ライフサイエンスコーパス: HSC

1 HSCs mediate hepatic fibrosis through their activation f

2 HSCs play an essential role in ConA-induced liver injury

3 ease-activated receptors (PARs) can activate HSCs through thrombin and factor Xa, which are known PAR

4 Activated HSC are also important sources of hydrogen peroxide resu

5 dulated alpha-smooth muscle actin (activated HSC marker) and collagen 1 in both WT and TLR4-KO HSCs.

6 localized with alphaSMA-expressing activated HSC.

7 her indicate that LPS signaling in activated HSCs might be a mechanism of limiting liver fibrosis.

8 omes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 axis.

9 During activation, HSCs lose their lipid droplets (LDs) containing triacylg

10 arly, hyperactivation of RagA did not affect HSC function.

11 se survival and hematopoietic recovery after HSC transplantation.

12 Exposure of aged HSCs to thrombin-cleaved OPN attenuates aging of old HSC

13 This allows us to specifically focus on aged HSCs presenting with a pronounced lineage skewing, a hal

14 eactive oxygen species, and rejuvenated aged HSCs.

15 formed therapeutic approach for ameliorating HSC phenotypes associated with aging.

16 In summary, we demonstrate an HSC-based gene therapy approach for IFNgammaR1 deficienc

17 reserving endogenous FOXP3 regulation for an HSC-based gene therapy approach for IPEX syndrome.

18 fibrosis genes in vitro in cholangiocyte and HSC lines.

19 Analysis of the composition of HSCs and HSC-derived multipotent progenitors (MPPs) revealed a si

20 omal abnormalities, genomic instability, and HSC aging and might promote hematological malignancies w

21 ion within the ER, induction of the UPR, and HSC apoptosis.

22 ype (GnRHR1) expressed by cholangiocytes and HSCs.

23 transposition is much lower in both MSCs and HSCs when compared to NPCs.

24 tential in the bone marrow (BM), and that as HSCs accumulate a divisional history, they progressively

25 cols are not capable of generating authentic HSCs with high efficiency.

26 Gene therapy using autologous HSCs should avoid these limitations and thus may be safe

27 The balance between HSC self-renewal and differentiation is maintained by va

28 w cells restore quiescence of myeloid-biased HSCs, with implications for blood disorders, aging, and

29 decreased IHVR, enhanced NO bioavailability, HSC deactivation, and reduced intrahepatic microthrombos

30 le marker of UM171-expanded human cord blood HSCs.

31 D41 expression is up-regulated within the BM HSC compartment in response to G-CSF treatment.

32 nd Hes1 were significantly activated in both HSC and MPP1 cells in anemic mice.

33 Lack of PDK1 caused HSCs to be less quiescent and to produce a higher number

34 rmal hematopoietic stem and progenitor cell (HSC/P) functions.

35 Hepatic stellate cell (HSC) activation and transforming growth factor-beta 1 (T

36 notypically defined hematopoietic stem cell (HSC) compartment in all investigated patients and were a

37 ote quiescent human hematopoietic stem cell (HSC) expansion ex vivo have been identified; however, th

38 poietic defects and hematopoietic stem cell (HSC) failure.

39 enia and to enforce hematopoietic stem cell (HSC) mobilization to the peripheral blood (PB).

40 racteristics of the hematopoietic stem cell (HSC) niche contain precursors that reform the niche.

41 regulate different hematopoietic stem cell (HSC) properties such as proliferation, differentiation,

42 when exposed to the hematopoietic stem cell (HSC) self-renewal agonist UM171.

43 ulting in decreased hematopoietic stem cell (HSC) self-renewal capacity, myeloid skewing, and immune

44 L-CSCs derived from hematopoietic stem cell (HSC)-enriched LSK population but not myeloid-granulocyte

45 p521 as a conserved hematopoietic stem cell (HSC)-enriched transcription factor in human and murine h

46 progenitor waves of hematopoietic stem cell (HSC)-independent hematopoiesis as well as for the normal

47 haematopoiesis or haematopoietic stem cell (HSC)-mediated reconstitution after transplantation is un

48 positivity in their hematopoietic stem cell (HSC)/progenitor/myeloid compartments at initial diagnosi

49 in hematopoetic stem cells/precursor cells (HSC/PC) and postnatal infections for human-like pB-ALL.

50 expressed by active hepatic stellate cells (HSC) and is a key monocyte recruitment signal.

51 ted by activation of hepatic stellate cells (HSC).

52 uce DNA damage in haematopoietic stem cells (HSC) and telomeres are sensitive to this damage.

