ライフサイエンスコーパス: hematopoiesis

1 e genetic diversity of healthy blood (clonal hematopoiesis).

2 ogenic endothelial cell development on adult hematopoiesis.

3 systematic integration of epigenomic data in hematopoiesis.

4 demonstrate its utility for modeling clonal hematopoiesis.

5 a more comprehensive future understanding of hematopoiesis.

6 SION website to aid research in genomics and hematopoiesis.

7 tion of this protein in normal and malignant hematopoiesis.

8 phages can originate from embryonic or adult hematopoiesis.

9 al repressor that plays an important role in hematopoiesis.

10 ypes covering a range of variation impacting hematopoiesis.

11 important role in the development of clonal hematopoiesis.

12 lls (LSCs/LICs) but not essential for normal hematopoiesis.

13 y contribution from fetal liver or postnatal hematopoiesis.

14 ion programs governing lineage allocation in hematopoiesis.

15 nsregulates Notch pathway genes required for hematopoiesis.

16 oid neoplasia, suggesting a critical role in hematopoiesis.

17 genes not previously associated with clonal hematopoiesis.

18 the development of the neural crest and for hematopoiesis.

19 r reestablishing homeostasis after emergency hematopoiesis.

20 ssociated with the lymphoid lineage in adult hematopoiesis.

21 SCs expressing the CAR-Stop sustained normal hematopoiesis.

22 It was shown critical for primitive hematopoiesis.

23 pendent of de novo generation by bone marrow hematopoiesis.

24 have provided important insights into human hematopoiesis.

25 gonism as well as stage-selective effects on hematopoiesis.

26 cting lncRNA that has physiological roles in hematopoiesis.

27 of innate-like B-1a lymphocytes during fetal hematopoiesis.

28 anaemic with splenomegaly and extramedullary hematopoiesis.

29 estriction of inflammation driven pathologic hematopoiesis.

30 lity in individuals with age-related, clonal hematopoiesis.

31 tion reduces myeloproliferation and improves hematopoiesis.

32 iption factor regulates normal and malignant hematopoiesis.

33 ents that disrupt multiple genes controlling hematopoiesis.

34 y expand and differentiate during definitive hematopoiesis.

35 (LSC) function but is dispensable for normal hematopoiesis.

36 and maintain gene expression patterns during hematopoiesis.

37 may not reflect the biology of steady-state hematopoiesis.

38 siological and pathological angiogenesis and hematopoiesis.

39 mechanism by which mutant p53 drives clonal hematopoiesis.

40 cancer) had features consistent with clonal hematopoiesis.

41 fects on hematopoietic stem cells (HSCs) and hematopoiesis.

42 in hematopoietic cell development and clonal hematopoiesis.

43 e DNA-binding chromatin factor DEK regulates hematopoiesis.

44 tor, can result in distinct changes in human hematopoiesis.

45 of master transcription factors involved in hematopoiesis.

46 roughout all measured stages and lineages of hematopoiesis.

47 ed regulatory molecules necessary for normal hematopoiesis.

48 ical insights into both normal and malignant hematopoiesis.

49 ied contexts, namely immunology, cancer, and hematopoiesis.

50 lylated and fucosylated glycans in zebrafish hematopoiesis.

51 ene may be proven to play a critical role in hematopoiesis.

52 tial for the long-term maintenance of normal hematopoiesis.

53 mouse development, meiotic recombination and hematopoiesis.

54 t with a retinoid-induced myeloid skewing of hematopoiesis.

55 d m(6)A modification in normal and malignant hematopoiesis.

56 ulates primitive myelopoiesis and definitive hematopoiesis.

57 ed overall survival without affecting murine hematopoiesis.

58 erations that affect important regulators of hematopoiesis.

59 y show iron overload that negatively affects hematopoiesis.

60 s as a master transcriptional corepressor in hematopoiesis.

61 of HR sufficient for normal development and hematopoiesis.

62 may regulate developmental processes beyond hematopoiesis.

63 sentiality of developmental enhancers during hematopoiesis.

64 we hypothesize that SCI disrupts bone marrow hematopoiesis.

65 ventral dorsal aorta (VDA), support lifelong hematopoiesis.

