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1 which requires maintenance and expansion of myeloid progenitors.
2 of the entire hematopoietic tree, including myeloid progenitors.
3 yeloid-derived suppressor cells (MDSCs) from myeloid progenitors.
4 row by inducing differentiation of committed myeloid progenitors.
5 ortality, self-renewal, and tumorigenesis in myeloid progenitors.
6 vents the expansion of Nras(G12D/+) HSCs and myeloid progenitors.
7 rentiation skewing of multipotent and common myeloid progenitors.
8 gh estrogen receptor (ER) alpha signaling in myeloid progenitors.
9 PU.1 and induces malignant reprogramming of myeloid progenitors.
10 gulatory factor (IRF)-4 in GM-CSF-stimulated myeloid progenitors.
11 ctor signaling or increased proliferation in myeloid progenitors.
12 ost related to haematopoietic stem cells and myeloid progenitors.
13 cell virus vectors and assayed the growth of myeloid progenitors.
14 f monocytes over neutrophils at the level of myeloid progenitors.
15 ing in these patients occurs at the level of myeloid progenitors.
16 cell progeny concomitant with an increase in myeloid progenitors.
17 d shortly after Setbp1 expression in primary myeloid progenitors.
18 n granulocyte-monocyte progenitors or common myeloid progenitors.
19 tial, and induces cell death specifically in myeloid progenitors.
20 d expansion of undifferentiated cells in 32D myeloid progenitors.
21 ation of hematopoietic stem cells (HSCs) and myeloid progenitors.
22 d myeloid-related genes could be detected in myeloid progenitors.
23 d of culture and an additional 2 d to expand myeloid progenitors.
24 not required for the proliferation of early myeloid progenitors.
25 leukemic cells from normal myeloid cells or myeloid progenitors.
26 ssential for neutrophil differentiation from myeloid progenitors.
27 nditionally deleted Nemo from osteoclast and myeloid progenitors.
28 suppressor cells (mMDSC) from human or mouse myeloid progenitors.
29 escence with concomitant expansion of murine myeloid progenitors.
30 sed sensitivity to DNA damage in bone marrow myeloid progenitors.
31 egulation of PtdIns(3,4,5)P3 signaling in BM myeloid progenitors.
32 matopoietic function of ICL-repair deficient myeloid progenitors.
37 PA re-activated replating activity of common myeloid progenitor and granulocyte macrophage progenitor
39 xhibit a decrease in myeloid-biased HSCs and myeloid progenitors and an increase in T cells and lymph
40 ic stem cells (HSCs) results in expansion of myeloid progenitors and co-operates with oncogenic Kras(
41 of the haematopoietic system, such as common myeloid progenitors and common lymphoid progenitors, inc
42 oter in vitro, and in vivo within both early myeloid progenitors and differentiating neutrophils.
44 uction of myeloid lineage precursors (common myeloid progenitors and granulocyte myeloid precursors)
47 reactive granulopoiesis," in which committed myeloid progenitors and more primitive progenitors cycle
51 Myeloid-derived suppressor cells (MDSCs) are myeloid progenitors and precursors that fail to differen
52 rs when IFN-gamma inhibits the generation of myeloid progenitors and prevents lineage differentiation
54 -derived suppressor cells (MDSCs) arise from myeloid progenitors and suppress both innate and adaptiv
55 hromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin struc
57 g the commitment of short-term HSC to common myeloid progenitors and these alterations were predomina
60 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
71 ly, both Flt3(+)CD150(-) and Flt3(-)CD150(-) myeloid progenitors are susceptible to Notch1-mediated T
72 an increase in the proportions of committed myeloid progenitors, as determined by colony-forming uni
74 topoiesis and highlights PN as a disorder of myeloid progenitors associated with bone marrow dysfunct
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 hly expressed in marrow monocytes and common myeloid progenitors but significantly lower in granulocy
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
91 o more pronounced suppression of bone marrow myeloid progenitor cell proliferation and monocytosis, a
92 leukemia is preceded by a period of extended myeloid progenitor cell proliferation and self-renewal.
