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1 tation of the hematopoietic system in stress myelopoiesis.
2 lon (C/EBPepsilon) is a critical mediator of myelopoiesis.
3 artment fails to induce LPS-driven emergency myelopoiesis.
4 hocyte development and is also implicated in myelopoiesis.
5 pression, enhanced self renewal and expanded myelopoiesis.
6 ral shortcomings, one of which is poor human myelopoiesis.
7 r-binding protein-alpha up-regulation during myelopoiesis.
8 to a loss of Notch-dependent suppression of myelopoiesis.
9 ts and myelocytes, as well as extramedullary myelopoiesis.
10 ease in B lymphopoiesis, and an elevation in myelopoiesis.
11 ced alpha2,6-sialylation results in elevated myelopoiesis.
12 abolic reprogramming underlies M-CSF-induced myelopoiesis.
13 SBP protects against the genotoxic stress of myelopoiesis.
14 presses HoxA9, Pbx1, and Meis1 during normal myelopoiesis.
15 gulatory T cells regulate the extramedullary myelopoiesis.
16 w insights into regulation of extramedullary myelopoiesis.
17 topoietic stem cells could support long-term myelopoiesis.
18 InsP3KB is also a physiological modulator of myelopoiesis.
19 on and G-CSF- or inflammation-induced stress myelopoiesis.
20 e progressive growth in our understanding of myelopoiesis.
21 d DUSP4 activation by HoxA10 decrease during myelopoiesis.
22 e for leptin in sustaining lymphopoiesis and myelopoiesis.
23 nding to the DUSP4 promoter decreases during myelopoiesis.
24 show that their interaction also suppressed myelopoiesis.
25 AML, which dephosphorylate HoxA10 throughout myelopoiesis.
26 ge progenitor stage and continues throughout myelopoiesis.
27 suggesting a mechanism by which NE regulates myelopoiesis.
28 ation provides important insight into normal myelopoiesis.
29 cooperates with C/EBPalpha to regulate early myelopoiesis.
30 ibutes to inappropriate cell survival during myelopoiesis.
31 Here, we show a role for Rbm15 in myelopoiesis.
32 d IL-3 also responded to IL-7 with increased myelopoiesis.
33 or (IRF)-8 plays an important role in normal myelopoiesis.
34 n and Mkp2 expression decrease during normal myelopoiesis.
35 gene transcription at various points during myelopoiesis.
36 IL-6, and IL-3) shifted the cultures toward myelopoiesis.
37 ession of CYBB and NCF2 transcription during myelopoiesis.
38 ing proteins (C/EBPs) play critical roles in myelopoiesis.
39 hopoiesis and a corresponding enhancement of myelopoiesis.
40 ulatory element) during normal and leukaemic myelopoiesis.
41 thereby constituting a feed-forward loop for myelopoiesis.
42 loid leukemia (AML) and results in defective myelopoiesis.
43 icroenvironmental) age-related changes favor myelopoiesis.
44 e results establish a critical role of PS in myelopoiesis.
45 cytic leukemic cells and during normal human myelopoiesis.
46 e stem cell genes, such as scl, in governing myelopoiesis.
47 actor JunB is a transcriptional regulator of myelopoiesis.
48 s by causing imbalances in lymphopoiesis and myelopoiesis.
49 L-RARA, initially has only modest effects on myelopoiesis.
50 ulation of HoxA10 repression activity during myelopoiesis.
51 e is known regarding GSL expression in early myelopoiesis.
52 C/EBPepsilon, have important roles in normal myelopoiesis.
53 viour in mice during emergency and leukaemic myelopoiesis.
54 expression of PU.1, a critical regulator of myelopoiesis.
55 ne at http://bioinfo.mbb.yale.edu/expression/myelopoiesis.
56 iation and suggest it is required for normal myelopoiesis.
57 bolism as a central node in mTORC1-dependent myelopoiesis.
58 m for the study of normal and aberrant human myelopoiesis.
59 l, mutants affecting erythropoiesis, but not myelopoiesis.
60 nse to different subsets of cytokines during myelopoiesis.
61 and HOX B7, which are expressed during early myelopoiesis.
62 creates specific defects in lymphopoiesis or myelopoiesis.
63 nonhematopoietic niche that controls normal myelopoiesis.
64 5 inhibits human erythropoiesis and promotes myelopoiesis.
65 that BNBD-4 synthesis is completed early in myelopoiesis.
66 serine phosphorylation also had no effect on myelopoiesis.
67 and the DNA binding domain are required for myelopoiesis.
68 nate regulation of immune effector cells and myelopoiesis.
69 which is transcriptionally regulated during myelopoiesis.
70 normal murine fetal liver erythropoiesis and myelopoiesis.