66 R using Rapamycin has deleterious effects on hematopoiesis.

67 applied this to study fate determination in hematopoiesis.

68 ification of alterations arising from clonal hematopoiesis.

69 or- cells, but only in the context of native hematopoiesis.

70 of HSCs to meet the physiological demand of hematopoiesis.

71 factor activity is fine-tuned during normal hematopoiesis.

72 well as lymphoid malignancies and in clonal hematopoiesis.

73 n hematological malignancies(1-3) and clonal hematopoiesis(4,5).

74 the utility of this system to study neonatal hematopoiesis, a developmental stage that has been diffi

75 w the role played by mutant DNMT3A in clonal hematopoiesis, accompanied by its effect on immune cell

76 sociated molecular patterns induce emergency hematopoiesis, activating hematopoietic stem and progeni

77 stic syndromes and are also common in clonal hematopoiesis, acute myeloid leukemia, chronic lymphocyt

78 em cells and impaired proper regeneration of hematopoiesis after DNA damage.

79 nt pathway as the key regulator of emergency hematopoiesis after injury.

80 bese diabetic mice have decreased "emergency hematopoiesis" after an acute infection.

81 oubtedly improve our understanding of normal hematopoiesis and ability to manipulate this in patholog

82 are enriched in binding of key regulators of hematopoiesis and AML pathogenesis.

83 clonal disorders that result in ineffective hematopoiesis and are associated with an increased risk

84 rs regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute my

85 vide a more holistic understanding of normal hematopoiesis and blood disorders.

86 yndromes (MDSs), contributing to ineffective hematopoiesis and clinical cytopenias.

87 e-S cluster biogenesis in erythropoiesis and hematopoiesis and define HSCB as a CSA gene.

88 ect to frequent missense mutations in clonal hematopoiesis and diverse neoplastic diseases.

89 nograft mouse models, restoring normal human hematopoiesis and eradicating aggressive pathologic MDS

90 l regulation and function of Runx factors in hematopoiesis and focus particularly on the biological e

91 associated with postradiation restoration of hematopoiesis and gastrointestinal repair.

92 lar vesicles (EVs) play a regulatory role in hematopoiesis and have been shown to promote the ex vivo

93 ave shown underwhelming rescue of endogenous hematopoiesis and have delivered the cells within 24 h o

94 sive description of injury-induced emergency hematopoiesis and identify an IL-1/MyD88/G-CSF-dependent

95 ediate cytokine signals in the regulation of hematopoiesis and immunity.

96 odel for understanding mechanisms underlying hematopoiesis and immunity.

97 rate novel PSEDN roles in vivo in Drosophila hematopoiesis and in human erythropoiesis in vitro Using

98 de clearance alone is therefore critical for hematopoiesis and in limiting mutagenesis in somatic tis

99 es (IBMFSs) are characterized by ineffective hematopoiesis and increased risk for developing myeloid

100 wever, the biological role of BRD4 in normal hematopoiesis and inflammation is not fully understood.

101 uperfamily is important in the regulation of hematopoiesis and is dysregulated in myelodysplastic syn

102 omplex, plays an essential role during early hematopoiesis and is frequently activated in T-cell acut

103 evels, recurrent MI caused reduced emergency hematopoiesis and less leukocytosis than a first MI.

104 Activation of hematopoiesis and myeloid differentiation in tumor-beari

105 understanding of the molecular regulation of hematopoiesis and offer opportunities to develop disease

106 romes (MDS) are characterized by ineffective hematopoiesis and often include a dysregulation and dysf

107 group of diseases characterized by defective hematopoiesis and often predisposing to myelodysplastic

108 how GATA2 enhancer disease mutations impact hematopoiesis and pathology are unclear, we generated mo

109 one marrow (BM) is the key anatomic site for hematopoiesis and plays a significant role in the homeos

110 PU.1 is a master regulator of hematopoiesis and promotes myeloid differentiation.

111 g hematopoietic clones confirmed oligoclonal hematopoiesis and revealed mutations in at least 27 gene

112 profiling, patients with MDS-PA have altered hematopoiesis and T regulatory cell distribution in the

113 Embryonic SSMs originated from yolk sac hematopoiesis and were replaced by a postnatal wave of b

114 se of cytokines involved in immune response, hematopoiesis, and homeostatic processes.

