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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.
33 ion centres originate from embryonic erythro-myeloid progenitors(21,22).
34                               Suppression of myeloid progenitors (6 h) occurs only for DMBA.
35         Conditional deletion of Hdac3 within myeloid progenitors accelerates healing of cortical bone
36                    Importantly, the abnormal myeloid progenitors (AMPs), a leukemia-initiating cell p
37 PA re-activated replating activity of common myeloid progenitor and granulocyte macrophage progenitor
38 ion and expansion, as well as an increase of myeloid progenitors and a decrease of mature cells.
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.
43 d LSCs was most similar to that of committed myeloid progenitors and distinct from HSCs.
44 uction of myeloid lineage precursors (common myeloid progenitors and granulocyte myeloid precursors)
45 EBPA overlapped an enhancer active in common myeloid progenitors and influenced its activity.
46                          Tumor cells recruit myeloid progenitors and monocytes to the tumor site, whe
47 reactive granulopoiesis," in which committed myeloid progenitors and more primitive progenitors cycle
48 ential onto otherwise committed lymphoid and myeloid progenitors and myeloid effector cells.
49 olon cancers transform the growth of primary myeloid progenitors and of Ba/F3 cells.
50                           Furthermore, mouse myeloid progenitors and patient leukemic cells with the
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
53                                 Sf3b1(K700E) myeloid progenitors and SF3B1-mutant MDS patient samples
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
56 ranulocyte macrophage CSF (GM-CSF) to expand myeloid progenitors and their progeny in culture.
57 g the commitment of short-term HSC to common myeloid progenitors and these alterations were predomina
58                             Irf8(-/-) common myeloid progenitors and, unexpectedly, Irf8(-/-) ALPs pr
59         Late MDSCs had more immature CD31(+) myeloid progenitors and, when treated ex vivo with granu
60 ing lineage(-)Sca-1(+)c-kit(+) (LSK), common myeloid progenitor, and granulocyte/macrophage progenito
61                 Further, inhibiting c-Maf in myeloid progenitors, and consequent myeloid-lineage cell
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
68                  We show that while inducing myeloid progenitor apoptosis, TNF-alpha promotes HSC sur
69                                              Myeloid progenitors are conditionally immortalized using
70                         Yet, Flt3(+)CD150(-) myeloid progenitors are not likely to efficiently traffi
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
73 ntributes to HOXB4-mediated expansion in our myeloid progenitor assays.
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
82                            Here we show that myeloid progenitors can be derived from embryonic stem c
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
86 n of haematopoietic stem cell/progenitor and myeloid progenitor cell genes.
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                    Using Kasumi-3 cells as a myeloid progenitor cell model endogenously expressing MH
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
94                           This impairment of myeloid progenitor cell proliferation was not attenuated
95 fection on MHC class II in Kasumi-3 cells, a myeloid-progenitor cell line that endogenously expresses
96 viral infection using a clonal population of myeloid progenitor cells (Kasumi-3 cells).
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
103           The oncoprotein BCR-ABL transforms myeloid progenitor cells and is responsible for the deve
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
112                             Apc heterozygous myeloid progenitor cells display an increased frequency
113           In contrast, HoxA10-overexpressing myeloid progenitor cells exhibited increased proliferati
114                                Consequently, myeloid progenitor cells expressing oncogenic Kras and l
115 d expression of Fap1 and Gas2 in bone marrow myeloid progenitor cells from Icsbp(-/-) mice in compari
116 the phenomenon of microglial augmentation by myeloid progenitor cells in the adult brain.
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.
119  trafficking was linked to redistribution of myeloid progenitor cells in the spleen.
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
126 es have relied on ex vivo differentiation of myeloid progenitor cells to DCs in culture.
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
132            We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1
133 and colleagues examine deletion of Dicer1 in myeloid progenitor cells using a conditional Cebpa-Cre a
134                            Normal numbers of myeloid progenitor cells were present in Nr4a1-/- mice,
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
144 ignancy characterized by clonal expansion of myeloid progenitor cells.
145 he gene encoding Fanconi C (Fancc) in murine myeloid progenitor cells.
146 and Ig synthesis, and enhances maturation of myeloid progenitor cells.
147 d a growth advantage over wild-type HOXB4 in myeloid progenitor cells.
148 n of Fap1 with the Apc complex in Bcr-abl(+) myeloid progenitor cells.
149  genes that are activated by beta-catenin in myeloid progenitor cells.
150  gene expression in T cells, mast cells, and myeloid progenitor cells.
151 e properties of the Pu/Gata toggle switch in myeloid progenitor cells.
152 iption factor that is maximally expressed in myeloid progenitor cells.
153 ow previously to inhibit colony formation by myeloid progenitor cells.
154  and short-term hematopoietic stem cells and myeloid progenitor cells.
155 ormal and transformed hematopoietic stem and myeloid progenitor cells.
156 that Tregs can affect the differentiation of myeloid progenitor cells.
157 ic and carcinogenic species in human CD34(+) myeloid progenitor cells.
158 ed fewer nucleated cells and was enriched in myeloid progenitor cells.
159 d1 is greater in mature granulocytes than in myeloid progenitor cells.
