ライフサイエンスコーパス: granulopoiesis

1 es production of cytokines that drive excess granulopoiesis.

2 control to G-CSF signaling and regulation of granulopoiesis.

3 i1 and G-CSF are linked in the regulation of granulopoiesis.

4 of C/EBPalpha occupancy during demand-driven granulopoiesis.

5 rentiation and the homeostatic regulation of granulopoiesis.

6 yeloid progenitor compartments to accelerate granulopoiesis.

7 ccelerated granulopoiesis known as emergency granulopoiesis.

8 role for their proliferation in inflammatory granulopoiesis.

9 tor cells but did not rescue Gfi1-/- blocked granulopoiesis.

10 lymphocytes from the BM along with increased granulopoiesis.

11 ion of myeloid progenitors, but not terminal granulopoiesis.

12 SCN patient) completely blocks G-CSF-induced granulopoiesis.

13 colony-stimulating factor (G-CSF)-stimulated granulopoiesis.

14 le receptor (sIL6R) contributes to emergency granulopoiesis.

15 ulted in a dominant-negative block to murine granulopoiesis.

16 acid receptor (RAR) and C/EBPepsilon direct granulopoiesis.

17 differentiation, including myelopoiesis and granulopoiesis.

18 little is known about the role of miRNAs in granulopoiesis.

19 penia (CN), a related but milder disorder of granulopoiesis.

20 dominant, cell-intrinsic fashion to disrupt granulopoiesis.

21 of cyclic neutropenia, a related disorder of granulopoiesis.

22 l neutropenia (SCN) is an inborn disorder of granulopoiesis.

23 genital neutropenia is an inborn disorder of granulopoiesis.

24 tially expressed >2-fold throughout terminal granulopoiesis.

25 In vivo expression profoundly stimulates granulopoiesis.

26 , and 67% of ET patients demonstrated clonal granulopoiesis.

27 anscriptional repressor that is required for granulopoiesis.

28 se signals regulate basal and stress-induced granulopoiesis.

29 yeloid disorders characterized by a block in granulopoiesis.

30 (G-CSF) is the principal cytokine regulating granulopoiesis.

31 ic differentiation, but downregulated during granulopoiesis.

32 favors monocyte differentiation by blocking granulopoiesis.

33 SF), consistent with their critical roles in granulopoiesis.

34 he C/EBPalpha basic region, are required for granulopoiesis.

35 ancer binding protein alpha) is critical for granulopoiesis.

36 forming unit and mature neutrophil stages of granulopoiesis.

37 onent of G-CSF-driven cell proliferation and granulopoiesis.

38 g induction of other C/EBP family members in granulopoiesis.

39 for G-CSF as the main mediator of emergency granulopoiesis.

40 of chemotherapy patients through accelerated granulopoiesis.

41 dentifying zebrafish mutants with defects in granulopoiesis.

42 CSF) plays a major role in the regulation of granulopoiesis.

43 e form of stem cell factor (SCF) for optimal granulopoiesis.

44 rmation of monocyte/macrophages and enhanced granulopoiesis.

45 phenotype, with dramatic effects on in vivo granulopoiesis.

46 d event in patients with pre-existing clonal granulopoiesis.

47 bp/Irf8) was required to terminate emergency granulopoiesis.

48 cols that recapitulate the major features of granulopoiesis.

49 epithelium in the outer medulla can regulate granulopoiesis.

50 uced Triad1 expression on emergency (stress) granulopoiesis.

51 sponse nor significantly alters steady-state granulopoiesis.

52 yeloid progenitor expansion during emergency granulopoiesis.

53 ZBTB11, as critical for basal and emergency granulopoiesis.

54 iPSCs through C/EBPbeta-dependent emergency granulopoiesis.

55 f G-CSF receptor-mediated signaling in human granulopoiesis.

56 the timed expression of C/EBP-epsilon during granulopoiesis.

57 iferation, cell cycle, and maturation during granulopoiesis.

58 generally show decreased methylation during granulopoiesis.

59 on of systemic infection into demand-adapted granulopoiesis.

60 ds of wild-type (WT) mice exhibited impaired granulopoiesis.

61 s,thereby directly linking TLR-triggering to granulopoiesis.