115 many processes, including immune responses, hematopoiesis, and organogenesis.

116 role in immune function, endocrine function, hematopoiesis, and oxidative stress regulation.

117 a, BM fibrosis, IL-6 release, extramedullary hematopoiesis, and splenomegaly.

118 ly appreciated as being essential for normal hematopoiesis, and they are understood to play fundament

119 The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved.

120 the most common cause of age-related clonal hematopoiesis (ARCH) in older individuals, and are among

121 a onset in the context of age-related clonal hematopoiesis (ARCH).

122 sing frequency with which people with clonal hematopoiesis are discovered and the need for counseling

123 minants connecting hypercholesterolemia with hematopoiesis are unclear.

124 f mutated hematopoietic cells, termed clonal hematopoiesis, are common in aging humans.

125 We find that deletion of Tet2 in native hematopoiesis as well as fully transformed acute myeloid

126 ic variation can impact on key mechanisms in hematopoiesis, as well as highlighting future prospects

127 sights into the cellular hierarchy of normal hematopoiesis, as well as the functional impact of drive

128 lly characterize the genetic architecture of hematopoiesis, assess the relevance of the omnigenic mod

129 ythropoietic anemia and other impairments in hematopoiesis associated with an intronic mutation in GA

130 , several studies have now shown that clonal hematopoiesis associates with increased risk of atherosc

131 er, the incidence and sequelae of dysplastic hematopoiesis at diagnosis are unknown.

132 ls from the bone marrow (BM) niche that tune hematopoiesis at steady state and in hematologic disorde

133 These data are consistent with clonal hematopoiesis being driven by a continuing risk of mutat

134 ional priming of DNMT3A-mutated human clonal hematopoiesis bone marrow progenitors.

135 Cs) and the HSC niche is likely important in hematopoiesis but not well demonstrated.

136 udies reveals an essential role for PDIA6 in hematopoiesis, but one extrinsic to cells of the hematop

137 results show that Nanog regulates primitive hematopoiesis by directly repressing critical erythroid

138 ing growth factor beta1 (Tgfb1) disorganized hematopoiesis by expanding the pre-EPO pool of progenito

139 text, somatic alterations can promote clonal hematopoiesis by improving the competitive fitness of sp

140 lecular mechanism whereby AML impairs normal hematopoiesis by remodeling the mesenchymal niche.

141 muscle development and muscular dystrophies, hematopoiesis, cancer, and neural stem cell biology, hig

142 udy this phenomenon in the context of clonal hematopoiesis (CH) and the development of therapy-relate

143 Clonal hematopoiesis (CH) arises when a substantial proportion

144 studies identified nearly ubiquitous clonal hematopoiesis (CH) in AA patients.

145 The discovery of clonal hematopoiesis (CH) in older individuals has changed the

146 Clonal hematopoiesis (CH) is associated with age and an increas

147 Clonal hematopoiesis (CH) is common in older persons and is ass

148 Clonal hematopoiesis (CH) of indeterminate potential (CHIP) is

149 many treated patients have persistent clonal hematopoiesis (CH) that may not reflect residual AML.

150 iable, ranging from clinically silent clonal hematopoiesis (CH) to leukemic progression.

151 We hypothesized that clonal hematopoiesis (CH), a state in which somatic mutations i

152 Clonal hematopoiesis (CH), as evidenced by recurrent somatic mu

153 become detectable, now referred to as clonal hematopoiesis (CH).

154 is the most commonly mutated gene in clonal hematopoiesis (CH).

155 DNA sequencing approach revealed that clonal hematopoiesis constitutes a pervasive biological phenome

156 Approaches that restore normal regulation of hematopoiesis could be effective treatment strategies.

157 nic development, epidermal regeneration, and hematopoiesis demonstrates robust identification of subp

158 lenomegaly, neutrophilia, and extramedullary hematopoiesis, despite normal numbers of DCs.