93 G-CSF signaling in the regulation of marrow myeloid progenitor cell proliferation in mice with Strep
95 fection on MHC class II in Kasumi-3 cells, a myeloid-progenitor cell line that endogenously expresses
97 ation of hematopoietic stem cells (HSCs) and myeloid progenitor cells (MPCs) has been shown to mediat
98 (MDS) at 24 months of age, with dysplasia of myeloid progenitor cells and anemia with abnormal circul
99 ignaling pathway, we observed an increase in myeloid progenitor cells and CDllb(lo)Gr1(lo) promyelocy
100 expression of HoxA10 is maximal in committed myeloid progenitor cells and decreases as differentiatio
101 GF2 promoter that are activated by HoxA10 in myeloid progenitor cells and differentiating phagocytes.
102 AcmvIL-10 during latent infection of primary myeloid progenitor cells and found that LAcmvIL-10 is re
104 support interleukin-3-independent growth of myeloid progenitor cells and long-term outgrowth of B-ly
105 survival of preleukemic short-term HSCs and myeloid progenitor cells and maintains the differentiati
106 is also expressed during latent infection of myeloid progenitor cells and monocytes and facilitates p
107 OPN (iOPN) diminished the population size of myeloid progenitor cells and myeloid cells, and secreted
108 romoted the outgrowth of Ly6C(+) and Ly6G(+) myeloid progenitor cells and their mobilization to tumor
109 all RNAs, termed microRNAs, encoded by human myeloid progenitor cells are capable of repressing a key
110 air of our bones are formed from bone marrow myeloid progenitor cells by a complex differentiation pr
111 interleukin-6 receptor (IL-6R) expression on myeloid progenitor cells by Delta-1 treatment combined w
115 d expression of Fap1 and Gas2 in bone marrow myeloid progenitor cells from Icsbp(-/-) mice in compari
117 ncer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secre
118 itment of bone marrow-derived CD11b(+)Gr1(+) myeloid progenitor cells in the premetastatic lungs.
120 lso determined that HoxA10 overexpression in myeloid progenitor cells increased Tgfbeta2 production b
121 on of the CML-related Bcr-abl oncoprotein in myeloid progenitor cells increases expression of Fas-ass
122 sed Fgf2 production by HoxA10-overexpressing myeloid progenitor cells induced a phosphoinositol 3-kin
123 e myeloid-derived suppressor cells, immature myeloid progenitor cells known for immunosuppressive pro
124 We determined that expression of Mll-Ell in myeloid progenitor cells resulted in autocrine productio
125 wth factor 2 (Fgf2) by HoxA10-overexpressing myeloid progenitor cells results in activation of beta-c
127 ed that differentiation of latently infected myeloid progenitor cells to dendritic or macrophage-like
128 Mcl1 facilitates AML development by allowing myeloid progenitor cells to evade Myc-induced cell death
129 JMML is acquired hypersensitivity by clonal myeloid progenitor cells to granulocyte macrophage-colon
130 nal activators involved in the commitment of myeloid progenitor cells to the DC lineage and predicted
131 tion-induced adaptation of hematopoietic and myeloid progenitor cells toward enhanced myelopoiesis mi
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
160 y elevated frequencies and numbers of common myeloid progenitor (CMP) and granulocyte/macrophage prog
161 -associated molecular patterns by the common myeloid progenitor (CMP) and is dependent on type I IFN
162 s classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing t
163 the developmental defect of DCs from common myeloid progenitor (CMP) in Mysm1(-/-) mice is associate
164 In Dhh-deficient bone marrow, the common myeloid progenitor (CMP) population was increased, but d
166 ved common lymphoid progenitor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progen
168 common lymphoid progenitors (CLP) or common myeloid progenitors (CMP) during this process remains el
170 )Sca-1(+)c-Kit(+)CD34(+)Flt3(hi)) and common myeloid progenitors (CMPs) (Lin(-)Sca-1(+)c-Kit(+)CD34(+
172 hematopoietic progenitor stem cells, common myeloid progenitors (CMPs) and granulocyte-macrophage pr
173 ther myeloid progenitor compartments [common myeloid progenitors (CMPs) and granulocyte/monocyte prog
174 as an ATM-independent function in the common myeloid progenitors (CMPs) by deletion of Atmin in the e
176 opulations are thought to derive from common myeloid progenitors (CMPs), and a hierarchical relations
177 ouse hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), and erythroblasts (ERYs).
