ライフサイエンスコーパス: HSPC

1 HSPCs differentiate and renew in other locations, ensuri

2 HSPCs exist in a quiescent state in vivo, and quiescence

3 HSPCs recruited to infected wounds were unaffected by AT

4 ibitor (JAKi) significantly reduced aberrant HSPCs and mitigated leukemia development in a mouse mode

5 d to verify the ability of agonist-activated HSPCs to reconstitute the bone marrow in lethally irradi

6 arabiotic zebrafish, we show that cxcr1 acts HSPC nonautonomously to improve the efficiency of donor

7 e to explore combination therapy of adoptive HSPC-NK cells and DAC in patients with AML.

8 -/-)) results in a marked reduction of adult HSPC activity, both in vitro and in vivo.

9 xa gene expression to proliferation of adult HSPCs.

10 The affected HSPCs and their progeny lack expression of glycosylphosp

11 ajor truncating BCOR gene mutation affecting HSPC and CMP was beneath the threshold of detection in G

12 wed that CYTH1 deficiency profoundly affects HSPC mobility and localization within the marrow space a

13 ions in SMARCAL1 by suggesting that it is an HSPC defect.

14 ng," HSPC residency time within the CHT, and HSPC mitotic rate.

15 Importantly, we showed HMAs and HSPC-NK cells could potently work together to target AML

16 ytopenia as well as recovered osteoblast and HSPC abundance and improved the hematopoietic-supportive

17 lting in increased vascular permeability and HSPC egress.

18 omology-directed editing in both T cells and HSPCs are expected to spur the development of even more

19 ical findings of CCR5 editing in T cells and HSPCs for HIV therapy and summarize other promising geno

20 and discovered that all of these factors are HSPC quiescence regulators.

21 te diverse aspects of hematopoiesis, such as HSPC trafficking, in steady-state and stress-induced con

22 Notch blockade reversed attenuated HSPC cycling, leukemia-associated abnormal blood lineage

23 In this study, we identified an atypical HSPC population in the spleen of C57BL/6 mice, with a li

24 cular sinusoidal portals, thereby augmenting HSPC trafficking to the circulation.

25 190-B RhoGAP-ROS-TGF-beta-p38(MAPK) balances HSPC self-renewal and differentiation.

26 erve as an effective method to expand the BM HSPC pool.

27 reen fluorescent protein (GFP) marking in BM HSPCs (Lin(-)Sca1(+)Kit(-) cells) in most of the mice wa

28 scent HSCs into cycle, was well tolerated by HSPC-depleted mice and did not induce expansion of the s

29 flammatory cytokines, perforin, and TRAIL by HSPC-NK cells.

30 e shown here as mechanisms of MkMP uptake by HSPC.

31 let-derived MPs (PMPs) cannot be taken up by HSPCs although they bind to and induce HSPC aggregation.

32 ered by the supportive line were taken up by HSPCs ex vivo and in vivo.

33 ing may serve as 'fate determinants' used by HSPCs to modulate their activity.

34 Cytokine treatments that cause HSPC trafficking to peripheral blood are associated with

35 promoted homing of transplanted UCB CD34(+) HSPC to BM.

36 Exposure of UCB CD34(+) HSPC to EPO inhibits their migration and enhances erythr

37 Overall, MSC/CD34+ HSPC composite grafts reduce inflammation, enhance an ea

38 models of Ssb1 or Ssb2 Mechanistically, cDKO HSPCs showed altered replication fork dynamics, massive

39 Transcriptional profiling of cDKO HSPCs revealed the activation of p53 and interferon (IFN

40 mation, haematopoietic stem progenitor cell (HSPC) activity and LV remodelling in response to myocard

41 dult hematopoietic stem and progenitor cell (HSPC) activity has been hampered by a combination of emb

42 from hematopoietic stem and progenitor cell (HSPC) attrition.

43 r of hematopoietic stem and progenitor cell (HSPC) biology.