159 Clonal hematopoiesis driven by mutations of DNMT3A (DNA methylt

160 Clonal hematopoiesis driven by somatic heterozygous TET2 loss i

161 The acquisition of clonal hematopoiesis-driver mutations (CHDMs) occurs with norma

162 n=6 patients with HF harboring DNMT3A clonal hematopoiesis-driver mutations and n=4 patients with HF

163 T cells of patients with HF harboring clonal hematopoiesis-driver mutations in DNMT3A exhibit a highl

164 erimental studies suggest that DNMT3A clonal hematopoiesis-driver mutations may enhance inflammation,

165 is an elegant genetic model for the study of hematopoiesis due to its many unique advantages.

166 is dispensable for steady-state myeloid-cell hematopoiesis due to their capacity to tap the glutathio

167 blood system, but neither observed impaired hematopoiesis during homeostatic conditions nor upon ser

168 Regulation of hematopoiesis during human development remains poorly de

169 l describe decreased clonal contributions to hematopoiesis during steady-state aging and after transp

170 ing global clonal complexity of steady-state hematopoiesis during the natural murine lifespan.

171 Q/-) mice died prematurely due to anemia and hematopoiesis failure.

172 role of PcG proteins in normal and malignant hematopoiesis, focusing on the compositional complexity

173 toxicity we observe no evidence of abnormal hematopoiesis following transplantation and no evidence

174 ion and disentangling known heterogeneity in hematopoiesis for different organisms.

175 nate-like lymphocytes develop early in fetal hematopoiesis from progenitors that emerge prior to, and

176 9.5) controls expression of the regulator of hematopoiesis GATA-2.

177 Embryonic definitive hematopoiesis generates hematopoietic stem and progenito

178 hile the significance of inflammation driven hematopoiesis has begun to unfold, molecular players tha

179 Hematopoiesis has long served as a paradigm of stem cell

180 n the nervous system, its regulatory role in hematopoiesis has not been reported.

181 Somatic mutations leading to clonal hematopoiesis have been described in IBMFSs, but the dis

182 c lineages) from 67 patients revealed clonal hematopoiesis in 13 (50%) of 26 cases with MDS-PA vs 9 (

183 ypical growth trajectories or extramedullary hematopoiesis in anemias such as SCD.

184 al advance in the understanding of emergency-hematopoiesis in cancer and opening new targets for ther

185 ver, mutations in BRCC36 are found in clonal hematopoiesis in humans.

186 BMF, thereby confirming its critical role in hematopoiesis in humans.

187 tanding of the processes that promote clonal hematopoiesis in IBMFSs may inform clinical surveillance

188 d that tissue injury alone induces emergency hematopoiesis in mice subjected to polytrauma.

189 ukocytosis but does not compromise emergency hematopoiesis in mice.

190 is well tolerated and did not impair normal hematopoiesis in mice.

191 ical and clinical significance of dysplastic hematopoiesis in newly diagnosed MM, which can be screen

192 partments showed significant platelet-biased hematopoiesis in old mice reflected by increased megakar

193 fying phases of many developmental processes-hematopoiesis in particular-is unclear.

194 Hematopoiesis in patients with cancer is characterized b

195 of Blood, Eskelund et al characterize clonal hematopoiesis in serial samples from persons with mantle

196 future investigation of human developmental hematopoiesis in the context of blood pathologies and re

197 the role of the TGase enzyme in controlling hematopoiesis in the crayfish, Pacifastacus leniusculus

198 rophages, microglia originate from primitive hematopoiesis in the embryonic yolk sac and self-renew t

199 stages, we found that Nanog blocks primitive hematopoiesis in the gastrulating embryo, resulting in a

200 These cells are generated through primitive hematopoiesis in the yolk sac and migrate into the brain

201 How the products of transient hematopoiesis in the yolk sac, dorsal aorta, and develop

202 icient to drive premature age-related clonal hematopoiesis in these inherited disorders.

203 titative systems pharmacology (QSP) model of hematopoiesis in vitro for quantifying the effects of an

204 reening, we identified 6 lncRNAs influencing hematopoiesis in vitro.

