ライフサイエンスコーパス: hematopoietic

1 Hematopoietic acute radiation syndrome (H-ARS) and delay

2 X-301, both pre- and post-radiation, against hematopoietic acute radiation syndrome with a broad wind

3 ral cancer initiation by the bone marrow and hematopoietic adaptation to distant noxia through transc

4 Hematopoietic ageing involves declining erythropoiesis a

5 more broadly, to study and characterize the hematopoietic and immune systems.

6 late leads to long-term viral replication in hematopoietic and mesenchymal cells, but not epithelial

7 The insights from hematopoietic and neural stem cell differentiation pathw

8 , numerous antigen-presenting partners, both hematopoietic and non-hematopoietic, were sufficient to

9 mouse models of allogeneic T-cell therapy of hematopoietic and solid cancers.

10 scriptional signatures of different types of hematopoietic and vascular progenitors are identified us

11 urface antigen CD19 has been demonstrated in hematopoietic cancers.

12 to SP and NK-A to protect the most primitive hematopoietic cell and also to maintain immune/hematopoi

13 ess functions of the Id3 and/or Tet2 gene in hematopoietic cell development and clonal hematopoiesis.

14 e the causal role of heterochromatin loss in hematopoietic cell development.

15 he effects of anti-cancer agents on multiple hematopoietic cell lineages.

16 ression pattern of metabolic pathways of two hematopoietic cell lines, we find that the relative posi

17 at Fbxl8 antagonizes cell cycle progression, hematopoietic cell proliferation, and oncogene-induced t

18 HE cells undergo an endothelial to hematopoietic cell transition, giving rise to HSPCs that

19 a significant complication facing allogeneic hematopoietic cell transplant (allo-HCT) recipients, as

20 use of morbidity and mortality in allogeneic hematopoietic cell transplant (allo-HCT) recipients.

21 eiving intensive chemotherapy and the use of hematopoietic cell transplant (HCT) for specific high-ri

22 associated with substantial morbidity among hematopoietic cell transplant (HCT) recipients, but the

23 V) infection causes significant morbidity in hematopoietic cell transplant (HCT) recipients.

24 tiocytosis, congenital immunodeficiency, and hematopoietic cell transplant are independently associat

25 Among patients without hematopoietic cell transplant, congenital immunodeficien

26 lood specimens from recipients of allogeneic hematopoietic cell transplant.

27 of morbidity and mortality after allogeneic hematopoietic cell transplantation (allo-HCT).

28 Allogeneic hematopoietic cell transplantation (alloHCT) benefits in

29 graft-vs-tumor effects following allogeneic hematopoietic cell transplantation (alloHCT), but retros

30 Post hematopoietic cell transplantation (HCT) autoimmune cyto

31 ary immunodeficiencies undergoing allogeneic hematopoietic cell transplantation (HCT) for difficult-t

32 Hematopoietic cell transplantation (HCT) is the primary

33 Hematopoietic cell transplantation (HCT) remains the onl

34 been effective in preventing acute GvHD post hematopoietic cell transplantation (HCT), its efficacy a

35 onditioning for HLA class I or II mismatched hematopoietic cell transplantation (HCT).

36 Allogeneic hematopoietic cell transplantation at the time of second

37 The success of allogeneic hematopoietic cell transplantation depends heavily on th

38 versus-host disease (aGVHD) after allogeneic hematopoietic cell transplantation have poor prognosis,

39 induced hematopoietic syndrome is allogeneic hematopoietic cell transplantation, a therapy unavailabl

40 analysis of a nonhematologic neoplasm, after hematopoietic cell transplantation, or as a result of ge

41 iders who care for patients after allogeneic hematopoietic cell transplantation.

42 life-threatening complication of allogeneic hematopoietic cell transplantation.

43 reduce the risk of relapse after allogeneic hematopoietic cell transplantation.

44 lly validating this model in unrelated donor hematopoietic cell transplantation.

45 In hematopoietic cell transplants, alloreactive T cells med

46 crophages (TAMs) represent the most abundant hematopoietic cell type in the solid tumor microenvironm

47 Hematopoietic cell-specific deletion of PTN suppressed C

48 se these cells express the cortactin homolog hematopoietic cell-specific lyn substrate-1.

49 current knowledge on cortactin expression in hematopoietic cells and discusses the functional implica

50 ggering apoptosis in specific cells, such as hematopoietic cells and endothelium.