71 ed it may be an important regulator of human myelopoiesis.
72 r a major role of SDF-1 on the regulation of myelopoiesis.
73 overexpression of evi1 acts to block normal myelopoiesis.
74 antibacterial properties, and regulation of myelopoiesis.
75 E or C/EBPalpha are resistant to HFD-induced myelopoiesis.
76 and this pathway was essential for emergency myelopoiesis.
77 the marrow, skewing toward the expansion of myelopoiesis.
78 o rapidly altered stem cells homeostasis and myelopoiesis.
79 tumor-derived soluble factors able to alter myelopoiesis.
80 they inhibited B lymphopoiesis and enhanced myelopoiesis.
81 a transcription factor that is essential for myelopoiesis.
82 wnstream genes and consequently deregulating myelopoiesis.
83 cking this pathway was sufficient to enhance myelopoiesis.
84 n, an miRNA gene known to play a key role in myelopoiesis.
85 ansposition and impaired spermatogenesis and myelopoiesis.
86 ce also drove type I IFN-dependent emergency myelopoiesis.
87 hibition of miR-9 with a miRNA sponge blocks myelopoiesis.
88 p-regulation of FoxO3 inhibits miR-9-induced myelopoiesis.
89 volved in orchestrating inflammation-induced myelopoiesis.
90 ative disease with splenomegaly and aberrant myelopoiesis.
91 ic shuttling activity in normal and leukemic myelopoiesis, a mutant defective in nuclear export was e
93 angioblast specification, and for subsequent myelopoiesis, acting as early as cloche and upstream of
94 demonstrated that norepinephrine stimulated myelopoiesis after burn injury and sepsis, but the site
96 -skewing potential from lymphopoiesis toward myelopoiesis, an increase in the long-term-HSC pool, and
97 iferation and expansion, which prevented the myelopoiesis and accelerated atherosclerosis of ApoE(-/-
98 of neutropenia with an intrinsic failure of myelopoiesis and an increase in the incidence of cytogen
99 TLR7.1 mice exhibited hallmarks of emergency myelopoiesis and contained a discrete population of Sca-
100 cytokine regulated anti-apoptotic protein in myelopoiesis and contributes to leukemia cell survival.
102 m a regulatory axis that specifies primitive myelopoiesis and definitive hematopoiesis, but not primi
105 mammalian hematopoiesis, embryonic zebrafish myelopoiesis and erythropoiesis occur in anatomically se
108 psilon deficiency, define SGD as a defect in myelopoiesis and establish the requirement for C/EBPepsi
109 restricted and stage-specific pattern during myelopoiesis and functions to promote monocyte different
112 ous unrecognized significant role for ACE in myelopoiesis and imply new perspectives for manipulating
113 d to play a role in vascular development and myelopoiesis and in the inflammatory responses of granul
114 ese results reveal a unique role of miR-9 in myelopoiesis and in the pathogenesis of EVI1-induced mye
117 summary, SMARCD2 is a key factor controlling myelopoiesis and is a potential tumor suppressor in leuk
119 cyclin A1 overexpression results in abnormal myelopoiesis and is necessary, but not sufficient in the
120 n factor C/EBPalpha is a master regulator of myelopoiesis and its inactivation is associated with acu
121 a critical transcription factor involved in myelopoiesis and its inactivation is associated with acu
122 he genes in this region may play in abnormal myelopoiesis and leukemia associated with trisomy 21 and
124 ygosity in Down Syndrome-associated abnormal myelopoiesis and leukemia, as well as the markers, which
125 l the SPI1-METTL14-MYB/MYC signaling axis in myelopoiesis and leukemogenesis and highlight the critic
128 core binding factor (CBF) family stimulates myelopoiesis and lymphopoiesis by activating lineage-spe
130 ls does not result in strict separation into myelopoiesis and lymphopoiesis, and that there might be
135 The results of this analysis indicated that myelopoiesis and primary lymphopoiesis were unaltered in
136 ssion of miR-9 strongly accelerates terminal myelopoiesis and promotes apoptosis in vitro and in vivo
138 usly unknown cytokine-RAR interaction during myelopoiesis and suggest that RAR activation might be a
139 a and systemic exposure to SAA can influence myelopoiesis and susceptibility to amebiasis via epigene
140 (-/-) mice significantly reduced bone marrow myelopoiesis and systemic CD11b(+)Ly6G(+) cell expansion
141 at Fas has a novel role in the regulation of myelopoiesis and that Fas may act as a tumor suppressor
142 ve a previously unknown function in limiting myelopoiesis and the development of dendritic cells.