44 )CD38(-) hematopoietic stem/progenitor cell (HSPC) compartment and interrogated dominant clones for M

45 nce haematopoietic stem and progenitor cell (HSPC) expansion in culture have been identified, but in

46 ting hematopoietic stem and progenitor cell (HSPC) fate choices remain ill-defined.

47 cols for hematopoietic stem/progenitor cell (HSPC) gene therapy, involving the transplantation of ex

48 late hematopoietic stem and progenitor cell (HSPC) homeostasis.

49 and haematopoietic stem and progenitor cell (HSPC) maintenance.

50 s in hematopoietic stem and progenitor cell (HSPC) numbers are also seen in a stage-specific manner i

51 to rare hematopoietic stem/progenitor cell (HSPC) populations.

52 tial for hematopoietic stem/progenitor cell (HSPC) proliferation and survival in vitro and in vivo up

53 ting hematopoietic stem and progenitor cell (HSPC) retention and quiescence in bone marrow.

54 rant hematopoietic stem and progenitor cell (HSPC) self-renewal in vitro and in vivo.

55 ed a hematopoietic stem and progenitor cell (HSPC)-specific silencer element (the Gata1 methylation-d

56 of hematopoietic stem and progenitor cells (HSPC) in tumor-bearing mice.

57 ive hematopoietic stem and progenitor cells (HSPC), associated specifically with reduced expression o

58 CD34(+) hematopoietic stem/progenitor cells (HSPC).

59 (+) hematopoietic stem and progenitor cells (HSPC-NK cells) in in vitro and in vivo AML models.

60 normal hematopoietic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t

61 reover, hematopoietic stem/progenitor cells (HSPCs) and developing thymocytes in Smarcal1-deficient m

62 in hematopoietic stem and progenitor cells (HSPCs) and inhibition of AHR results in a marked expansi

63 DS haematopoietic stem and progenitor cells (HSPCs) and reverses the clinical features of MDS.

64 rate in hematopoietic stem/progenitor cells (HSPCs) and/or by promoting clonal hematopoiesis.

65 Hematopoietic stem/progenitor cells (HSPCs) are capable of supporting the lifelong production

66 fic hematopoietic stem and progenitor cells (HSPCs) are generated de novo.

67 Hematopoietic stem and progenitor cells (HSPCs) are vulnerable to endogenous damage and defects i

68 imitive hematopoietic stem/progenitor cells (HSPCs) compared with lineage-committed myeloid-restricte

69 man hematopoietic stem and progenitor cells (HSPCs) expressing MLL-AF9 or MLL-Af4 into immunodeficien

70 ted hematopoietic stem and progenitor cells (HSPCs) from FA patients, either after autologous transpl

71 nal hematopoietic stem and progenitor cells (HSPCs) from human pluripotent stem cells (PSCs) has been

72 4+ haematopoietic stem and progenitor cells (HSPCs) from patients with Myelodysplastic syndromes (MDS

73 in hematopoietic stem and progenitor cells (HSPCs) from patients with paroxysmal nocturnal hemoglobi

74 of hematopoietic stem and progenitor cells (HSPCs) from the bone marrow (BM) into the peripheral blo

75 Hematopoietic stem and progenitor cells (HSPCs) function to replenish the immune cell repertoire

76 of hematopoietic stem and progenitor cells (HSPCs) has the potential to address the short supply of

77 ted hematopoietic stem and progenitor cells (HSPCs) in adult mice in situ and found that LT-HSCs reco

78 of hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM) microenvironment.

79 of hematopoietic stem and progenitor cells (HSPCs) into functional megakaryocytes.

80 in hematopoietic stem and progenitor cells (HSPCs) is a promising novel technology for the treatment

81 (+) hematopoietic stem and progenitor cells (HSPCs) may be safer using targeted integration (TI) of t

82 ects of hematopoietic stem/progenitor cells (HSPCs) on the cerebral microcirculation after ischemia-r

83 n human hematopoietic stem/progenitor cells (HSPCs) promotes cell differentiation, coupled with reduc

84 for hematopoietic stem and progenitor cells (HSPCs) released EVs that could affect the gene expressio

85 Hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow.

86 rom hematopoietic stem and progenitor cells (HSPCs) that also traffic to infected skin wounds.