51 a ubiquitous pathogen that latently infects hematopoietic cells and has the ability to reactivate wh

52 py on PI-PLCbeta1 inositide signaling, using hematopoietic cells and MDS samples.

53 tibodies inhibited leukemic, but not normal, hematopoietic cells and synergized with other antileukem

54 marrow transplantation experiments identify hematopoietic cells as the predominant source of plasma

55 has been until recently considered absent in hematopoietic cells because these cells express the cort

56 raftment of normal and diseased human immune/hematopoietic cells has made in vivo functional characte

57 d infer cellular dynamics of differentiating hematopoietic cells in vitro and in vivo.

58 he hypomethylation phenotype of Dnmt3a (-/-) hematopoietic cells is reversible, we developed an induc

59 on factor in the terminal differentiation of hematopoietic cells to the monocytes has been well estab

60 tal stage in which HCMV infects, HCMV drives hematopoietic cells towards a weaker immune-responsive m

61 c stem cell niche and are thought to protect hematopoietic cells under stress.

62 ound that constitutive MDR1 expression among hematopoietic cells was observed in cytolytic lymphocyte

63 era experiments showed that CD137L-deficient hematopoietic cells were able to confer T1D resistance.

64 ned by the continuous interactions of mobile hematopoietic cells within specialized microenvironments

65 ecular bone and collagen fibers that replace hematopoietic cells, resulting in abnormal bone marrow f

66 ed a conditioning regimen, infusion of donor hematopoietic cells, then immunosuppressive drugs and an

67 n in thymic epithelial cells (TECs), but not hematopoietic cells, was sufficient for complete deletio

68 ated mice lacking LIFR in either CD11c(+) or hematopoietic cells.

69 diation preconditioning to ablate endogenous hematopoietic cells.

70 of induced RASGRP1 overexpression in primary hematopoietic cells.

71 s during short-term or long-term tracking of hematopoietic cells.

72 In conclusion, non-hematopoietic cellular sources, rather than plasmacytoid

73 However, a comprehensive analysis of hematopoietic changes caused by heterochromatin loss is

74 Hematopoietic changes were associated with modifications

75 s of rejection status, and in tolerant mixed hematopoietic chimeras, the co-existence of these cells

76 T cell responses and thereby enhanced donor hematopoietic chimerism and T cell deletion after bone m

77 Hematopoietic clones with leukemogenic mutations arise i

78 ted YAP activation enhanced RUNX1 levels and hematopoietic colony-forming potential.

79 lammasome stimulation increased multilineage hematopoietic colony-forming units and T cell progenitor

80 Finally, mice carrying Tet2 mutations in the hematopoietic compartment (a common model for CH) displa

81 es that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasi

82 As a consequence, the hematopoietic compartment reconstitution was improved be

83 d negatively with the expansion of the human hematopoietic compartment.

84 ent membrane composition in the formation of hematopoietic compartments.

85 GT3-Nano can facilitate rapid recovery of hematopoietic components in mice treated with the endora

86 Hematopoietic Cx43-deficient chimeric mice show reduced

87 We show that the absence of hematopoietic CXCL4 ameliorates the MPN phenotype, reduc

88 little is known about its role in mammalian hematopoietic development.

89 essenger RNA (mRNA) translation during human hematopoietic development.

90 ious innate immune response during mammalian hematopoietic development.

91 It is important for hematopoietic differentiation and plays a central role i

92 transcription reprogramming associated with hematopoietic differentiation poses a major threat to ge

93 ata show that DNAme shapes the topography of hematopoietic differentiation, and support a model in wh

94 ing to dyserythropoiesis and an imbalance of hematopoietic differentiation.

95 GS may contain germline, somatic, and clonal hematopoietic DNA alterations, and distinguishing the et

96 The hematopoietic effects of SP and NK-A are mostly mediated

97 er studies are warranted to assess long-term hematopoietic effects.

98 Cell fate decisions involved in vascular and hematopoietic embryonic development are still poorly und

99 portance of accessory, non-HSC to accelerate hematopoietic engraftment.

100 atopoietic stem cell transplantation for the hematopoietic features of SMARCD2 deficiency.

101 an RNA-binding protein associated with fetal hematopoietic gene expression programs, and these cells

102 cells (MSCs) without co-administration of a hematopoietic graft have shown underwhelming rescue of e

103 superoxide in the mediating pathways and of hematopoietic GSTM1 on renal inflammation.

104 iesis, these tools reconstruct the classical hematopoietic hierarchy and detect couplings between mon

105 matopoietic cell and also to maintain immune/hematopoietic homeostasis.

