphoid progenitors, inc
41 oter in vitro, and in vivo within both early myeloid progenitors and differentiating neutrophils.
43 uction of myeloid lineage precursors (common myeloid progenitors and granulocyte myeloid precursors)
44 on assays and defective in generating common myeloid progenitors and granulocyte-monocyte progenitors
45 ment of myeloid precursors, including common myeloid progenitors and granulocytic-monocytic precursor
48 reactive granulopoiesis," in which committed myeloid progenitors and more primitive progenitors cycle
52 Myeloid-derived suppressor cells (MDSCs) are myeloid progenitors and precursors that fail to differen
53 rs when IFN-gamma inhibits the generation of myeloid progenitors and prevents lineage differentiation
55 -derived suppressor cells (MDSCs) arise from myeloid progenitors and suppress both innate and adaptiv
56 hromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin struc
58 g the commitment of short-term HSC to common myeloid progenitors and these alterations were predomina
61 ing lineage(-)Sca-1(+)c-kit(+) (LSK), common myeloid progenitor, and granulocyte/macrophage progenito
62 ctivation of ERK, excessive proliferation of myeloid progenitors, and consequently an acute myeloprol
63 n of immature lineage-negative cells, common myeloid progenitors, and granulocyte/macrophage progenit
64 icant reduction of HSCs, common lymphoid and myeloid progenitors, and lymphoid cell populations in th
65 human long-term HSC, short-term HSC, common myeloid progenitors, and megakaryocyte-erythrocyte proge
66 rythrocyte progenitors, a decrease in common myeloid progenitors, and reduced beta-catenin signaling
67 onal repressors for the survival of CD11b(+) myeloid progenitors, and then they are required as activ
70 ly, both Flt3(+)CD150(-) and Flt3(-)CD150(-) myeloid progenitors are susceptible to Notch1-mediated T
71 an increase in the proportions of committed myeloid progenitors, as determined by colony-forming uni
73 topoiesis and highlights PN as a disorder of myeloid progenitors associated with bone marrow dysfunct
74 to the phenotype, stem cell marker CD34 and myeloid progenitor-associated antigen CD13 were analyzed
75 nt DC development from multiple lymphoid and myeloid progenitors autonomously of cellular context.
76 successful establishment of HCMV latency in myeloid progenitors begins at the point of virus entry.
77 s in acquisition of self-renewal capacity by myeloid progenitors, biased myeloid differentiation, and
78 mpartment, consisting of depletion of common myeloid progenitors but relative sparing of granulocyte-
79 he accumulation and lineage specification of myeloid progenitors, but not terminal granulopoiesis.
80 f normal hematopoiesis, that the loss of MDS myeloid progenitors by programmed cell death and program
81 studies identified autocrine stimulation of myeloid progenitors by Tgfbeta2 as one mechanism by whic
83 oreover, ectopic miR-223 expression in human myeloid progenitors causes heterochromatic repression of
84 eletion of 2 alleles of p53 rescued both the myeloid progenitor cell and long-term hematopoietic stem
85 y increases atherogenesis through regulating myeloid progenitor cell expansion and differentiation, f
87 n of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and
88 ivation of STAT3-p27(Kip1) pathway in murine myeloid progenitor cell line 32D-G-CSFR cells was marked
89 phages, and ectopic expression of VentX in a myeloid progenitor cell line triggered its differentiati
90 o more pronounced suppression of bone marrow myeloid progenitor cell proliferation and monocytosis, a
91 G-CSF signaling in the regulation of marrow myeloid progenitor cell proliferation in mice with Strep
94 ation of hematopoietic stem cells (HSCs) and myeloid progenitor cells (MPCs) has been shown to mediat
95 induces a select set of micro-RNAs (miR) in myeloid progenitor cells and AML patients with t(8;21).