62 uring repeated, failed episodes of emergency granulopoiesis.

63 ibutes to genomic stability during emergency granulopoiesis.

64 matopoietic activity shifts toward promoting granulopoiesis.

65 novel important target of C/EBPalpha during granulopoiesis.

66 L-1beta, an essential cytokine for emergency granulopoiesis.

67 he development of neutrophil immunity during granulopoiesis.

68 progenitors and that exogenous RUNX1 rescues granulopoiesis.

69 structive lesions of the spleen and impaired granulopoiesis.

70 d promoter histone acetylation, and inhibits granulopoiesis.

71 rvival but have little impact on bone marrow granulopoiesis.

72 ion with G193X Elane, had no effect on basal granulopoiesis.

73 plays a key role in stimulating bone marrow granulopoiesis.

74 so found that repeated episodes of emergency granulopoiesis accelerated progression to acute myeloid

75 Basal and stress granulopoiesis after myeloablative therapy are normal in

76 e mechanism that is required for recovery of granulopoiesis after radiation injury.

77 -1+/c-kit+ cells produced PGE2 and underwent granulopoiesis after TLR2 stimulation.

78 IL-17A and IL-17F regulate granulopoiesis and are produced by memory T cells.

79 AT, and translated into reduced bone marrow granulopoiesis and cardiac neutrophil infiltration 3 day

80 e of inhibition of proliferative pathways in granulopoiesis and demonstrate that several regions of t

81 lude that AT-induced IL-1beta promotes local granulopoiesis and effective resolution of S. aureus-inf

82 scription factor C/EBP alpha is required for granulopoiesis and frequently disrupted in human acute m

83 -21 has been implicated in the regulation of granulopoiesis and hepatic gene expression.

84 ings demonstrate an essential role for AR in granulopoiesis and host defense against microbial infect

85 coinhibitory receptor for G-CSFR regulating granulopoiesis and host innate immune response to bacter

86 nto Ceacam1(-/-) bone marrow restored normal granulopoiesis and host sensitivity to LM infection, whi

87 al network controlled by C/EBPepsilon during granulopoiesis and identifies Trem1 as one of its downst

88 target pathways in neutrophils required for granulopoiesis and innate immunity.

89 alpha (C/EBPalpha) is a master regulator in granulopoiesis and is frequently disrupted in acute myel

90 on of Bcl3 in recipients inhibited emergency granulopoiesis and limited acute graft damage.

91 We demonstrate that granulopoiesis and lymphopoiesis are coupled specificall

92 w that STAT3 has a crucial role in emergency granulopoiesis and mature neutrophil function.

93 c finger transcription factor that regulates granulopoiesis and may have a regulatory role in cellula

94 that restricted erythropoiesis but permitted granulopoiesis and megakaryopoiesis.

95 cific cytokines that play a dominant role in granulopoiesis and monopoiesis, respectively.

96 chemic graft storage enhances G-CSF-mediated granulopoiesis and neutrophil graft infiltration, result

97 important regulator of host defense through granulopoiesis and neutrophil trafficking.

98 neutrophil apoptosis, the role of CEACAM1 in granulopoiesis and neutrophil-dependent host immune resp

99 Integrin alpha9beta1 was required for granulopoiesis and played a permissive role in the G-CSF

100 hich fail to develop lobulated nuclei during granulopoiesis and present an in vitro model for Pelger-

101 e gain-of-function of Stat5 causes excessive granulopoiesis and prolonged survival of granulocytes in

102 sh Lyn and Hck as key negative regulators of granulopoiesis and raise the possibility that loss of Sr

103 rovide direct evidence for STAT3-independent granulopoiesis and suggest that STAT3 directs a negative

104 itical role for Bcl3 in regulating emergency granulopoiesis and suggest that targeting the differenti

105 nd transcriptional changes that occur during granulopoiesis and supports the role of DNA methylation

106 prominent role of IL-23 in the regulation of granulopoiesis and the prevalence of IL-17A-producing Tn

107 em, can result in a differentiation block in granulopoiesis and thus contribute to leukemic transform

108 role specifically for the SMARCD2 subunit in granulopoiesis, and further investigation implicates the

109 They also displayed enhanced entry into granulopoiesis, and inhibited postmitotic terminal diffe

110 ances 32D cell survival, promotes entry into granulopoiesis, and inhibits postmitotic differentiation

111 rdial AT coordinates immune cell activation, granulopoiesis, and outcome after MI.

