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1 ion to susceptibility to leukemia (malignant hematopoiesis).
2 ulates primitive myelopoiesis and definitive hematopoiesis.
3 ion of H2AV is primarily required for normal hematopoiesis.
4 transcription factor in normal and malignant hematopoiesis.
5 oiesis, which may include support to failing hematopoiesis.
6 s a master regulator of normal and malignant hematopoiesis.
7 ukemic HSCs, correlating with loss of normal hematopoiesis.
8 congenital neutropenia to assess for clonal hematopoiesis.
9 d cell cycle regulators in the regulation of hematopoiesis.
10 SC, further sustaining and driving malignant hematopoiesis.
11 bone marrow that contributes to ineffective hematopoiesis.
12 enance and HSC engraftment capacity in adult hematopoiesis.
13 ed overall survival without affecting murine hematopoiesis.
14 of the hepatic microvasculature in embryonic hematopoiesis.
15 uding their ability to form bone and support hematopoiesis.
16 icrobiota in the maintenance of steady-state hematopoiesis.
17 D9L in regulating IFN-driven, demand-adapted hematopoiesis.
18 HR) plays an important physiological role in hematopoiesis.
19 with myeloid cell dysplasia and ineffective hematopoiesis.
20 n, where we observed enhanced extramedullary hematopoiesis.
21 ng the RUNX transcription factor involved in hematopoiesis.
22 o be essential for adult but not early fetal hematopoiesis.
23 DH GRN and the HE, as well as into primitive hematopoiesis.
24 ying the maintenance of normal and malignant hematopoiesis.
25 -suppressive effects on normal and malignant hematopoiesis.
26 MDS specimens with this compound stimulated hematopoiesis.
27 hopoiesis without affecting other aspects of hematopoiesis.
28 xpansion of HSCs without compromising normal hematopoiesis.
29 factor Runx1 has essential roles throughout hematopoiesis.
30 s that affect biological processes including hematopoiesis.
31 that had not previously been associated with hematopoiesis.
32 se CD26, which modulates critical aspects of hematopoiesis.
33 with only minor contribution to steady-state hematopoiesis.
34 ystem recapitulates fetal erythroid-dominant hematopoiesis.
35 D proteins, have significant roles in normal hematopoiesis.
36 immune cells, distinguishes fetal from adult hematopoiesis.
37 ly been shown to support improved human cell hematopoiesis.
38 role for Rad18 in FA pathway function during hematopoiesis.
39 tudy of Gata2 expressing cells during normal hematopoiesis.
40 ogenic progenitors, which create a niche for hematopoiesis.
41 investigation of healthy and malignant human hematopoiesis.
42 may control both physiological and malignant hematopoiesis.
43 erroportin was increased probably to sustain hematopoiesis.
44 res of cytological dysplasia and ineffective hematopoiesis.
45 nism by which VEGF pathway inhibition alters hematopoiesis.
46 adiated mice entirely failed to reconstitute hematopoiesis.
47 ) mice exhibited normal body mass and normal hematopoiesis.
48 , little is known about the role of ATMIN in hematopoiesis.
49 nitiate the myeloid and lymphoid branches of hematopoiesis.
50 ation of lineage decisions is imperative for hematopoiesis.
51 elopment of endothelium producing adult-type hematopoiesis.
52 ecific deletion of Rargamma had no impact on hematopoiesis.
53 provide insight into the regulation of human hematopoiesis.
54 investigated the function of Usp16 in mouse hematopoiesis.
55 n mutation in the spliceosomal gene SF3B1 on hematopoiesis.
56 cal reduction in red pulp and extramedullary hematopoiesis.
57 us recapitulating important aspects of human hematopoiesis.
58 is required in all three waves of embryonic hematopoiesis.
59 t cell mediator release, and disturbances of hematopoiesis.
60 first blood cells generated during embryonic hematopoiesis.
61 s, and is essential during embryogenesis and hematopoiesis.
62 via activation of AGC protein kinases during hematopoiesis.
63 ion of primitive myelopoiesis and definitive hematopoiesis.
64 fumarate metabolism, in normal and leukemic hematopoiesis.
65 and BMSCs from only three centers supported hematopoiesis.
66 on and chorion, to human embryonic and fetal hematopoiesis.
67 interferon might have a particular effect on hematopoiesis.
68 n shown to regulate various stages of normal hematopoiesis.
69 s demonstrated residual aberrant oligoclonal hematopoiesis.