96 (MDS) at 24 months of age, with dysplasia of myeloid progenitor cells and anemia with abnormal circul
97 ignaling pathway, we observed an increase in myeloid progenitor cells and CDllb(lo)Gr1(lo) promyelocy
98 expression of HoxA10 is maximal in committed myeloid progenitor cells and decreases as differentiatio
99 GF2 promoter that are activated by HoxA10 in myeloid progenitor cells and differentiating phagocytes.
100 AcmvIL-10 during latent infection of primary myeloid progenitor cells and found that LAcmvIL-10 is re
102 support interleukin-3-independent growth of myeloid progenitor cells and long-term outgrowth of B-ly
103 survival of preleukemic short-term HSCs and myeloid progenitor cells and maintains the differentiati
104 is also expressed during latent infection of myeloid progenitor cells and monocytes and facilitates p
105 OPN (iOPN) diminished the population size of myeloid progenitor cells and myeloid cells, and secreted
106 romoted the outgrowth of Ly6C(+) and Ly6G(+) myeloid progenitor cells and their mobilization to tumor
107 all RNAs, termed microRNAs, encoded by human myeloid progenitor cells are capable of repressing a key
108 tro phenotypes observed with loss of Gfi1 in myeloid progenitor cells but did not rescue Gfi1-/- bloc
109 air of our bones are formed from bone marrow myeloid progenitor cells by a complex differentiation pr
110 interleukin-6 receptor (IL-6R) expression on myeloid progenitor cells by Delta-1 treatment combined w
112 neovasculogenesis and that CD133(+)CXCR4(+) myeloid progenitor cells directly participate in new blo
116 d expression of Fap1 and Gas2 in bone marrow myeloid progenitor cells from Icsbp(-/-) mice in compari
118 LHRHa), increases the number of lymphoid and myeloid progenitor cells in the bone marrow and developi
119 ncer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secre
120 itment of bone marrow-derived CD11b(+)Gr1(+) myeloid progenitor cells in the premetastatic lungs.
122 lso determined that HoxA10 overexpression in myeloid progenitor cells increased Tgfbeta2 production b
123 on of the CML-related Bcr-abl oncoprotein in myeloid progenitor cells increases expression of Fas-ass
124 sed Fgf2 production by HoxA10-overexpressing myeloid progenitor cells induced a phosphoinositol 3-kin
125 We determined that expression of Mll-Ell in myeloid progenitor cells resulted in autocrine productio
126 wth factor 2 (Fgf2) by HoxA10-overexpressing myeloid progenitor cells results in activation of beta-c
128 ed that differentiation of latently infected myeloid progenitor cells to dendritic or macrophage-like
129 Mcl1 facilitates AML development by allowing myeloid progenitor cells to evade Myc-induced cell death
130 JMML is acquired hypersensitivity by clonal myeloid progenitor cells to granulocyte macrophage-colon
131 nal activators involved in the commitment of myeloid progenitor cells to the DC lineage and predicted
133 and colleagues examine deletion of Dicer1 in myeloid progenitor cells using a conditional Cebpa-Cre a
135 marily attributable to autonomous defects in myeloid progenitor cells, although the hematopoietic mic
136 pa was associated with a marked reduction in myeloid progenitor cells, and Gabpalpha null myeloid cel
137 and survival of hematopoietic stem cells and myeloid progenitor cells, and increased Fgf2-expression
138 that HoxA9 repressed ARIH2 transcription in myeloid progenitor cells, antagonizing the effect of Hox
139 ted C57BL/6 mice, we observed a reduction in myeloid progenitor cells, as defined both phenotypically
140 s, we demonstrated that AML EVs are taken-up myeloid progenitor cells, resulting in the selective pro
141 of p53 in limiting aberrant self-renewal of myeloid progenitor cells, such that loss of p53 counters
142 oxidase (MPO), an enzyme found in developing myeloid progenitor cells, the likely origin for myeloid
143 ucing transcription factors IRF8 and PU.1 in myeloid progenitor cells, whereas it reduces G-CSF-drive
162 vere anemia and thrombocytopenia and expands myeloid-progenitor cells, indicating that FOG-1 is requi
163 y elevated frequencies and numbers of common myeloid progenitor (CMP) and granulocyte/macrophage prog
164 -associated molecular patterns by the common myeloid progenitor (CMP) and is dependent on type I IFN
165 s classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing t
166 the developmental defect of DCs from common myeloid progenitor (CMP) in Mysm1(-/-) mice is associate
167 In Dhh-deficient bone marrow, the common myeloid progenitor (CMP) population was increased, but d
169 ved common lymphoid progenitor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progen
171 common lymphoid progenitors (CLP) or common myeloid progenitors (CMP) during this process remains el
173 )Sca-1(+)c-Kit(+)CD34(+)Flt3(hi)) and common myeloid progenitors (CMPs) (Lin(-)Sca-1(+)c-Kit(+)CD34(+
175 hematopoietic progenitor stem cells, common myeloid progenitors (CMPs) and granulocyte-macrophage pr
176 ther myeloid progenitor compartments [common myeloid progenitors (CMPs) and granulocyte/monocyte prog
177 as an ATM-independent function in the common myeloid progenitors (CMPs) by deletion of Atmin in the e
180 opulations are thought to derive from common myeloid progenitors (CMPs), and a hierarchical relations
181 ouse hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), and erythroblasts (ERYs).