112 vivo G-CSF levels and stimulation of marrow granulopoiesis, and was comparable to that of exogenousl

113 Steady-state and emergency granulopoiesis are both dependent on TLR signaling.

114 ular events involved in initiating emergency granulopoiesis are known, but termination of this proces

115 isms controlling infection-induced emergency granulopoiesis are poorly defined.

116 mechanisms by which these mutations disrupt granulopoiesis are unclear.

117 rowth factor that has a role in steady state granulopoiesis, as well as in mature neutrophil activati

118 y be clinically useful to enhance neutrophil granulopoiesis, as well as to study the mechanisms invol

119 ed reduction of Stat3 amounts rescued normal granulopoiesis, attenuating host sensitivity to LM infec

120 normal progenitors, C/EBPs are required for granulopoiesis beyond their ability to induce receptors

121 l elastase in providing negative feedback to granulopoiesis by direct antagonism of G-CSF.

122 STAT3 as an essential mediator of emergency granulopoiesis by its regulation of transcription factor

123 rovide evidence that the G-CSFR may regulate granulopoiesis by several mechanisms.

124 a and miR-182 for the maintenance of healthy granulopoiesis.C/EBPalpha is a critical transcription fa

125 h these mice did not display the increase in granulopoiesis commonly found in chronic myeloid leukemi

126 sis in the blood under both basal and stress granulopoiesis conditions primarily by regulating neutro

127 The observed failure of granulopoiesis could be rescued by the addition of solub

128 nt mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutr

129 tive of neutrophil homeostasis and emergency granulopoiesis determined by innate immunologic signalin

130 igation of the effect of C/EBPalphap30-ER on granulopoiesis downstream of G-CSF signalling, we coexpr

131 plays a critical role in mediating emergency granulopoiesis during acute infection.

132 Impaired bone marrow granulopoiesis during burn sepsis often results in neutr

133 mulating factor (G-CSF) mediates "emergency" granulopoiesis during infection, a process that is mimic

134 ions or adjuvant usage can trigger emergency granulopoiesis (EG), leading to dysregulation in neutrop

135 the interrelated processes of hematopoiesis, granulopoiesis, erythropoiesis, and lymphopoiesis.

136 he bone marrow via the circulation and local granulopoiesis from hematopoietic stem and progenitor ce

137 her blood cell lineages, its function during granulopoiesis has remained elusive.

138 t drive reactive neutrophilias and emergency granulopoiesis have been inferred but not demonstrated.

139 dition, some ET and MMM patients with clonal granulopoiesis have somatic mutations other than JAK2V61

140 ltiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vi

141 neutrophil homeostasis in the steady state, granulopoiesis in 'emergency' conditions and interaction

142 ranulocyte colony-stimulating factor-induced granulopoiesis in 32D cells or retinoic acid- and vitami

143 beta-ER or C/EBPdelta-ER can induce terminal granulopoiesis in 32D cl3 cells.

144 IL-23 also regulates granulopoiesis in a neutrostat regulatory feedback loop

145 the accumulation of Bcl3 protein attenuated granulopoiesis in an NF-kappaB p50-dependent manner.

146 an and rodents and is essential for terminal granulopoiesis in both species.

147 ta in granulopoiesis; therefore, we examined granulopoiesis in C/EBPbeta-deficient mice.

148 Failed emergency granulopoiesis in Fancc(-/-) mice was associated with ex

149 r neutrophils during G-CSF-induced emergency granulopoiesis in humans.

150 on of G-CSF in vivo, as a model of emergency granulopoiesis in humans.

151 emonstrated that the early increase in human granulopoiesis in NSG-3GS mice reflects an expanded outp

152 ggesting that TLR2/MyD88 activation promotes granulopoiesis in part by production and autocrine activ

153 d for induction of C/EBPalpha expression and granulopoiesis in response to G-CSF or other cytokines i

154 We conclude that granulopoiesis in S aureus-infected wounds is induced by

155 nsight into the mechanism underlying reduced granulopoiesis in the absence of NF-kappaB p50, we asses

156 rculation and in the liver, through enhanced granulopoiesis in the bone marrow.