70 o induced pluripotent stem cells (iPSCs) and hematopoiesis.
71 ctive in vivo niche model for studying human hematopoiesis.
72 d m(6)A modification in normal and malignant hematopoiesis.
73 s in MDS patients as a result of ineffective hematopoiesis.
74 tor cells (HSPCs) and/or by promoting clonal hematopoiesis.
75 s in which recurrent mutations define clonal hematopoiesis.
76 ructure, composition, and function in normal hematopoiesis; (2) its alteration and functional relevan
77 niche changes and their suspected impact on hematopoiesis; (4) ongoing efforts to develop new models
78 the utility of this system to study neonatal hematopoiesis, a developmental stage that has been diffi
79 t only to MPN, but also to JAK2 V617F clonal hematopoiesis, a more common phenomenon that may foresha
81 increased cell cycling with improved stress hematopoiesis after 5-FU treatment, and this results in
83 clonal disorder characterized by ineffective hematopoiesis and a tendency to evolve into acute myeloi
84 t role in homeostatic as well as "emergency" hematopoiesis and are involved in the pathogenesis of se
85 committed to the adipocytic lineage inhibit hematopoiesis and bone healing, potentially by producing
86 Thus, alternative physiological patterns of hematopoiesis and bone marrow cell outputs depend on the
88 widely used diabetes drug metformin improves hematopoiesis and delays tumor formation in Fancd2(-/-)
89 during embryonic, fetal and adult stages of hematopoiesis and discusses the possible origins and con
90 in a narrow window of embryonic fetal liver hematopoiesis and do not persist in adult bone marrow.
91 EMH during pregnancy but normal bone marrow hematopoiesis and EMH in response to bleeding or G-CSF t
92 l regulation and function of Runx factors in hematopoiesis and focus particularly on the biological e
93 g the molecular mechanisms that govern human hematopoiesis and for developing novel therapies for dis
94 echanisms play important regulatory roles in hematopoiesis and hematopoietic stem cell (HSC) function
95 the critical role of the MPL-THPO pathway in hematopoiesis and highlight the importance of accurate g
96 are chronic diseases characterized by clonal hematopoiesis and hyperproliferation of terminally diffe
97 lent chromatin regulator BRPF1 in definitive hematopoiesis and illuminate a potentially new avenue fo
104 molecular and clinical studies indicate that hematopoiesis and leukemogenesis are dependent upon hypo
108 KDM2B as a critical regulator of definitive hematopoiesis and lineage commitment of murine hematopoi
109 stem cell (HSC) is capable of reconstituting hematopoiesis and maintaining homeostasis by balancing s
110 hanistically, FTY720 enhanced extramedullary hematopoiesis and massive accumulation of myeloid-derive
111 way to model the complex genetics of clonal hematopoiesis and myeloid disorders using CRISPR-Cas9 ge
112 tic gene regulation, the role of AID loss in hematopoiesis and myeloid transformation remains to be i
115 te that haploinsufficiency for Dnmt3a alters hematopoiesis and predisposes mice (and probably humans)
116 an unexpected fundamental role for ACKR1 in hematopoiesis and provide the mechanism that links its a
117 a morpholino oligomer (gata1aMO) suppressing hematopoiesis and resulting in attenuated trabeculation;
118 s, we have investigated the role of Plvap in hematopoiesis and show that deletion of Plvap results in
120 g evidence that Brca1 is critical for normal hematopoiesis and that Brca1 is a bona fide FA-like gene
122 effects of LEDGF/p75 depletion in postnatal hematopoiesis and the initiation of MLL leukemogenesis.