106 g the central nervous, endocrine, metabolic, hematopoietic, immune and, finally, the cardiovascular s

107 n multiple cell types, except those from the hematopoietic lineage.

108 ineage modulate the differentiation of other hematopoietic lineages is largely unknown.

109 tiation and is not observed in non-erythroid hematopoietic lineages or healthy erythroblasts.

110 "memory" via a circulating signal, reducing hematopoietic maintenance factor expression in bone marr

111 cancers in a single patient, diagnosis of a hematopoietic malignancy at a younger age than seen in t

112 s establishing an association between CH and hematopoietic malignancy, discuss features of CH that ar

113 oth the development of CH and progression to hematopoietic malignancy.

114 The majority of TdT(OSX)+ cells express the hematopoietic marker CD45, have a genetic and phenotypic

115 0, and CD105, whereas they were negative for hematopoietic markers, including CD34 and CD45.

116 lood cell homing and their interactions with hematopoietic microenvironments remain poorly understood

117 imeras confirmed that vascular Nck1, but not hematopoietic Nck1, mediated this effect.

118 he interactions between gametocytes and this hematopoietic niche have not been investigated.

119 es of recent studies have suggested that the hematopoietic niche of the bone marrow (BM) is a major r

120 The Drosophila lymph gland, the larval hematopoietic organ comprised of prohemocytes and mature

121 Using Drosophila hematopoietic organ: lymph gland, we demonstrate that Fa

122 most cancers with infectious etiology or of hematopoietic origin were driven by multiple HLA regions

123 rticularly those with infectious etiology or hematopoietic origin, given its role in immune presentat

124 wed by genetic lineage tracing to have a non-hematopoietic origin.

125 The hematopoietic potential of patient-derived induced pluri

126 ecific tissue microenvironments that nurture hematopoietic precursors and promote their self-renewal,

127 Bacteria, cytokines, leukocytes, and hematopoietic precursors were quantified in blood, bone

128 Here we show that murine HSCs and committed hematopoietic progenitor cells (HPCs) undergo a gradual,

129 nant-negative ETS1 p27 isoform in cord blood hematopoietic progenitor cells, we show that the transcr

130 implicated in regulating embryonic stem and hematopoietic progenitor cells.

131 We found that AXL interacts with hematopoietic progenitor kinase 1 (HPK1) and demonstrate

132 In this perspective review, the role Hematopoietic Progenitor Kinase 1 (HPK1) in tumor immuni

133 CD21 promoter enabled Xlf deletion in early hematopoietic progenitors and splenic mature B cells, re

134 Whether developing hematopoietic progenitors of a particular lineage modula

135 ization of the thymus by bone-marrow-derived hematopoietic progenitors that migrate through the blood

136 o such effects were observed in CD34+ normal hematopoietic progenitors, although CDK6 was efficiently

137 ted in both CD11b + and CD11b- cells, and in hematopoietic progenitors.

138 Macrophages derive from multiple sources of hematopoietic progenitors.

139 ction to enforce self-renewal in bone marrow hematopoietic progenitors.

140 However, early phases of hematopoietic reconstitution following bone marrow trans

141 y or other fitness-reducing mutations during hematopoietic reconstitution following bone marrow trans

142 n of Vegfc from the microenvironment delayed hematopoietic recovery after transplantation by decreasi

143 that suppresses BM inflammation and enhances hematopoietic recovery following myelosuppression.

144 rradiation (TBI) promoted rapid and complete hematopoietic recovery, whereas recovery of controls sta

145 We show that hematopoietic regeneration in vivo following total body

146 nstrate that EGF promotes HSC DNA repair and hematopoietic regeneration in vivo via augmentation of N

147 F has therapeutic potential to promote human hematopoietic regeneration, and further studies are warr

148 gnificant therapeutic opportunity to improve hematopoietic regeneration.

149 pts through the application of PRAM to mouse hematopoietic RNA-seq data sets.

150 stem cells, HSCs transition through multiple hematopoietic sites during development.

151 oming mechanism that specifies and maintains hematopoietic sites in Drosophila.

152 2-expressing HSPCs demonstrate enrichment of hematopoietic-specific enhancers associated with pro-dif

153 ring mutations in NCKAP1L, which encodes the hematopoietic-specific HEM1 protein.