157 ut they initiate differentiation and undergo granulopoiesis in the presence of granulocyte CSF (G-CSF

158 reduces C/EBPalpha protein level and impairs granulopoiesis in vitro and in vivo.

159 ogenitors showed decreased emergency-induced granulopoiesis in vitro and in vivo.

160 3, elastase, azurocidin, and cathepsin G) on granulopoiesis in vitro.

161 role for the G-CSFR as a major regulator of granulopoiesis in vivo and provide evidence that the G-C

162 ate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or I

163 nt mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals.

164 role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR i

165 urine IL-17 is a cytokine that can stimulate granulopoiesis in vivo.

166 This pattern is consistent with "reactive granulopoiesis," in which committed myeloid progenitors

167 slowed G1, but did not induce early or late granulopoiesis, indicating that cell cycle inhibition as

168 In vitro models of granulopoiesis involving the inducible expression of eit

169 Emergency granulopoiesis is a component of the innate immune respo

170 'Steady-state' granulopoiesis is absolutely dependent on the C/EBPalpha

171 oid progenitors accumulate, whereas terminal granulopoiesis is blocked.

172 we demonstrate that this specialization for granulopoiesis is determined by inflammation-induced red

173 mouse lung allografts unless G-CSF-mediated granulopoiesis is inhibited.

174 myeloid maturation, indicating that resting granulopoiesis is normal.

175 ates that conversion to a state of emergency granulopoiesis is temporally delayed, allowing B cells o

176 to the switch from steady-state to emergency granulopoiesis is, however, unknown.

177 timulating factor (G-CSF) receptor-triggered granulopoiesis, is downregulated in granulocytic progeni

178 that NFI-A promoter silencing, which allows granulopoiesis, is guaranteed by epigenetic events, incl

179 ed by a hematopoietic program of accelerated granulopoiesis known as emergency granulopoiesis.

180 etics of infection, circulating blood cells, granulopoiesis, lesions, and cellular populations in the

181 Our findings identify granulopoiesis-mediated augmentation of alloimmunity as

182 Rather than a deficit in granulopoiesis, mice lacking STAT3 in their hematopoieti

183 pment (miR-150 and miR-17 approximately 92), granulopoiesis (miR-223), immune function (miR-155) and

184 During granulopoiesis, miR-223 localizes inside the nucleus and

185 L; p<0.0001), bone marrow erythropoiesis and granulopoiesis, more venous thromboses, and a higher rat

186 C/EBPalpha(BRM2)-ER induced early markers of granulopoiesis much less efficiently than C/EBPalpha-ER

187 icated that G-CSFR independent mechanisms of granulopoiesis must exist.

188 uggest that G-CSFR-independent mechanisms of granulopoiesis must exist.

189 le for Runx1 tyrosine phosphorylation during granulopoiesis, mutation of the five Src-modified residu

190 Emergency granulopoiesis occurs in response to infectious or infla

191 colony-stimulating factor (G-CSF) to promote granulopoiesis of human hematopoietic stem cells (HSCs),

192 regulation of C/EBPalpha by microRNAs during granulopoiesis or acute myeloid leukemia development has

193 he disruption of CD18 functions essential to granulopoiesis or basal leukocyte trafficking.

194 ers normal leukocyte production by promoting granulopoiesis over lymphopoiesis, a response that suppo

195 nt by evicting resident B cells and favoring granulopoiesis over lymphopoiesis.

196 hopoiesis, and higher C/EBP levels may favor granulopoiesis over monopoiesis.

197 row into TTP KO mice and found the "reactive granulopoiesis" phenocopied, indicating a non-hematopoie

198 Moreover, we also identified C/EBPalpha, a granulopoiesis-promoting transcription factor, as a subs

199 Emergency granulopoiesis refers to the increased production of neu

200 ne expression pattern with overexpression of granulopoiesis-related and interferon (IFN)-induced gene

201 nscriptional mechanisms underlying emergency granulopoiesis remain unclear.

202 stage, whereas progenitor cell expansion or granulopoiesis remained unimpaired.