178 on of Scf from LepR(+) cells depleted common myeloid progenitors (CMPs), common lymphoid progenitors
179 ) mice revealed that short-term HSCs, common myeloid progenitors (CMPs), erythroid burst-forming unit
180 , common lymphoid progenitors (CLPs), common myeloid progenitors (CMPs), granulocyte/macrophage proge
181 ttern of mutations may differ between common myeloid progenitors (CMPs), granulomonocytic progenitors
182 III-A mRNA transcription increased as common myeloid progenitors committed to become granulocyte-macr
183 -myb inactivation also causes defects in the myeloid progenitor compartment, consisting of depletion
184 A mice in early myeloid development in other myeloid progenitor compartments [common myeloid progenit
188 loss of in vivo myeloid potential as common myeloid progenitors differentiate into common DC progeni
192 erochronic factor Lin28b decreases in common myeloid progenitors during hematopoietic maturation to a
194 the formation of yolk sac-derived erythroid/myeloid progenitors (EMPs) and hematopoietic stem cells
195 p during organogenesis from yolk-sac erythro-myeloid progenitors (EMPs) distinct from haematopoietic
198 tion of primitive erythroid cells or erythro-myeloid progenitors (EMPs) in the yolk sac, but it decre
199 opoietic-stem-cell (HSC)-independent erythro-myeloid progenitors (EMPs) present in the murine yolk sa
200 bodies, and that these correspond to erythro-myeloid progenitors (EMPs) that first appear in the yolk
201 initive hematopoietic progenitors (erythroid/myeloid progenitors [EMPs]) emerges in the yolk sac begi
202 eased in frequency compared with normal, and myeloid progenitors evade phagocytosis due to up-regulat
204 ing normal hematopoiesis, HoxA10 facilitates myeloid progenitor expansion and impedes myeloid differe
205 cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult but not fetal
206 oduction in the BM played a critical role in myeloid progenitor expansion during emergency granulopoi
207 etion of Bap1 and Ezh2 in vivo abrogates the myeloid progenitor expansion induced by Bap1 loss alone.
208 a cell line mimicking CP-CML, we found that myeloid progenitor expansion is driven by the exposure o
210 enesis proceeds normally but endothelial and myeloid progenitors fail to initiate differentiation, mi
211 rmed macrophages by differentiating ER-Hoxb8 myeloid progenitors from Cas9-expressing transgenic mice
212 In contrast, ectopic expression of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mi
215 ession with BCR/ABL transforms primary mouse myeloid progenitors, generating aggressive leukemias in
216 roach allowed the long-term culture of mouse myeloid progenitors (HoxB8 progenitors) in estrogen-cont
217 bines cell proliferation as a consequence of myeloid progenitor hypersensitivity to granulocyte-macro
218 nimal region sufficient for MLL-AF6 mediated myeloid progenitor immortalization in vitro and short la
219 on decreased the bone marrow Gr1(+) CD11b(+) myeloid progenitors, improved bacterial clearance, and r
220 al changes may promote expansion of abnormal myeloid progenitors in del(5q) MDS, and in rare cases dr
223 hanism conferring self-renewal capability to myeloid progenitors in myeloid leukemia development.
225 TNF-alpha or IFN-gamma blocked expansion of myeloid progenitors in the bone marrow and also limited
226 athway of human NK cell differentiation from myeloid progenitors in the bone marrow and suggest the u
227 ood, and mutations were observed in HSCs and myeloid progenitors in the bone marrow of 4 patients.