53 cRNA-seq on murine hematopoietic stem cells (HSC) and their progeny MPP1 separated the cells into 3 m

54 of damaged DNA in hematopoietic stem cells (HSC) is associated with chromosomal abnormalities, genom

55 nregulated Tet1 in hematopoietic stem cells (HSC), resulting in reduced expression of genes critical

56 ll production, and hematopoietic stem cells (HSC), which provide a quiescent cellular reserve.

57 Hepatic stellate cells (HSCs) are key players in the development of liver fibros

58 , is up-regulated in hepatic stellate cells (HSCs) during chronic liver injury.

59 of LPS on fibrogenic hepatic stellate cells (HSCs) from WT and TLR4-KO mice were assessed in vitro.

60 Activation of hepatic stellate cells (HSCs) in response to injury is a key step in hepatic fib

61 Hepatic stellate cells (HSCs) induce hepatic inflammation and immunological reac

62 Activation of hepatic stellate cells (HSCs) is a critical step in the development of liver fib

63 ocytes and activated hepatic stellate cells (HSCs) participate in the promotion of liver fibrosis dur

64 gnature of activated hepatic stellate cells (HSCs), the primary collagen-secreting cell in liver, and

65 ighly expressed in hematopoietic stem cells (HSCs) and acute myeloid leukemia stem cells (LSCs) compa

66 lar niches sustain hematopoietic stem cells (HSCs) and are drastically remodeled in leukemia to suppo

67 ow (BM) long-term haematopoietic stem cells (HSCs) and granulocyte-macrophage progenitors compared wi

68 DDT in maintaining hematopoietic stem cells (HSCs) and progenitors, we used Pcna(K164R/K164R) mice as

69 Hematopoietic stem cells (HSCs) are mobilized from niches in the bone marrow (BM)

70 Hematopoietic stem cells (HSCs) are the therapeutic component of bone marrow trans

71 f patient-specific hematopoietic stem cells (HSCs) could be generated from induced pluripotent stem c

72 developing embryo, hematopoietic stem cells (HSCs) emerge from the aorta-gonad-mesonephros (AGM) regi

73 ntion or egress of hematopoietic stem cells (HSCs) from bone marrow (BM).

74 Single hematopoietic stem cells (HSCs) have been functionally shown to generate all matur

75 Hematopoietic stem cells (HSCs) in the bone marrow (BM) form mature blood cells of

76 Hematopoietic stem cells (HSCs) produce most cellular energy through glycolysis ra

77 from quiescence by hematopoietic stem cells (HSCs) progressively impairs their homeostasis in the bon

78 Hematopoietic stem cells (HSCs) remain mostly quiescent under steady-state conditi

79 Hematopoietic stem cells (HSCs) reside at the top of the hematopoietic hierarchy a

80 graftment of human hematopoietic stem cells (HSCs) that can lead to human hematopoiesis within the mu

81 Hematopoietic stem cells (HSCs) that sustain lifelong blood production are created

82 in the response of hematopoietic stem cells (HSCs) to liver fibrosis in mice.

83 h specification of hematopoietic stem cells (HSCs) to the myeloid and lymphoid lineages.

84 use of allogeneic hematopoietic stem cells (HSCs) to treat genetic blood cell diseases has become a

85 Upon aging, hematopoietic stem cells (HSCs) undergo changes in function and structure, includi

86 gnals can activate hematopoietic stem cells (HSCs), but how HSCs regain quiescence after stress is un

87 or ECD arises from hematopoietic stem cells (HSCs), nor which potential blood borne precursors lead t

88 otypically defined hematopoietic stem cells (HSCs).

89 es the behavior of hematopoietic stem cells (HSCs).

90 environment is formed and establish complete HSC niches, which are functionally supportive of hematop

91 anti-interferon beta antibody mitigated ConA/HSC-induced injury.

92 In vitro, effects of ConA-conditioned HSC medium on hepatocytes were determined.

93 l of parallel signaling pathways controlling HSC specification: Wnt16/DeltaC/DeltaD and Vegfa/Tgfbeta

94 As a consequence, genetically corrected HSC-derived macrophages were able to suppress T-cell act

95 Transplantation of genetically corrected HSCs into Ifngammar1(-/-) mice before BCG infection prev

96 In vitro, cultured HSCs were stimulated with cholangiocyte supernatants and

97 tent inhibitor of Jak2 signaling, in cycling HSCs.