182 ) mice revealed that short-term HSCs, common myeloid progenitors (CMPs), erythroid burst-forming unit
183 , common lymphoid progenitors (CLPs), common myeloid progenitors (CMPs), granulocyte/macrophage proge
184 ttern of mutations may differ between common myeloid progenitors (CMPs), granulomonocytic progenitors
185 III-A mRNA transcription increased as common myeloid progenitors committed to become granulocyte-macr
186 -myb inactivation also causes defects in the myeloid progenitor compartment, consisting of depletion
187 A mice in early myeloid development in other myeloid progenitor compartments [common myeloid progenit
188 trophilias by expanding both pluripotent and myeloid progenitor compartments to accelerate granulopoi
191 loss of in vivo myeloid potential as common myeloid progenitors differentiate into common DC progeni
195 ors, which are largely akin to the mammalian myeloid progenitors, display increased levels of ROS und
196 erochronic factor Lin28b decreases in common myeloid progenitors during hematopoietic maturation to a
197 the formation of yolk sac-derived erythroid/myeloid progenitors (EMPs) and hematopoietic stem cells
198 p during organogenesis from yolk-sac erythro-myeloid progenitors (EMPs) distinct from haematopoietic
201 tion of primitive erythroid cells or erythro-myeloid progenitors (EMPs) in the yolk sac, but it decre
202 bodies, and that these correspond to erythro-myeloid progenitors (EMPs) that first appear in the yolk
203 initive hematopoietic progenitors (erythroid/myeloid progenitors [EMPs]) emerges in the yolk sac begi
204 eased in frequency compared with normal, and myeloid progenitors evade phagocytosis due to up-regulat
206 ing normal hematopoiesis, HoxA10 facilitates myeloid progenitor expansion and impedes myeloid differe
207 cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult but not fetal
208 oduction in the BM played a critical role in myeloid progenitor expansion during emergency granulopoi
209 etion of Bap1 and Ezh2 in vivo abrogates the myeloid progenitor expansion induced by Bap1 loss alone.
210 a cell line mimicking CP-CML, we found that myeloid progenitor expansion is driven by the exposure o
213 enesis proceeds normally but endothelial and myeloid progenitors fail to initiate differentiation, mi
214 In contrast, ectopic expression of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mi
217 ession with BCR/ABL transforms primary mouse myeloid progenitors, generating aggressive leukemias in
219 cells and cardiac valvular tissues leads to myeloid progenitor hyperplasia and pulmonary stenosis du
220 bines cell proliferation as a consequence of myeloid progenitor hypersensitivity to granulocyte-macro
221 nimal region sufficient for MLL-AF6 mediated myeloid progenitor immortalization in vitro and short la
222 on decreased the bone marrow Gr1(+) CD11b(+) myeloid progenitors, improved bacterial clearance, and r
225 hanism conferring self-renewal capability to myeloid progenitors in myeloid leukemia development.
227 T cells greatly increased the number of the myeloid progenitors in spleen during immune responses.
228 TNF-alpha or IFN-gamma blocked expansion of myeloid progenitors in the bone marrow and also limited
229 athway of human NK cell differentiation from myeloid progenitors in the bone marrow and suggest the u
230 ood, and mutations were observed in HSCs and myeloid progenitors in the bone marrow of 4 patients.