203 -/-) non-granulated defect and suggests that granulopoiesis requires a structural motif that is conse

204 In this study, we show that IL-17-mediated granulopoiesis requires G-CSF release and the presence o

205 Early granulopoiesis requires the C/EBPalpha, PU.1, RAR, CBF,

206 uction or silencing boosts erythropoiesis or granulopoiesis, respectively.

207 xhibited an overwhelming and fatal emergency granulopoiesis response that was characterized by tissue

208 echanisms of STAT3 function in the emergency granulopoiesis response to G-CSF administration or infec

209 The stress granulopoiesis response, as measured by neutrophil recov

210 /EBPbeta), a crucial factor in the emergency granulopoiesis response.

211 (-/-) mice after stimulation of an emergency granulopoiesis response.

212 G-CSF-independent effect of IL-17 on splenic granulopoiesis, resulting in a preservation of mature ci

213 accumulation was attributable to attenuated granulopoiesis secondary to assessed lower levels of IL-

214 unaffected in CN, suggests the presence of a granulopoiesis-specific mechanism downstream of G-CSF re

215 The granulopoiesis-stimulating agents (GSAs) have been effec

216 bed role for HoxA10 in terminating emergency granulopoiesis, suggesting an important contribution by

217 iant unable to bind NF-kappaB p50 stimulated granulopoiesis, suggesting their cooperation with C/EBPa

218 in myeloid cells, are negative regulators of granulopoiesis that act at distinct stages of granulocyt

219 l neutropenia (SCN) is an inborn disorder of granulopoiesis that in many cases is caused by mutations

220 topoietic response program termed "emergency granulopoiesis" that is characterized by increased de no

221 than the hours required to induce "emergency granulopoiesis," the relevance of having high numbers of

222 ttle is known about the role of C/EBPbeta in granulopoiesis; therefore, we examined granulopoiesis in

223 n to the effect of THP on the epithelium and granulopoiesis, this new immunomodulatory role could exp

224 e show that IL-17, a cytokine that regulates granulopoiesis through G-CSF, is made by gammadelta T ce

225 IL-23 and IL-17A regulate granulopoiesis through G-CSF, the main granulopoietic cy

226 proteins act as dominant negatives to block granulopoiesis through selective deregulation of a subse

227 Cytokines stimulate granulopoiesis through signaling via receptors whose exp

228 ibit the alternate cell fate choice, that of granulopoiesis, through inhibition of C/EBPalpha.

229 tor B cell leukemia/lymphoma 3 (Bcl3) limits granulopoiesis under emergency (i.e., inflammatory) cond

230 the transcriptional mechanisms that regulate granulopoiesis under inflammatory conditions are poorly

231 n DNA methylation and gene expression during granulopoiesis using 4 distinct cell populations ranging

232 have assessed the effect of C/EBPalphap30 on granulopoiesis utilizing C/EBPalphap30-ER, containing th

233 nd SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPalpha homodime

234 principally by CD4(+) T cells, which induces granulopoiesis via granulocyte colony-stimulating factor

235 After stimulation of emergency granulopoiesis, we found increased and sustained express

236 explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 x G-CSFR doubly defici

237 h lamin A is typically down-regulated during granulopoiesis, we genetically modified HL-60 cells to g

238 To delineate the role of C/EBPalpha in human granulopoiesis, we studied its expression and function i

239 igate the effects of mutant NE expression on granulopoiesis, we used the HL-60 promyelocytic cell lin

240 omatic repression of NFI-A gene and channels granulopoiesis, whereas its stable knockdown produces th

241 aureus-infected skin wounds in mice undergo granulopoiesis, whereas other authors have demonstrated

242 ve Stat5 in diseased animals restored normal granulopoiesis, which also resulted in a swift clearance

243 critical function for C/EBPbeta in emergency granulopoiesis, which demands both differentiation and p

244 Although C/EBPalpha is known to induce granulopoiesis while suppressing monocyte differentiatio

245 fut1(-/-) embryonic stem cells show enhanced granulopoiesis with depressed lymphoid lineage developme

246 xamined this pathway in HSPC trafficking and granulopoiesis within S aureus-infected wounds.