87 rom hematopoietic stem and progenitor cells (HSPCs) through to mature T cells.

88 d from, hematopoietic stem/progenitor cells (HSPCs) to identify candidate niche factors.

89 hCD34+ hematopoietic stem/progenitor cells (HSPCs) using human immunodeficiency virus, type 1-derive

90 el, hematopoietic stem and progenitor cells (HSPCs) were decreased in NHD13 mice by flow cytometric a

91 nase in hematopoietic stem/progenitor cells (HSPCs), and its uncontrolled activation is a prominent o

92 man hematopoietic stem and progenitor cells (HSPCs), the cells of origin for myeloid pre-malignant an

93 and hematopoietic stem and progenitor cells (HSPCs), which allows the virus to persist in infected in

94 osis of hematopoietic stem/progenitor cells (HSPCs), which raised serious concerns about the side eff

95 ult hematopoietic stem and progenitor cells (HSPCs).

96 of hematopoietic stem and progenitor cells (HSPCs).

97 of hematopoietic stem and progenitor cells (HSPCs).

98 odel of hematopoietic stem/progenitor cells (HSPCs).

99 ine hematopoietic stem and progenitor cells (HSPCs).

100 y human hematopoietic stem/progenitor cells (HSPCs).

101 as hematopoietic stem and progenitor cells (HSPCs).

102 ved hematopoietic stem and progenitor cells (HSPCs).

103 in MDS hematopoietic stem/progenitor cells (HSPCs).

104 metastatic process and identify circulating HSPCs as potential clinical indicators of metastatic nic

105 tization resulted in decrease of circulating HSPCs in five patients with WS.

106 s lineage priming and thus represent a CLOUD-HSPC.

107 opulation in FA patients with gene corrected HSPCs, opening new prospects for gene therapy of FA pati

108 n the generation of phenotypically corrected HSPCs capable of repopulating and developing proliferati

109 creases in HSPC-endothelial cell "cuddling," HSPC residency time within the CHT, and HSPC mitotic rat

110 However, current models for culturing HSPCs and for infecting T cells in vitro require that th

111 by Pak2-KD; defective homing of Pak2-deleted HSPCs was rescued by constitutive active CDC42.

112 a) HSPCs, and consistently, Eed(Delta/Delta) HSPCs exhibited increased attachment to a major extracel

113 e significantly enriched in Eed(Delta/Delta) HSPCs, and consistently, Eed(Delta/Delta) HSPCs exhibite

114 l cell protrusions seen in Pak2 (Delta/Delta)HSPCs were rescued by wild-type (WT) Pak2 but not by a P

115 ine activation of CDC42 in Pak2 (Delta/Delta)HSPCs, which was rescued by expression of Pak2-WT but no

116 SPCs activated Gata1 expression and depleted HSPCs, thus recapitulating the HSC phenotype associated

117 ansion of human umbilical cord blood-derived HSPCs following cytokine stimulation.

118 human induced pluripotent stem cell-derived HSPCs (hiPS-HSPCs).

119 C niche associated with previously described HSPC expansion strategies were not detected in bones tre

120 vation from latency than more differentiated HSPCs and that quiescent HSPCs are resistant to reactiva

121 e actively proliferating and differentiating HSPCs obtain predominantly active infections.

122 onomously to improve the efficiency of donor HSPC engraftment.

123 o hematopoietic stem and progenitor cell/EC (HSPC/EC) coculture system as well as in vivo EC infusion

124 e in vivo, reinforcing that CCR5 gene-edited HSPCs are capable of long-term engraftment.