144 nsient effects of the monoclonal antibody on myelopoiesis and the more persistent effects on lymphopo
145 appeared to be specific for that lineage, as myelopoiesis and thymopoiesis were normal in dwarf and h
147 that can serve as a model for the failure of myelopoiesis, and dissection of its pathogenesis has yie
148 lly inactive until the promyelocyte stage of myelopoiesis, and in mature phagocytes, expression of gp
149 viability, B lymphopoiesis, and bone marrow myelopoiesis, and is a potent monocyte and T-lymphocyte
150 s known to inhibit lymphopoiesis and elevate myelopoiesis, and its expression was MAPK dependent.
151 sulted in enhanced embryonic erythropoiesis, myelopoiesis, and lymphopoiesis, including a 2- 3-fold i
152 ntifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for t
153 emonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzyma
154 program that underlies both human and murine myelopoiesis, and that is central to the pathogenesis of
161 factors that have important roles in normal myelopoiesis as well as associated with myeloid disorder
162 ignaling was essential for microbiota-driven myelopoiesis, as microbiota colonization or transferring
163 macrophages are essential to extramedullary myelopoiesis because these macrophages use the adhesion
164 icroRNAs whose regulation is required during myelopoiesis, but also provide an example of synergy in
168 y ST6Gal-1, mostly of hepatic origin, limits myelopoiesis by a mechanism independent of hepatic sialy
170 n negatively regulate splenic extramedullary myelopoiesis by suppressing the naive T cell differentia
171 e demonstrated minimal stimulation of normal myelopoiesis by the TEL/PDGFbetaR-expressing cells.
172 We also show that MBT-1 appears to influence myelopoiesis by transiently enhancing p57(KIP2) expressi
173 llowed by specification to hematopoiesis and myelopoiesis by vascular endothelial growth factor and h
174 gest that DC differentiation, during induced myelopoiesis, can be regulated by the nature of the Notc
175 hat Kit(W-sh) causes aberrant extramedullary myelopoiesis characterized by the expansion of immature
177 nt (TR) in the zebrafish results in impaired myelopoiesis, despite normal development of haematopoiet
179 o bias hematopoietic progenitor cells toward myelopoiesis directly by replacing cytokine and differen
180 the suppressive effects of Notch ligands on myelopoiesis, do not transcribe Notch1 target genes when
182 r Erk2 disruption did not grossly compromise myelopoiesis, dual Erk1/2 disruption rapidly ablated gra
183 ion of this revealed the cause to be massive myelopoiesis due to ectopic granulocyte/ colony-stimulat
185 idence that LAL is an important regulator of myelopoiesis during hematopoietic development, different
187 c mice displayed enhanced marrow and splenic myelopoiesis: greatly increased progenitor cell cycling
189 y serve as important markers for analysis of myelopoiesis, hepatic development, and other development
190 tivities for these C/EBP-epsilon isoforms in myelopoiesis, human CD34(+) progenitors were transduced
191 eloid cell autonomous defect led to abnormal myelopoiesis, immune suppression, and lung adenocarcinom
193 n of several genes activated during terminal myelopoiesis in BM cells and identified a group of them
197 ve severely reduced B-lymphopoiesis, reduced myelopoiesis in fetal liver, and a virtual absence of my
199 , these observations indicate that defective myelopoiesis in IL-2(-/-) mice is at least in part a con
200 s from IL-2(-/-) mice were unable to sustain myelopoiesis in lethally irradiated mice and in long-ter
203 with NF-kappaB p65, we have now investigated myelopoiesis in nfkb1(-/-) mice lacking NF-kappaB p50.