123 tors as possible drug candidates that act on hematopoiesis and the niche to prevent transformation of
125 se-modifying drugs that can eradicate clonal hematopoiesis and/or prevent progression to more aggress
126 d megakaryopoiesis, increased extramedullary hematopoiesis, and accelerated the development of MF in
128 togenesis, osteoclastogenesis, marrow T-cell hematopoiesis, and extra-skeletal endocrine organ functi
129 reminiscent of premature aging and stressed hematopoiesis, and indeed progressed with age and were e
131 rin proteins, discuss shelterin functions in hematopoiesis, and review emerging knowledge implicating
132 Specific functions of JAK1 in the context of hematopoiesis, and specifically within hematopoietic ste
133 GATAs 1, 2, and 3, are essential for normal hematopoiesis, and their mutations are responsible for a
139 of hematopoietic stem cell (HSC)-independent hematopoiesis as well as for the normal function of HSCs
140 tion of hematopoietic stem cells (definitive hematopoiesis), as shown by decreased expression of runx
141 ers, etsrp, fli1a, and scl; blocks primitive hematopoiesis, as shown by decreased expression of pu.1,
142 ur findings support the occurrence of clonal hematopoiesis-associated mutations as a widespread mecha
143 tors regulating lineage specification during hematopoiesis (ASXL1, IRF8, IKZF1, JMJD1C, ETS2-PSMG1),
147 microenvironment, called 'niche', regulates hematopoiesis both under homeostatic and immune stress c
148 ntributor to the maintenance of multilineage hematopoiesis, both in the steady state and during cytok
150 at LEDGF/p75 is dispensable for steady-state hematopoiesis but essential for the initiation of MLL-me
151 ion generated myeloid cells unfit for normal hematopoiesis but prone to immunogenic death, leading to
153 marrow microenvironment influences malignant hematopoiesis, but how it promotes leukemogenesis has no
154 cifies primitive myelopoiesis and definitive hematopoiesis, but not primitive erythropoiesis or vascu
155 d for their ability to form bone and support hematopoiesis by in vivo transplantation (defining featu
156 re, we investigated the function of BRPF1 in hematopoiesis by selectively deleting its gene in murine
157 a non-cell-autonomous role in regulation of hematopoiesis by simultaneously preserving HSPC stemness
158 Multilineage involvement of bone marrow (BM) hematopoiesis by the somatic KIT D816V mutation is prese
159 set out to study the role of MOF in general hematopoiesis by using a Vav1-cre-induced conditional mu
164 characterized by BM fibrosis, extramedullary hematopoiesis, circulating CD34+ cells, splenomegaly, an
167 ed bone marrow compromised in reconstituting hematopoiesis, demonstrating that HSCs and early progeni
168 and bone marrow/thymic niches during normal hematopoiesis, describes the main signaling pathways imp
175 ortant to iron acquisition, homeostasis, and hematopoiesis (enterocytes, hepatocytes, macrophages, he
176 types, and its absence results in perturbed hematopoiesis, especially during stress conditions and a
177 bone marrow serves as the primary niche for hematopoiesis, extramedullary mobilization and different
178 to mimic in vitro a key early stage in human hematopoiesis for the generation of AGM-derived hematopo
180 ndings have important implications for human hematopoiesis, given the similarities between macaque an
181 (SC) compartment in both normal and leukemic hematopoiesis has been challenging due to the inability
182 mphoid and myeloid neoplasms in which normal hematopoiesis has gone awry and together account for app
186 dvances in our understanding of steady-state hematopoiesis have allowed us to explore the effects of
187 the requirement for ARID3a for normal human hematopoiesis, hematopoietic stem cell progenitors from
188 developmental timing processes in vertebrate hematopoiesis, highlighting how identification and manip
189 re critical for both normal and pathological hematopoiesis; however, it is unclear which of the sever
191 of bone and immune compartments critical for hematopoiesis, immunological memory, and bone regenerati
196 serve as a prime signal in the commitment to hematopoiesis in both mammals and Drosophila In this stu
197 w insights into cell-extrinsic disruption of hematopoiesis in CML associated with clinical outcome.
198 oietic colonies in vitro and to reconstitute hematopoiesis in irradiated recipients, consistent with
201 ich RUNX1C(+) blood cells emerge, similar to hematopoiesis in the aorta-gonad-mesonephros (AGM).