125 r, these data demonstrate that genome-edited HSPCs engraft, and contribute to multilineage repopulati

126 These genome-edited HSPCs support multilineage engraftment and generate prog

127 Here we show that the CNS controls embryonic HSPC numbers via the hypothalamic-pituitary-adrenal/inte

128 opoietic tissue (CHT), the site of embryonic HSPC expansion in fish.

129 ATOs initiated with TCR-engineered HSPCs produced T cells with antigen-specific cytotoxicit

130 sis following MI, accompanied by exaggerated HSPC activity and impaired macrophage phenotype.

131 E confirmed the compound's ability to expand HSPCs and inhibit differentiation.

132 or hematopoietic defects in TRAF6-expressing HSPCs.

133 Recent advances marking fluorescent HSPCs have allowed exquisite visualization of HSPCs in t

134 r identifying molecular signals critical for HSPC proliferation and differentiation in the zebrafish.

135 interaction with beta-Pix are essential for HSPC filopodia formation, cytoskeletal integrity, and ho

136 at Vectofusin-1 remains the lead peptide for HSPC transduction enhancement with LVs pseudotyped with

137 growth factor beta (TGFbeta) is required for HSPC specification and that it regulates the expression

138 how that MkMP RNA is largely responsible for HSPC programming into Mk differentiation.

139 We provide further evidence that Foxo3(-/-) HSPC are defective in DNA damage repair.

140 unaddressed in efforts to derive functional HSPCs from human PSCs.

141 myeloid leukemia (AML) cells than in healthy HSPCs or other types of tumor cells.

142 However, glycoengineered hiPS-HSPCs did not engraft long-term, indicating that additio

143 ed pluripotent stem cell-derived HSPCs (hiPS-HSPCs).

144 nt progress, a complete understanding of how HSPC homing and engraftment are regulated is still elusi

145 Specifically, proliferation of Hoxa(-/-) HSPCs is reduced compared with wild-type (WT) cells in v

146 e age-related clonal expansions in the human HSPC pool, which was termed in the past age-related clon

147 Murine and human HSPCs were isolated from bone marrow and umbilical cord

148 Injection of murine and human HSPCs, which had been pretreated with treprostinil and f

149 o models induce T cell commitment from human HSPCs; however, differentiation into mature CD3(+)TCR-al

150 AAV) 6 delivery of donor constructs in human HSPCs approaches clinically relevant levels of TI into t

151 gulator of adhesion and engraftment in human HSPCs through mechanisms that, at least in part, involve

152 novel culture system in which primary human HSPCs cultured under hypothermic conditions are maintain

153 The human HSPCs produce immune cells that home into the tumor and

154 MLL-CHD fusion protein failed to immortalize HSPCs in myeloid conditions in vitro, it could successfu

155 Mice lacking CD26 or NPY exhibited impaired HSPC trafficking that was restored by treatment with tru

156 trated that this is a result of increases in HSPC-endothelial cell "cuddling," HSPC residency time wi

157 GAP and non-canonical TGF-beta signalling in HSPC differentiation.

158 inosine-5'-monophosphate dehydrogenase 2 in HSPCs, leading to altered levels of amino acids and puri

159 in transduction efficiency exceeding ~90% in HSPCs at significantly reduced vector doses.

160 izes TGF-beta levels and p38MAPK activity in HSPCs and is correlated with increased HSC self-renewal

161 ctor, do not increase the mutation burden in HSPCs in congenital neutropenia.

162 with TLR4 and endosomal Rab5 compartments in HSPCs.

163 Furthermore, genetic deletion of Dnmt1 in HSPCs activated Gata1 expression and depleted HSPCs, thu

164 -optimized AAV6 vectors in genome editing in HSPCs.

165 signature, modulated the gene expression in HSPCs after uptake, and maintained the survival and clon

166 o permit visualization of gene expression in HSPCs at single-cell resolution for any gene of choice.

167 mice exhibited abundant GATA1 expression in HSPCs, in a GATA2-dependent manner.