205 gamma 1 (Plcgamma1) has been implicated for hematopoiesis in vivo and in vitro and is also required

206 e the pathogenic role of PTPRJ deficiency in hematopoiesis in vivo, we carried out CRISPR/Cas9-mediat

207 ent of siderocytes and more broadly perturbs hematopoiesis in vivo.

208 Proper glycosylation is critical to normal hematopoiesis, in particular to megakaryocyte and platel

209 ript and Osx protein expression early during hematopoiesis, in subsets of hematopoietic stem cells an

210 ical considerations for patients with clonal hematopoiesis, including important points for hematologi

211 Furthermore, Epcr expression in Mpl(-/-) hematopoiesis increased the number of megakaryocytes in

212 ot induce any toxicity to splenocytes and on hematopoiesis, induced protective cytokines, and did not

213 cular disease and are associated with clonal hematopoiesis, inflammation, and adverse vascular remode

214 Hematopoiesis is a dynamic system that requires balanced

215 ed consequence of mutation-associated clonal hematopoiesis is an increased risk of hematologic cancer

216 ork operates in mammals to control emergency hematopoiesis is an open question.

217 Here, we show that endocardial hematopoiesis is critical for cardiac valve remodeling a

218 Hematopoiesis is disrupted profoundly, with a reduction

219 Since bone marrow hematopoiesis is essential for proper immune function, w

220 Clonal hematopoiesis is exceptionally common with human aging,

221 In part, this continuous nature of hematopoiesis is made possible by the emergent outcomes

222 This process of hematopoiesis is maintained throughout life by hematopoi

223 Because clonal hematopoiesis is not deterministic of malignant transfor

224 ever, the effect of sterile tissue injury on hematopoiesis is not well described.

225 Hematopoiesis is partly regulated by soluble factors, su

226 Hematopoiesis is responsible for numerous functions, ran

227 Hematopoiesis is tightly regulated by the bone marrow (B

228 Similarly, the role of PHF6 in hematopoiesis is unknown.

229 This outgrowth, called "clonal hematopoiesis," is highly prevalent in the elderly popul

230 s recent advances in our knowledge of clonal hematopoiesis, its relationship to malignancies, its lin

231 d modulate immune cell phenotypes, reviewing hematopoiesis, leukocyte trafficking, and innate immune

232 g to define the "switch" from fetal to adult hematopoiesis, Li et al.

233 r event in an individual patient with clonal hematopoiesis may be low, the possibility of future clin

234 People with clonal hematopoiesis may come to clinical attention in a variet

235 nesis, a process in which vasculogenesis and hematopoiesis occur simultaneously.

236 hich show that an early and distinct wave of hematopoiesis occurs for all major hematopoietic lineage

237 Dysregulated hematopoiesis occurs in several chronic inflammatory dis

238 During mammalian embryogenesis, de novo hematopoiesis occurs transiently in multiple anatomical

239 fects of CAR-mediated tonic signaling on the hematopoiesis of CAR-armed HSCs is unclear.

240 ons in the peripheral blood is termed clonal hematopoiesis of indeterminate potential (CHIP) and is a

241 Clonal hematopoiesis of indeterminate potential (CHIP) increase

242 Clonal hematopoiesis of indeterminate potential (CHIP) is a rec

243 Clonal hematopoiesis of indeterminate potential (CHIP) refers t

244 Clonal hematopoiesis of indeterminate potential (CHIP), the age

245 This phenomenon, termed clonal hematopoiesis of indeterminate potential (CHIP), was ass

246 lar risk factor has recently emerged: clonal hematopoiesis of indeterminate potential (CHIP).

247 al as underscored by the incidence of clonal hematopoiesis of indeterminate potential associated with

248 ribe the emergence and prevalence of "clonal hematopoiesis of indeterminate potential" in aged human

249 undaries between MDS, MDS/MPNs, sAML, clonal hematopoiesis of indeterminate potential, clonal cytopen

250 without MDS/AML also had evidence of clonal hematopoiesis of indeterminate potential-related mutatio

251 ten preceded by a premalignant state (clonal hematopoiesis or myelodysplastic syndrome).

252 adult Drosophila melanogaster as a model for hematopoiesis or organismal immunity has been debated.