204 study, the potential function of ROS during hematopoiesis in the crayfish Pacifastacus leniusculus w
206 m E10.5 onward did not compromise definitive hematopoiesis in the liver, and Vegfc deletion in adult
208 ed minimal inhibitory effect on normal human hematopoiesis in vitro and was very well tolerated in an
211 partment that reconstitutes short-term human hematopoiesis in xenotransplantation models is usually t
212 nces in peripheral blood cell counts (normal hematopoiesis) in addition to susceptibility to leukemia
213 most commonly mutated gene linked to clonal hematopoiesis, in the hematopoietic cells of atheroscler
214 study show that ROS are involved in crayfish hematopoiesis, in which a low ROS level is required to m
215 The absence of erythroid ACKR1 altered mouse hematopoiesis including stem and progenitor cells, which
225 of the most studied transcription factors in hematopoiesis is the leucine zipper CCAAT-enhancer bindi
227 ed genes has been associated with defects in hematopoiesis, it remains unclear whether hyperactivated
231 s particular environment is also the site of hematopoiesis, megakaryocytopoiesis, and platelet produc
233 ET2 occur frequently in patients with clonal hematopoiesis, myelodysplastic syndrome (MDS), and acute
234 s not affect erythropoiesis during primitive hematopoiesis (no effect on gata1 or h-bae1) or vasculog
235 the orthotopic BALB/cJ model, extramedullary hematopoiesis occurred in the spleen, resulting in a fou
242 n characterized as frequent events in clonal hematopoiesis of indeterminate potential, suggesting a m
243 ical organization of malignant clones in the hematopoiesis of myelodysplastic syndromes (MDS) and its
244 viduals with idiopathic cytopenias or clonal hematopoiesis of undetermined significance, the identifi
245 emia (AML) and largely dispensable for basal hematopoiesis, plays an important role in facilitating l
246 e most abundantly expressed isoform in adult hematopoiesis, present in all RUNX1-expressing populatio
247 EphrinB2 as an essential regulator of adult hematopoiesis provides important insight in the regulati
249 ce were viable but showed several defects in hematopoiesis, reduced colony-forming activity in vitro,
251 ure of hematopoietic stem cells under normal hematopoiesis remained largely unknown due to the limite
252 These patients have BCR-ABL1-positive clonal hematopoiesis resembling a chronic myeloid leukemia (CML
253 nate-like B cell population of fetal-derived hematopoiesis, responsible for natural Ab production and
257 ell function, contributing to extramedullary hematopoiesis, splenomegaly, BM failure, and decreased l
259 n turn are recruited from sites of embryonic hematopoiesis such as the yolk sac by way of blood flow.
260 his metabolic activity changes during stress hematopoiesis, such as bone marrow transplantation.
261 vasculature and regulate diverse aspects of hematopoiesis, such as HSPC trafficking, in steady-state
262 B coordinate distinct developmental fates in hematopoiesis, suggesting that their functional differen
263 d for adult but not early and midgestational hematopoiesis supports the notion that multiple chromati
265 y individuals along with clonal expansion of hematopoiesis that confers an increased risk for the dev
267 myeloid malignancies and clonal disorders of hematopoiesis that may give rise to these disorders have
270 patients suffering from myriad disorders of hematopoiesis, their application for therapeutic modific
271 important for both skeletal development and hematopoiesis, through the formation of HS proteoglycans
272 s disease evolution from asymptomatic clonal hematopoiesis to frank MDS, and, ultimately, to secondar
273 esponse is regulated at various stages, from hematopoiesis to monocyte changes and macrophage activat
274 s a phenotypic continuum ranging from clonal hematopoiesis to myelodysplastic syndrome (MDS) and acut
276 exist on a spectrum from asymptomatic clonal hematopoiesis to overt leukemia and exhibit substantial
278 f pathogens and inflammatory cytokines skews hematopoiesis toward myeloid development, although the p
281 could provide a new standard tool to analyze hematopoiesis under physiological condition without tran
282 ma responsible for the suppression of normal hematopoiesis using a T-ALL mouse model and human T-ALL
283 urviving patients, improvement in trilineage hematopoiesis was achieved following treatment with a TH
286 d massive reduction of LT-HSCs, steady-state hematopoiesis was unaffected and residual HSCs remained
287 st the hypothesis that Brca1 is essential in hematopoiesis, we developed a conditional mouse model wi
288 Although it has little impact on normal hematopoiesis, we found that PGE1 treatment impaired the
290 xpression of HMGA2 and JAK2V617F mutation in hematopoiesis, we transduced bone marrow cells from Jak2
291 ed included 40 regions known to drive clonal hematopoiesis when mutated and 64 novel candidate loci.
292 or both blood vessel formation and embryonic hematopoiesis, whereas the possible involvement of VEGF-
293 gulated epigenetic modifiers in normal aging hematopoiesis, which may include support to failing hema
294 nalyses have begun to define fetal and adult hematopoiesis, while cell-fate mapping studies have reve
295 mal, healthy elderly individuals with clonal hematopoiesis who are at increased risk of subsequently
296 hed transcription factor in human and murine hematopoiesis whose function in HSC biology remains elus
298 pirate and biopsy revealed normal trilineage hematopoiesis with no evidence of lymphoma and a normal
299 ologic remission may continue to have clonal hematopoiesis with populations closely related to the fo
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