168 perdurance of a key transcription factor in HSPCs.

169 lecular pathways mediating Pak2 functions in HSPCs are unknown.

170 wild-type (WT) AAV6 vector varies greatly in HSPCs from different donors.

171 omatic mutations per exome was identified in HSPCs from patients with SCN compared with 3.9 +/- 0.4 f

172 hat p38MAPK is immediately phosphorylated in HSPCs after a hematological stress, preceding increased

173 rived jagged-2 activates Notch2 signaling in HSPCs to promote hematopoietic recovery and has potentia

174 y1, while tempering Notch2/Hes1 signaling in HSPCs.

175 a hematological stress, preceding increased HSPC cycling.

176 up by HSPCs although they bind to and induce HSPC aggregation.

177 of intact fluorescently-tagged MkMPs inside HSPCs demonstrates endocytosis as one mechanism of cargo

178 maging show that direct fusion of MkMPs into HSPCs is also engaged in cargo delivery.

179 ges leading to full adsorption of MkMPs into HSPCs.

180 ists restored vascular integrity and limited HSPC mobilization, demonstrating that the enzymatically

181 with widely differing abilities to maintain HSPCs ex vivo, we demonstrate that stromal EVs play a cr

182 that regulates JAK2 in normal and malignant HSPCs and suggest new therapeutic strategies for treatin

183 posure to blood plasma increases bone marrow HSPC ROS levels, augmenting their migration and differen

184 explored as therapeutic targets against MDS HSPCs.

185 3, and CD123 have begun to differentiate MDS HSPCs from healthy counterparts.

186 naling pathways has been demonstrated in MDS HSPCs and is being targeted therapeutically in preclinic

187 We isolated migrated HSPCs from the brain; using RNA sequencing to investigat

188 HSC cycling defects, and partially mitigates HSPC DNA damage.

189 nsplantation of ex vivo genetically modified HSPCs are complex and not without risk for the patient.

190 The ability to stably genetically modify HSPCs without the need of myeloablative conditioning is

191 We found that TRAF6 overexpression in mouse HSPC results in impaired hematopoiesis and bone marrow f

192 ylcytosine formation in Tet2-deficient mouse HSPCs and suppresses human leukemic colony formation and

193 Finally, Muller-HSPC hybrids differentiated into photoreceptors.

194 nhanced survival and proliferation of Muller-HSPC hybrids as well as their reprogramming into interme

195 n human cell lines as well as primary murine HSPCs.

196 result of elevated ROS in Foxo3(-/-) mutant HSPC is at least partially reversible.

197 us selective pressure to expand TP53-mutated HSPCs, suggesting that acquisition of TP53 mutations is

198 quantification of PIGA-mutant (GPI-negative) HSPC-derived peripheral blood cell populations.

199 ole of PUM1/2 and FOXP1 in regulating normal HSPC and leukemic cell growth.

200 s terminal myeloid differentiation of normal HSPCs and AML cells and inhibits AML cell survival/proli

201 RNA sequencing of Kdm2b-null HSPCs and genome-wide ChIP studies in human leukemias re

202 pair after stroke maybe via direct action of HSPC-derived MT-I and could therefore be exploited as a

203 o bone marrow (BM) is an important aspect of HSPC biology that has remained unaddressed in efforts to

204 ly, Ssb1 and Ssb2 control crucial aspects of HSPC function, including proliferation and survival in v

205 brogated the metastasis-promoting effects of HSPC mobilization.

206 , our results point to ECs as gatekeepers of HSPC trafficking and identify a CD26-mediated NPY axis t

207 , treatment resulted in increased numbers of HSPC-NK cells in the bone marrow compartment, suggesting

208 er expansion of HSPCs and altered pattern of HSPC mobilisation 8 days post-myocardial infarction, wit

209 8/cxcr1 signaling as a positive regulator of HSPC colonization.