154 The hematopoietic-specific protein tyrosine phosphatase nonr

155 s were due to an intrinsic property of fetal hematopoietic stem and precursor cells (HSPCs) caused by

156 Recent studies demonstrate that in the hematopoietic stem and progenitor cell (HSPC) compartmen

157 Inflammatory signaling is required for hematopoietic stem and progenitor cell (HSPC) developmen

158 Hematopoietic stem and progenitor cell (HSPC) formation

159 Aging leads to a decline in hematopoietic stem and progenitor cell (HSPC) function.

160 ents who received ex vivo autologous CD34(+) hematopoietic stem and progenitor cell-based lentiviral

161 The fate of hematopoietic stem and progenitor cells (HSPC) is tightl

162 port on LSC proteomes to healthy age-matched hematopoietic stem and progenitor cells (HSPCs) and corr

163 Definitive hematopoietic stem and progenitor cells (HSPCs) arise fr

164 Hematopoietic stem and progenitor cells (HSPCs) develop

165 h may be related to dysregulated activity of hematopoietic stem and progenitor cells (HSPCs) in the b

166 Hematopoietic stem and progenitor cells (HSPCs) in the b

167 Conditional deletion of EGFR in hematopoietic stem and progenitor cells (HSPCs) signific

168 ence of myeloid- and lymphoid-dominant human hematopoietic stem and progenitor cells (HSPCs) using cl

169 In gene therapy with human hematopoietic stem and progenitor cells (HSPCs), each ge

170 tome profiling of 135,929 CD34(+) lineage(-) hematopoietic stem and progenitor cells (HSPCs), single-

171 ction of WAS mutations in up to 60% of human hematopoietic stem and progenitor cells (HSPCs), without

172 the specification of human cDCs from CD34(+) hematopoietic stem and progenitor cells (HSPCs).

173 alternative method for RNA delivery to human hematopoietic stem and progenitor cells (HSPCs).

174 sis to characterize latency in monocytes and hematopoietic stem and progenitor cells (HSPCs).

175 mia (FA) patients results from dysfunctional hematopoietic stem and progenitor cells (HSPCs).

176 ity, dormant label-retaining (LR) and non-LR hematopoietic stem and progenitor cells both had indisti

177 the proliferation of Lin(-)Sca-1(+)c-Kit(+) hematopoietic stem and progenitor cells in the bone marr

178 receptor (interleukin 1 receptor type 1) on hematopoietic stem and progenitor cells in the bone marr

179 nges that underlie abnormal proliferation of hematopoietic stem and progenitor cells is critical for

180 marrow cellularity, numbers and function of hematopoietic stem and progenitor cells, and frequency o

181 CPI203-mediated reprogramming of cord blood hematopoietic stem and progenitor cells.

182 Hematopoietic stem cell (HSC) attrition is considered th

183 ed fitness and increased myeloid bias of the hematopoietic stem cell (HSC) compartment, causing incre

184 ate harmful inflammatory reactions and cause hematopoietic stem cell (HSC) exhaustion; therefore, IFN

185 We have identified that hematopoietic stem cell (HSC) fitness response to stress

186 , including increased inflammation, impaired hematopoietic stem cell (HSC) function, and increased in

187 ls (MSPCs) are a critical constituent of the hematopoietic stem cell (HSC) niche.

188 nce is a fundamental property that maintains hematopoietic stem cell (HSC) potency throughout life.

189 s in patient and donor is indeed required in hematopoietic stem cell and solid-organ transplantation,

190 show that Grasp55 deficiency does not affect hematopoietic stem cell differentiation, engraftment, or

191 severely short telomeres, often resulting in hematopoietic stem cell failure in the most severe cases

192 1 nor Suv39h2 individually had any effect on hematopoietic stem cell function or the development of m

193 hanges associated with aging such as reduced hematopoietic stem cell function, thymic involution and

194 ng of various factors interacting to control hematopoietic stem cell generation, both in time and spa

195 al cells serve as critical components of the hematopoietic stem cell niche and are thought to protect

196 d fungal infection, as well as assessment of hematopoietic stem cell transduction and engraftment.

197 ported outcomes among survivors of pediatric hematopoietic stem cell transplant (HSCT) are understudi

198 Therapeutic hematopoietic stem cell transplant (HSCT) during chronic

199 ients who are recipients of a solid organ or hematopoietic stem cell transplant are living longer wit

200 ention of cytomegalovirus (CMV) infection in hematopoietic stem cell transplant patients.

201 py or graft versus host disease treatment in hematopoietic stem cell transplant recipients often resu

202 t morbidity and mortality in solid organ and hematopoietic stem cell transplant recipients.