229 essential cross-talk between tumor cells and myeloid progenitors in the bone microenvironment as a re
231 red STAT3 for cytokine-independent growth of myeloid progenitors in vitro, and mitochondrially restri
232 ficiently confers self-renewal capability to myeloid progenitors in vitro, causing their immortalizat
234 ion Notch1 mutations occurring in developing myeloid progenitors, in addition to known T-lineage prog
235 in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution
236 y genes promotes malignant transformation of myeloid progenitors into BC LSCS that are quiescent in t
237 sequently controls proper differentiation of myeloid progenitors into granulocytes in steady-state an
238 tor (CSF-1R) promotes the differentiation of myeloid progenitors into heterogeneous populations of mo
240 strate that M-CSF-induced differentiation of myeloid progenitors into Mo is not impaired by the loss
241 s 1-3 days show increased differentiation of myeloid progenitors into neutrophils and monocytes but r
242 actor; and (iii) directed differentiation of myeloid progenitors into neutrophils, eosinophils, dendr
244 ion of the "don't eat me" signal CD47 on MDS myeloid progenitors is an important transition step lead
247 enomic analysis demonstrates that ERG causes myeloid progenitor leukemia characterized by an inductio
248 uent G-CSF production by ECs is required for myeloid progenitor lineage skewing toward granulocyte-ma
251 ation in CMML and that GM-CSFR expression on myeloid progenitors may be a biomarker for this therapy.
252 uggest that targeting the differentiation of myeloid progenitors may be a therapeutic strategy for pr
254 nslatome in LSK (Lin(-)Sca-1(+)c-Kit(+)) and myeloid progenitor (MP; Lin(-)Sca-1(-)c-Kit(+)) cells.
255 RNA depletion affected neither the number of myeloid progenitors nor the percentage of C/EBPA-positiv
257 ere we aimed to investigate the influence of myeloid progenitors on CD34(+) cell differentiation into
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
263 be determined earlier than thought and that myeloid progenitor populations are aggregates of individ
265 as(G12D) promote the survival of preleukemic myeloid progenitors primed for leukemia by activation of
268 ene expression analysis of mirn23a-deficient myeloid progenitors revealed a decrease in TLR and IFN s
271 duction in neutrophil myeloperoxidase to the myeloid progenitors showing down-regulated pu.1 expressi
272 ulations ranging from the oligopotent common myeloid progenitor stage to terminally differentiated ne
273 ion was observed in multipotent progenitors, myeloid progenitors, T-cell progenitors, and B-cell prog
274 driver mutation is present in a BM-resident myeloid progenitor that can be mobilized to the blood.
275 d that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8.
276 aptive T lymphocytes are derived from lympho-myeloid progenitors that colonize the thymus, while lymp
277 sion of functionally enhanced extramedullary myeloid progenitors that correlated with the peripheral
278 irst wave of yolk sac (YS)-derived primitive myeloid progenitors that seed the skin before the onset
279 t Setbp1 led to the immortalization of mouse myeloid progenitors that showed enhanced proliferative c
281 naturally-existing, rapidly-cycling immature myeloid progenitors, this cell state becomes perpetuated
282 Acquisition of self-renewal capability by myeloid progenitors to become leukemic stem cells during
283 ta argue that the differentiation in vivo of myeloid progenitors to circulating DCs promotes the reac
284 his study shows that type I IFN can act upon myeloid progenitors to promote the development of emerge
285 ve apoptosis of hematopoietic stem cells and myeloid progenitors, together with elevated DNA damage,
286 dies reported conditional immortalization of myeloid progenitors using retroviral expression of an es
289 nctions, the production of both lymphoid and myeloid progenitors was impaired in the absence of Atg7.
290 ) Sca-1(-) cells containing primarily common myeloid progenitors were cultured in vitro without or wi
291 previously found that HoxA10-overexpressing myeloid progenitors were hypersensitive to a variety of
294 racterized by expansion of phenotypic common myeloid progenitors, whereas higher-risk cases revealed
295 ing factor receptor signaling in bone marrow myeloid progenitors, whereas in platelets cholesterol lo
296 R-139-3p strongly inhibited proliferation of myeloid progenitors, whereas inhibition of miR-139-3p ac
297 f innate immune cells occurs at the level of myeloid progenitors, which adds exciting opportunities f
299 effect by up-regulating the number of common myeloid progenitors while inhibiting development of pre-
300 ls; (ii) short-term expansion of multipotent myeloid progenitors with a high dose of granulocyte-macr