210 We identified 17 regulators of HSPC repopulation: Arhgef5, Armcx1, Cadps2, Crispld1, Em

211 o, low-dose HMAs did not impair viability of HSPC-NK cells.

212 d in WS mice and mirrored by accumulation of HSPCs in the spleen, where we observed enhanced extramed

213 Knockdown of CYTH1 disrupted adhesion of HSPCs to primary human mesenchymal stroma cells.

214 Cell cycle analysis of HSPCs demonstrated increased S-phase fraction coupled wi

215 and induced erythropoiesis and apoptosis of HSPCs.

216 dispensable for maintaining the capacity of HSPCs to repopulate under steady-state conditions, by ac

217 the proliferative and functional defects of HSPCs derived from FA mice and FA patients.

218 edullary mobilization and differentiation of HSPCs occur in the spleen during acute Plasmodium infect

219 is critical for lymphoid differentiation of HSPCs, and its impairment is a key mechanism underpinnin

220 egulates mobilisation and differentiation of HSPCs.

221 A1 (-/-) mice exhibited greater expansion of HSPCs and altered pattern of HSPC mobilisation 8 days po

222 ressors result in the selective expansion of HSPCs carrying specific gene mutations.

223 defined as the gradual, clonal expansion of HSPCs carrying specific, disruptive, and recurrent genet

224 Engraftment and/or expansion of HSPCs was dependent on the expression of endothelial-der

225 istant primary tumor drives the expansion of HSPCs within the bone marrow and their mobilization to t

226 target, deliver cargo and alter the fate of HSPCs is important for exploring such applications.

227 d affect the gene expression and function of HSPCs.

228 specifically jagged-2, to the homeostasis of HSPCs is unknown.

229 Homing of HSPCs from bloodstream to bone marrow (BM) is an importa

230 stinil-enhanced CXCR4-dependent migration of HSPCs.

231 Moreover, pharmacologic mobilization of HSPCs increased metastasis, whereas depletion of Gr1(+)

232 ned the survival and clonogenic potential of HSPCs, presumably by preventing apoptosis.

233 ceted approach to optimize the production of HSPCs from human PSCs.

234 Gene expression profiling of HSPCs from the MSI2 MDS mice identifies a signature that

235 Notch2 it did contribute to the recovery of HSPCs in response to myelosuppressive conditions.

236 Vs play a critical role in the regulation of HSPCs.

237 r the first time Foxa genes as regulators of HSPCs.

238 nventional human T cells from all sources of HSPCs.

239 Transplantation of HSPCs with activated Wnt functionally rescued the retina

240 Treatment of HSPCs in I/RI for up to 2 wk after cerebral I/RI led to

241 SPCs have allowed exquisite visualization of HSPCs in the caudal hematopoietic tissue (CHT) of the de

242 was reversed by depleting EPOR expression on HSPC.

243 the loss of Hoxa genes had little impact on HSPC differentiation.

244 (ICAM-1), CD11b, CD18 and CD43, localized on HSPC uropods, are involved in MkMP binding to HSPCs.

245 6, a receptor that is uniformly expressed on HSPCs.

246 t biological effects of MkMPs versus PMPs on HSPCs.

247 In others, HSPCs expand.

248 Most importantly, only DAC potentiated HSPC-NK cell anti-leukemic activity in vivo.

249 Furthermore, low-dose DAC preserved HSPC-NK killing, proliferation, and interferon gamma pro

250 f hematopoiesis by simultaneously preserving HSPC stemness and promoting MyePro proliferation.

251 relates with PUM1 and PUM2 levels in primary HSPCs and myeloid leukemia cells.

252 ows for the stable transduction of primitive HSPCs.

253 xpression of E-selectin ligands that program HSPC trafficking to BM.