203 5% CI, 11.3-13.2) in those who had undergone hematopoietic stem cell transplant.

204 definitive treatment for primary disease is hematopoietic stem cell transplant.

205 success and wider utilization of allogeneic hematopoietic stem cell transplantation (allo-HSCT) is l

206 Allogeneic hematopoietic stem cell transplantation (alloSCT) is an

207 GVHD) has been observed after haploidentical hematopoietic stem cell transplantation (h-HSCT) with po

208 Hematopoietic stem cell transplantation (HSCT) improves

209 e potential therapeutic effect of allogeneic hematopoietic stem cell transplantation (HSCT) in autoin

210 tal body irradiation (TBI) before allogeneic hematopoietic stem cell transplantation (HSCT) in pediat

211 disease (GVHD) biology beyond 3 months after hematopoietic stem cell transplantation (HSCT) is comple

212 whether treated with conventional therapy or hematopoietic stem cell transplantation (HSCT), and that

213 a major cause of morbidity and mortality in hematopoietic stem cell transplantation (HSCT).

214 S) is a serious complication post allogeneic hematopoietic stem cell transplantation (HSCT).

215 r molecular diagnosis, our patient underwent hematopoietic stem cell transplantation and is well 8 ye

216 Hematopoietic stem cell transplantation and NF-kappaB1 p

217 ith hematological malignancies or undergoing hematopoietic stem cell transplantation are vulnerable t

218 tients >60 years of age undergoing allogenic hematopoietic stem cell transplantation at our instituti

219 ediatric patients undergoing chemotherapy or hematopoietic stem cell transplantation for hematologica

220 ia, and sensorineural deafness that requires hematopoietic stem cell transplantation for survival.

221 uman myelopoiesis and the curative effect of hematopoietic stem cell transplantation for the hematopo

222 Because poor B-cell reconstitution after hematopoietic stem cell transplantation has been observe

223 Finally, hematopoietic stem cell transplantation in patients redu

224 Hematopoietic stem cell transplantation is the only cura

225 y, no estimates can be made on the impact of hematopoietic stem cell transplantation on allergy trans

226 patient with Hurler's syndrome treated with hematopoietic stem cell transplantation was referred for

227 Hematopoietic stem cell transplantation would result in

228 (2020) show that hematopoietic stem cell transplantation, an established

229 y, whereas underlying malignancy, allogeneic hematopoietic stem cell transplantation, and neutropenia

230 s T-cell reconstitution following allogeneic hematopoietic stem cell transplantation.

231 ory disease that affects patients undergoing hematopoietic stem cell transplantation.

232 lt CMV-seropositive recipients of allogeneic hematopoietic stem cell transplantation.

233 egarding allergic diseases in the context of hematopoietic stem cell transplantation.

234 ption of adding olanzapine in the setting of hematopoietic stem cell transplantation.

235 Hematopoietic stem cells (HSC) self-renew to sustain ste

236 -CreER enables permanent genetic labeling of hematopoietic stem cells (HSCs) and distinguishes HSC-de

237 Hematopoietic stem cells (HSCs) are regulated by signals

238 Culture conditions in which hematopoietic stem cells (HSCs) can be expanded for clin

239 multipotent and self-renewing capabilities, hematopoietic stem cells (HSCs) can maintain hematopoies

240 Hematopoietic stem cells (HSCs) develop from the hemogen

241 Fetal and adult hematopoietic stem cells (HSCs) have distinct proliferat

242 The exact localization of hematopoietic stem cells (HSCs) in their native bone mar

243 Expansion of human hematopoietic stem cells (HSCs) is a rapidly advancing f

244 Somatic DNMT3A mutations arise in hematopoietic stem cells (HSCs) many years before malign

245 ceptor subunit alpha (IL-27Ra) expression on hematopoietic stem cells (HSCs) mediates changes in HSCs

246 As humans age, hematopoietic stem cells (HSCs) occasionally acquire mut

247 Hematopoietic stem cells (HSCs) remain quiescent to pres

248 Hematopoietic stem cells (HSCs) reside in the bone marro

249 ying mechanisms and interactions of residual hematopoietic stem cells (HSCs) within the leukemic nich

250 otherapy and irradiation cause DNA damage to hematopoietic stem cells (HSCs), leading to HSC depletio

251 nce is critical for the maintenance of adult hematopoietic stem cells (HSCs).

252 ma thrombopoietin (TPO) levels and perturbed hematopoietic stem cells (HSCs).