204 nhibition of erythropoiesis and promotion of myelopoiesis in the absence of any demonstrable effect o
205 pectedly, in vivo ablation of pDCs increased myelopoiesis in the bone marrow and specifically induced
206 ced chronic arthritis, severe bone loss, and myelopoiesis in the bone marrow and spleen, which result
207 oid cells of lal(-/-) mice reversed abnormal myelopoiesis in the bone marrow starting at the granuloc
210 e data identify BCAP as a novel inhibitor of myelopoiesis in the steady state and of emergency myelop
211 ght important regulatory effects of IL-33 on myelopoiesis in vitro and in vivo, where excessive IL-33
212 rophages increases their capacity to support myelopoiesis in vitro, an effect mediated mainly through
213 cate that Notch-dependent signaling controls myelopoiesis in vivo and in vitro and identifies a requi
214 t to Dll1, Jag1, in vitro and during induced myelopoiesis in vivo, prevented DC differentiation by pr
216 g lymphoid development and suppressing overt myelopoiesis, in part through processes controlled by O-
220 L-ENL-induced AML but dispensable for normal myelopoiesis, indicating a specific requirement for Hhex
221 essive AML in vivo without preventing normal myelopoiesis, indicating that strategies to inhibit Myb-
222 myeloid differentiation, known as emergency myelopoiesis, involves recognition of pathogen-associate
225 idence for their participation in modulating myelopoiesis is much less clear, and roles for posttrans
233 be used to clarify the molecular genetics of myelopoiesis, it was found that the developmental hierar
234 ause IFN-gamma-deficient mice also increased myelopoiesis, it was suggested that IL-7 induced product
235 pression stimulates megakaryocytopoiesis and myelopoiesis leading to thrombocytosis and granulocytosi
236 hrombocytosis, and a marked dysregulation of myelopoiesis, leading to an important increase in myeloi
237 On transfer to IL-3, IL-6, and SCF to induce myelopoiesis, levels of granulocytic RNAs are reduced an
239 considered the alternative possibility that myelopoiesis may be regulated not by the hepatic sialyl
240 etic nervous system-induced up-regulation of myelopoiesis mediates the proinflammatory component of t
241 ence of JAK2(V617F)) and putative pattern of myelopoiesis (monoclonal versus polyclonal), it is yet t
242 ther has the balance between the two arms of myelopoiesis (monocytopoiesis and granulocytopoiesis) be
246 w that IFN-gamma-dependent infection-induced myelopoiesis occurs via the direct effect of the cytokin
247 ctivator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocytes and neutrophils an
248 tem cells and at more moderate levels during myelopoiesis of murine cell lines and primary murine cel
250 evelopment in the thymus but did not inhibit myelopoiesis or natural killer (NK) cell development in
251 ; cell cycle arrest is required for terminal myelopoiesis, perhaps due to expression of p53 or hypo-p
256 potential, but enhanced megakaryopoiesis and myelopoiesis, recapitulating the major phenotypes of the
257 ut there is increasing evidence that altered myelopoiesis, reduced effector T-cell function, and expa
258 neutrophil elastase acts as an inhibitor of myelopoiesis, substantiating a chalone hypothesis propos
260 syndrome neonates for the transient abnormal myelopoiesis (TAM) disorder based on blood cell morpholo
262 particular miRNAs and the unique features of myelopoiesis that are being uncovered by experimental ma
264 jury and sepsis results from an imbalance in myelopoiesis that is driven by the increased expression
265 tive erythropoiesis and, to a lesser extent, myelopoiesis that is independent of effects on vasculatu
266 (W-sh) mutation broadly affects key steps in myelopoiesis that may have an impact on mast cell resear
267 enic signaling, and (2) these data extend to myelopoiesis the growing body of evidence that the cellu
269 e cells regulate hematopoiesis, constraining myelopoiesis through a Gsalpha-mediated mechanism that a
270 s reveal a novel mechanism for inhibition of myelopoiesis through defective mitosis and cytokinesis d
271 gs suggest that HOTAIRM1 plays a role in the myelopoiesis through modulation of gene expression in th
272 omatous plaques of ApoE(-/-) mice with their myelopoiesis through regulation of hematopoietic stem an
273 usly to negatively regulate HSC function and myelopoiesis through Tet2-dependent and Tet2-independent
274 s, HFD feeding rapidly activates bone marrow myelopoiesis through the NE-dependent C/EBPalpha-GFI-1 p
275 place in LT-HSC, and not at later stages of myelopoiesis, to induce MPD and that only junB-deficient
277 liferation and infringed preferentially upon myelopoiesis under both steady-state and stressful condi
278 function provides insight into regulation of myelopoiesis under normal conditions and in myeloprolife
283 le of Janus kinase-2 (JAK2) in regulation of myelopoiesis was established 2 decades ago, but identifi
285 edian, 50% vs 18%; P < .0001), and wild-type myelopoiesis was suppressed in CALR(MUT) but not JAK2(V6
288 genic mice (line 215), resulting in aberrant myelopoiesis, we analyzed 17 cytokines in the peripheral
291 of creating a resource for in-depth study of myelopoiesis, we have executed a 2-pronged strategy to o
292 n that MDSCs are a manifestation of aberrant myelopoiesis, we hypothesized that MDSCs arise from pert
293 nesis screen to identify genes essential for myelopoiesis, we identified an insertional allele hi1727
294 Although best known as a potent inducer of myelopoiesis, we previously reported that G-CSF also pro
295 xamine the effect of the inv(16)(p13;q22) on myelopoiesis, we used the hMRP8 promoter element to gene
298 mily member IRF-8 is a critical regulator of myelopoiesis, which when deleted in mice results in a sy
299 of MN1-TEL-expressing mice developed altered myelopoiesis with severe anemia after long latency.
300 th interleukin-3 (IL-3) resulted in expanded myelopoiesis without a block in differentiation, PML-RAR
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