254 als from cancer and other conditions promote HSPC mobilization into circulation and subsequent homing

255 whereas the more permeable sinusoids promote HSPC activation and are the exclusive site for immature

256 the hematopoietic niche remodels to promote HSPC engraftment and suggests that cxcl8/cxcr1 signaling

257 Treatment of purified HSPCs cultured ex vivo with tumor-conditioned media indu

258 We furthered tracked purified HSPCs in vivo and found they differentiated into myeloid

259 ys, which enforced cell cycling in quiescent HSPCs, resulting in their apoptotic death.

260 emonstrate that the most primitive quiescent HSPCs are more resistant to spontaneous reactivation fro

261 more differentiated HSPCs and that quiescent HSPCs are resistant to reactivation by histone deacetyla

262 We show that these quiescent HSPCs are susceptible to predominantly latent infection

263 responses to crosslinking agents, Rad18(-/-) HSPC were sensitive to in vivo treatment with the myelos

264 EPHB4/ephrin B2 blockade also reduced HSPC infiltration into tumors as well as tumor progressi

265 ged-2 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence during regeneration.

266 12 axis represents an approach that releases HSPC with efficiency superior to any other known mobiliz

267 -infiltrated hematopoietic niche may restore HSPC homeostasis and improve the outcome of ALL patients

268 ly, mice lacking Smarcal1 showed significant HSPC defects when challenged to respond to other replica

269 etention of multi-lineage capacity in single HSPC myeloid cell cultures, further suggesting a link be

270 sequencing to profile more than 1600 single HSPCs, and deep sequencing has enabled detection of an a

271 th asymmetric fate choice in vitro in single HSPCs via p38MAPK activity and this is correlated with t

272 pectively assign cells to 12 commonly sorted HSPC phenotypes while also capturing intermediate cells

273 We demonstrate that FOXP1 by itself supports HSPC and leukemic cell growth, thus mimicking PUM activi

274 e distinct from Mk exosomes (MkExos), target HSPCs with high specificity since they have no effect on

275 We show that HSPC uropods are the preferential site for MkMP binding,

276 mice with engrafted human CD34(+) cells that HSPCs transduced in the periphery home back to the BM wh

277 lymphopenia in WS arises from defects at the HSPC level.

278 ted by human cytokines expressed by both the HSPC progeny and the tumor cells.

279 Clonal architecture of the HSPC compartment and mutations selected during different

280 s that EVs are an important component of the HSPC niche, which may have major applications in regener

281 ng to a twofold to fourfold expansion of the HSPC pool in the BM was observed.

282 c inhibition of the CXCR4/CXCL12 axis on the HSPC compartment were investigated by using 3 structural

283 Furthermore, major changes within the HSPC niche associated with previously described HSPC exp

284 urface molecules not previously connected to HSPC biology-the secreted RNase angiogenin, the cytokine

285 demonstrate that the G1MDR holds the key to HSPC maintenance and suggest that release from this supp

286 ensive genome-scale data that is relevant to HSPC biology.

287 duced neuroprotection in a manner similar to HSPC treatment.

288 SPC uropods, are involved in MkMP binding to HSPCs.

289 very of nucleic acids and other molecules to HSPCs for targeted molecular therapy.

290 ut the persistence of adoptively transferred HSPC-NK cells was not affected.

291 Upon transplantation, HSPCs express high amounts of bioactive TGF-beta1 protei

292 ed cell sorting analyses showed transplanted HSPCs emigrate preferentially into ischemic cortex brain

293 ivation of Wnt signaling in the transplanted HSPCs enhanced survival and proliferation of Muller-HSPC

294 expansion mediated by injection of wild-type HSPCs directly into wounds.

295 ing the dynamic molecular changes underlying HSPC differentiation.

296 Lentiviral vector HSPC gene therapy generates a human hematopoietic system

297 Up to 58% Venus(+) HSPCs with 6-16% human cell marking were observed follow

298 transgenic mice, we showed that our in vivo HSPC transduction approach allows for the stable transdu

299 Only upon 5-fluorouracil treatment was HSPC-depleted bone marrow compromised in reconstituting

300 el evidence that the mechanism through which HSPCs promote repair after stroke maybe via direct actio