231 essential cross-talk between tumor cells and myeloid progenitors in the bone microenvironment as a re
233 red STAT3 for cytokine-independent growth of myeloid progenitors in vitro, and mitochondrially restri
234 ficiently confers self-renewal capability to myeloid progenitors in vitro, causing their immortalizat
237 ion Notch1 mutations occurring in developing myeloid progenitors, in addition to known T-lineage prog
239 in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution
240 y genes promotes malignant transformation of myeloid progenitors into BC LSCS that are quiescent in t
241 tor (CSF-1R) promotes the differentiation of myeloid progenitors into heterogeneous populations of mo
243 y by which Muc1 regulates the development of myeloid progenitors into MDSCs would also be very useful
244 s 1-3 days show increased differentiation of myeloid progenitors into neutrophils and monocytes but r
245 actor; and (iii) directed differentiation of myeloid progenitors into neutrophils, eosinophils, dendr
247 ion of the "don't eat me" signal CD47 on MDS myeloid progenitors is an important transition step lead
249 enomic analysis demonstrates that ERG causes myeloid progenitor leukemia characterized by an inductio
250 uent G-CSF production by ECs is required for myeloid progenitor lineage skewing toward granulocyte-ma
253 ation in CMML and that GM-CSFR expression on myeloid progenitors may be a biomarker for this therapy.
254 uggest that targeting the differentiation of myeloid progenitors may be a therapeutic strategy for pr
257 RNA depletion affected neither the number of myeloid progenitors nor the percentage of C/EBPA-positiv
258 NOTCH and p38MAPK pathways balance primitive myeloid progenitor output downstream of the BMP pathway.
259 R-125b induces myeloid leukemia by enhancing myeloid progenitor output from stem cells as well as ind
260 actor that is involved in maintenance of the myeloid progenitor population and implicated in myeloid
262 be determined earlier than thought and that myeloid progenitor populations are aggregates of individ
264 as(G12D) promote the survival of preleukemic myeloid progenitors primed for leukemia by activation of
265 Mef2c, a transcription factor that promotes myeloid progenitor proliferation, is a target of miR-223
270 duction in neutrophil myeloperoxidase to the myeloid progenitors showing down-regulated pu.1 expressi
271 ulations ranging from the oligopotent common myeloid progenitor stage to terminally differentiated ne
272 ion was observed in multipotent progenitors, myeloid progenitors, T-cell progenitors, and B-cell prog
273 d that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8.
274 sion of functionally enhanced extramedullary myeloid progenitors that correlated with the peripheral
275 irst wave of yolk sac (YS)-derived primitive myeloid progenitors that seed the skin before the onset
276 t Setbp1 led to the immortalization of mouse myeloid progenitors that showed enhanced proliferative c
278 CD45+ hematopoietic cells highly enriched in myeloid progenitors through coculture of hESCs with OP9
279 Acquisition of self-renewal capability by myeloid progenitors to become leukemic stem cells during
280 ta argue that the differentiation in vivo of myeloid progenitors to circulating DCs promotes the reac
281 his study shows that type I IFN can act upon myeloid progenitors to promote the development of emerge
283 immune system, including bone-marrow-derived myeloid progenitors, to generate an inflammatory microen
284 ve apoptosis of hematopoietic stem cells and myeloid progenitors, together with elevated DNA damage,
287 nctions, the production of both lymphoid and myeloid progenitors was impaired in the absence of Atg7.
288 r important for development of erythroid and myeloid progenitors, was one of the most differentially
289 ) Sca-1(-) cells containing primarily common myeloid progenitors were cultured in vitro without or wi
290 previously found that HoxA10-overexpressing myeloid progenitors were hypersensitive to a variety of
293 racterized by expansion of phenotypic common myeloid progenitors, whereas higher-risk cases revealed
294 ing factor receptor signaling in bone marrow myeloid progenitors, whereas in platelets cholesterol lo
295 R-139-3p strongly inhibited proliferation of myeloid progenitors, whereas inhibition of miR-139-3p ac
296 nstead established the existence of lymphoid-myeloid progenitors, which possess lymphoid and myeloid
298 effect by up-regulating the number of common myeloid progenitors while inhibiting development of pre-
299 ls; (ii) short-term expansion of multipotent myeloid progenitors with a high dose of granulocyte-macr
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