253 of Gdf11 in blood cells might perturb normal hematopoiesis or recovery from hematopoietic insult.

254 multiple physiological processes, including hematopoiesis, organogenesis, inflammation, tissue repai

255 ML cure and the impact of preleukemic clonal hematopoiesis persistence in predisposing to second AML.

256 e most abundantly expressed isoform in adult hematopoiesis, present in all RUNX1-expressing populatio

257 demonstrate that dysregulated necroptosis in hematopoiesis promotes bone marrow progenitor cell death

258 The classical model of hematopoiesis proposes a hierarchy in which a small numb

259 not drift, is the major force shaping clonal hematopoiesis, provide bounds on the number of hematopoi

260 Clonal hematopoiesis provides a glimpse into the process of mut

261 Hematopoiesis provides an accessible system for studying

262 erload, bilirubin gallstones, extramedullary hematopoiesis, pulmonary hypertension, and thrombosis, a

263 However, the proteomics of hematopoiesis remains incompletely understood.

264 e technique has been rapidly embraced by the hematopoiesis research community, and like other technol

265 Clonal hematopoiesis results from somatic mutations in hematopo

266 Waves of hematopoiesis separated in anatomical space and time giv

267 concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin acce

268 ected by conditioning and identifies the key hematopoiesis stages that may be manipulated to control

269 Proposed models of hematopoiesis suggest that quantitative changes in linea

270 mmatory diseases are associated with altered hematopoiesis that could result in neutrophilia and anem

271 Hematopoiesis, the formation of blood cells, involves th

272 When applied to barcoding data in hematopoiesis, these tools reconstruct the classical hem

273 pecific proteins for degradation to regulate hematopoiesis through cell processes, such as cell cycle

274 Numerous cell types modulate hematopoiesis through soluble and membrane bound molecul

275 hematopoietic stem cells (HSCs) can maintain hematopoiesis throughout life.

276 he numbers of clones supporting steady-state hematopoiesis throughout mammalian life is lacking.

277 we will review recent studies linking clonal hematopoiesis to altered immune function, inflammation,

278 novel methods of cell tracking have revealed hematopoiesis to be more of a continuous and less of a d

279 Inflammation alters bone marrow hematopoiesis to favor the production of innate immune e

280 Cancer induces alteration of hematopoiesis to fuel disease progression.

281 esponse is regulated at various stages, from hematopoiesis to monocyte changes and macrophage activat

282 effects of depleting KDM4 activity on normal hematopoiesis to probe potential side effects of continu

283 reptozotocin-induced diabetes in mice skewed hematopoiesis toward the myeloid lineage via hematopoiet

284 rast, knockdown of TAZ did not impair normal hematopoiesis under basal conditions.

285 on the key cells and products that regulate hematopoiesis under homeostatic conditions, during ather

286 We assessed here the role of Lsh in hematopoiesis using conditional Lsh knockout mice with e

287 ed that ginger treatment promoted definitive hematopoiesis via Bmp signaling.

288 we investigated a possible effect of VKAs on hematopoiesis via the BMM.

289 eptor-related protein 6 (Lrp6) mice in adult hematopoiesis via Vav-Cre Loxp system.

290 model, whereas the capacity to sustain human hematopoiesis was evaluated in humanized ossicle models.

291 early lineage commitment and found that SDS hematopoiesis was left-shifted with selective loss of gr

292 ts motif mutant was viable, and steady-state hematopoiesis was normal.

293 Nbn (-/mid8vav) mice hematopoiesis was profoundly defective, exhibiting reduc

294 id progenitors, did not express IL7R, and YS hematopoiesis was unperturbed in IL7R-deficient mice.

295 mal, healthy elderly individuals with clonal hematopoiesis who are at increased risk of subsequently

296 Prevailing models of hematopoiesis with distinct intermediates are challenged

297 t in different murine tumor models activated hematopoiesis with increased proliferation of long-term

298 Emerging data also associate clonal hematopoiesis with other nonhematologic diseases.

299 tic stem cells (HSCs) that can lead to human hematopoiesis within the murine host.

300 ere that Hmces-deficient mice display normal hematopoiesis without global alterations in 5hmC.