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
165 is associated with an increase in the common myeloid progenitor (CMP) population.
166 ved common lymphoid progenitor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progen
167 tream APC progenitor cells, including common myeloid progenitor (CMP)-Flk2(+).
168  common lymphoid progenitors (CLP) or common myeloid progenitors (CMP) during this process remains el
169 d that induces the differentiation of common myeloid progenitors (CMP) to megakaryocytes.
170 )Sca-1(+)c-Kit(+)CD34(+)Flt3(hi)) and common myeloid progenitors (CMPs) (Lin(-)Sca-1(+)c-Kit(+)CD34(+
171                 Herein, we found that common myeloid progenitors (CMPs) and granulocyte-macrophage pr
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
175                                       Common myeloid progenitors (CMPs) were first identified as prog
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
185                               Bcl3-deficient myeloid progenitors demonstrated an enhanced capacity to
186                                These erythro-myeloid progenitor-derived osteoclasts are required for
187                                              Myeloid progenitor-derived suppressor cells (MDSCs) aris
188  loss of in vivo myeloid potential as common myeloid progenitors differentiate into common DC progeni
189                    We observed inhibition in myeloid progenitor differentiation despite an increase i
190 ting that IL-R1 deficiency does not abrogate myeloid progenitor differentiation potential.
191 telomere biology, aberrant RNA splicing, and myeloid progenitor differentiation.
192 erochronic factor Lin28b decreases in common myeloid progenitors during hematopoietic maturation to a
193                             Yolk sac erythro-myeloid progenitors (EMP) contribute substantially to ad
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
196 cellular pathway generating Csf1r(+) erythro-myeloid progenitors (EMPs) distinct from HSCs.
197 Both YS MFs and fetal MOs arise from erythro-myeloid progenitors (EMPs) generated in the YS.
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
203                        HoxA10 contributes to myeloid progenitor expansion and differentiation block,
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
209 ription factors that direct G-CSF-responsive myeloid progenitor expansion.
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
213                                              Myeloid progenitors from patients with heritable and/or
214                 In addition, Ercc1-deficient myeloid progenitors gain elevated levels of miR-139-3p a
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
221          Hematopoietic stem cells (HSCs) and myeloid progenitors in MDS have not been extensively cha
222                  We report here that erythro-myeloid progenitors in mice generate premacrophages (pMa
223 hanism conferring self-renewal capability to myeloid progenitors in myeloid leukemia development.
224 ensable for growth of normal or K-Ras-mutant myeloid progenitors in response to cytokines.
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.
228 ient induction requires direct engagement of myeloid progenitors in the bone marrow.
229 essential cross-talk between tumor cells and myeloid progenitors in the bone microenvironment as a re
230 nted the ability of oncogenic JAK2 to expand myeloid progenitors in vitro and in vivo.
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
233         Setbp1 also promotes self-renewal of myeloid progenitors in vivo as its coexpression with BCR
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
239                           Differentiation of myeloid progenitors into mature myeloid cells requires a
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
243 est that miR-29a initiates AML by converting myeloid progenitors into self-renewing LSC.
244 ion of the "don't eat me" signal CD47 on MDS myeloid progenitors is an important transition step lead
245  however, its role in the differentiation of myeloid progenitors is less clear.
246                     Moreover, CD34(+)PRLR(+) myeloid progenitors lacked lymphoid developmental potent
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
249 cipient's thymus from donor-derived lymphoid-myeloid progenitors (LMPs).
250                                              Myeloid progenitors lose their potential to generate neu
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
253                          We investigated the myeloid progenitor (MP) compartment in KO mice, arguing
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
256                   Long-term reprogramming of myeloid progenitors occurs in response to inflammatory s
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
261        We have examined the CD34+c-Kit+Flt3+ myeloid progenitor population as potential mutation carr
262 ism by which HoxA10 controls the size of the myeloid progenitor population.
263  be determined earlier than thought and that myeloid progenitor populations are aggregates of individ
264             Here we demonstrated that lympho-myeloid progenitor populations in cord blood - lymphoid-
265 as(G12D) promote the survival of preleukemic myeloid progenitors primed for leukemia by activation of
266                                Hematopoietic myeloid progenitors released into the circulation are ab
267        Blocking calreticulin on low risk MDS myeloid progenitors rescues them from phagocytosis in vi
268 ene expression analysis of mirn23a-deficient myeloid progenitors revealed a decrease in TLR and IFN s
269       In vitro, loss of FAK in erythroid and myeloid progenitor's results in impaired cytokine induce
270  AML and, like human LSC, miR-29a-expressing myeloid progenitors serially transplant AML.
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
280                           MDSCs are immature myeloid progenitors that suppress T-cell effector functi
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
287 ell-produced ROS stimulated proliferation of myeloid progenitors via a paracrine mechanism.
288 n that conferred autonomous proliferation to myeloid progenitors was found.
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
292             Therefore, these Flt3(+)CD150(-) myeloid progenitors were T/myeloid potent.
293              The embryonic stem cell-derived myeloid progenitors, when immortalized with estrogen-reg
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
298                           Clonal analysis of myeloid progenitors, which produce short-lived granulocy
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

 
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