253 rgt(m1Wjl)/SzJ mice reconstituted with human hematopoietic stem cells (Hu-NSG mice) and infected with

254 iased progenitors, followed by precursors of hematopoietic stem cells (pre-HSCs).

255 is disrupted profoundly, with a reduction of hematopoietic stem cells and common lymphoid progenitors

256 of the bone marrow that caused depletion of hematopoietic stem cells and impaired proper regeneratio

257 on early during hematopoiesis, in subsets of hematopoietic stem cells and multipotent progenitor popu

258 for the long-term encoding of ncAAs in human hematopoietic stem cells and reconstitution of this gene

259 the aortic microenvironment, where the first hematopoietic stem cells are generated during developmen

260 tential (CHIP) refers to clonal expansion of hematopoietic stem cells attributable to acquired leukem

261 Hematopoietic stem cells develop in a specialized niche

262 n in humanized mice reconstituted with human hematopoietic stem cells from donors homozygous for a fu

263 ic leukemia and underwent transplantation of hematopoietic stem cells from his human leukocyte antige

264 ic leukemia and underwent transplantation of hematopoietic stem cells from his human leukocyte antige

265 e bone marrow, where they differentiate from hematopoietic stem cells in a process called granulopoie

266 ia-associated somatic mutations by 1 or more hematopoietic stem cells is inevitable with advancing ag

267 DL1 expression is significantly increased in hematopoietic stem cells of patients with TP53 mutations

268 que MUSASHI-2 (MSI2) mRNA binding network in hematopoietic stem cells that changes during transition

269 matopoiesis, provide bounds on the number of hematopoietic stem cells, and quantify the fitness advan

270 w, CSF1R-FRed was absent in lineage-negative hematopoietic stem cells, arguing against a direct role

271 tion of proreparatory CD150(+)CD48(-)CCR2(+) hematopoietic stem cells.

272 Hematopoietic stem progenitor cells (HSPCs) stimulate re

273 human erythroleukemia TF1 cells and primary hematopoietic stem-progenitor cells.

274 he fact that at early stages, tumors recruit hematopoietic stem/progenitor cells (HSPC) from the bone

275 Mobilization of hematopoietic stem/progenitor cells (HSPC) from the bone

276 Bone marrow-derived hematopoietic stem/progenitor cells are vasculogenic and

277 s from Hoxa(neg/low) Kit(+)CD41(+)CD16/32(+) hematopoietic-stem-cell (HSC)-independent erythro-myeloi

278 There is emerging evidence suggesting that hematopoietic stressors contribute to both the developme

279 eukemic progression, and explore the role of hematopoietic stressors in the evolution of CH to acute

280 hat drive stromal activation and fibrosis by hematopoietic-stromal cross-talk remain elusive.

281 amily ligands (GFLs) as potential drivers of hematopoietic survival and self-renewal in the bone marr

282 h or 30 h in ameliorating radiation-induced hematopoietic syndrome and show that pancytopenia persis

283 available option to treat radiation-induced hematopoietic syndrome is allogeneic hematopoietic cell

284 Mice expressing active Kras(G12D) in the hematopoietic system developed myeloproliferation and cy

285 ing sufficient H3K9me3 to protect the entire hematopoietic system from changes associated with premat

286 Together, our results indicate that the hematopoietic system has a remarkable tolerance for majo

287 We further characterized the hematopoietic system in individuals with CH as follows:

288 econstitution of this genetically engineered hematopoietic system in mice.

289 s associated with significant changes in the hematopoietic system, including increased inflammation,

290 In the hematopoietic system, the function of the pathway has be

291 rsed in Kras(G12D) mice lacking NLRP3 in the hematopoietic system.

292 e but experienced equivalent collapse of the hematopoietic system.

293 odynamic and histological evidence of PAH in hematopoietic Tet2-knockout mice.

294 e HSCs, and conditional knockout of Sel1L in hematopoietic tissues drives HSCs to hyperproliferation,

295 dritic cells (DCs) is controlled by multiple hematopoietic transcription factors, including IRF8.

296 The mechanisms of this endothelial-to-hematopoietic transition (EHT) are poorly understood.

297 criptional regulators for the endothelial-to-hematopoietic transition, validating our overall approac

298 Hematopoietic transplantation is the preferred treatment

299 Solid and hematopoietic tumors often experience genomic instabilit

300 senting partners, both hematopoietic and non-hematopoietic, were sufficient to reactivate lung CD8+ T