98 Rivaroxaban deactivated HSC, with decreased alpha-smooth muscle actin and mRNA e

99 esulting in increased engraftment, decreased HSC frequency, increased stem cell polarity and a restor

100 trong cell intrinsic defect of DDT-deficient HSCs in reconstituting lethally irradiated mice and a st

101 PDK1-deficient HSCs were also unable to reconstitute the hematopoietic

102 Sin3B-deleted HSCs accumulate and fail to properly differentiate follo

103 cholesterol (27HC) induced ERalpha-dependent HSC mobilization and EMH but not HSC division in the bon

104 fficiency limits the number of donor-derived HSCs and B lymphopoiesis.

105 lopment is a promising approach to directing HSC specification in vitro, but current protocols are no

106 esting that G-CSF does not stimulate dormant HSC proliferation.

107 t result in H2BGFP label dilution of dormant HSCs, suggesting that G-CSF does not stimulate dormant H

108 Our results show that dormant HSCs are preferentially mobilized to the PB on G-CSF tre

109 Previous work has shown that dormant HSCs contain all the long-term repopulation potential in

110 gether, our results demonstrate that dormant HSCs mobilize in response to G-CSF treatment without div

111 he unfolded protein response (UPR) and drive HSC apoptosis.

112 ubsequent induction of chemokines that drive HSC recruitment in CFLD.

113 TANGO1 regulation during HSC activation occurs through a UPR-dependent mechanism

114 is not required for engraftment of embryonic HSCs.

115 can serve as adjuvant modalities to enhance HSC engraftment and accelerate hematopoietic recovery in

116 ss, Aid loss does not contribute to enhanced HSC self-renewal or cooperate with Flt3-ITD to induce my

117 tains HSC activity and can be used to expand HSC numbers ex vivo.Repeated cell divisions induce DNA d

118 eased repopulating ability, FOXP3 expressing HSC showed significantly enhanced expression of genes co

119 into immunodeficient mice, FOXP3-expressing HSC showed significantly enhanced engraftment ability.

120 alters the expression of genes critical for HSC self-renewal, differentiation and apoptosis in Lin(-

121 RagA was also dispensable for HSC function under nutritional stress conditions.

122 ulator of two crucial pathways necessary for HSC specification.

123 ical role for reduced stroma-derived OPN for HSC aging and identify thrombin-cleaved OPN as a novel n

124 Evaluating the prospects for HSC rejuvenation therefore ultimately requires approachi

125 We find that Rspo1 is required for HSC specification through control of parallel signaling

126 s a correlate of, but not a requirement for, HSC maturation.

127 ed ROS levels result in defective Foxo3(-/-) HSC cycling, among many other deficiencies.

128 re important for B-cell differentiation from HSCs by maintaining immunological homoeostasis in the bo

129 re critical to the maintenance of functional HSCs.

130 We generated HSC-specific NOX4 KO mice and these were pair-fed on alc

131 This emergent CD41(Hi) HSC fraction demonstrates no observable engraftment pote

132 ate hematopoietic stem cells (HSCs), but how HSCs regain quiescence after stress is unclear.

133 However, HSCs lacking mitochondrial Fh1 (which had normal fumarat

134 and compared the transcriptomes of pre-HSCs, HSCs matured ex vivo, and fetal liver HSCs.

135 to identify compounds that inactivate human HSC myofibroblasts through the quantification of lipid d

136 exogenous human POT1 protein maintains human HSC activity in culture.

137 tissue, which was also able to support human HSC engraftment.

138 -dependently reduced collagen I in the human HSC line, TWNT-4.

139 -bearing mice engrafted and maintained human HSCs in the niche.

140 uired for the repopulating activity of human HSCs.

141 Primary human HSCs and immortalized HSCs (LX2 cells) were incubated wi

142 ifferent stromal cell types to support human HSCs.

143 Primary human I148M HSCs displayed significantly higher expression and relea

144 ith BCR-ABL1-positive BCP-ALL, we identified HSC involvement in 40% of the patients.

145 To identify HSCs from in vitro sources, it will be necessary to refi

146 Primary human HSCs and immortalized HSCs (LX2 cells) were incubated with conditioned medium

147 ignaling pathways and cell types may improve HSC bioengineering, which could significantly advance cr

148 the potential of stroma recovery to improve HSC transplantation.

149 ew tools to manipulate primitive features in HSC for clinical applications.

150 n and murine hematopoiesis whose function in HSC biology remains elusive.

151 Despite this marked improvement in HSC phenotype, no significant changes in LF were identif

152 data highlight an essential role for Jak1 in HSC homeostasis and stress responses.

153 ntrol mice, which were strongly minimized in HSC-depleted mice.

154 We propose that the role of mitochondria in HSC biology may have to be revisited in light of these f

155 activation of the STAT3-TGF-beta pathway in HSC.

156 onstrate that FAK plays an essential role in HSC activation and liver fibrosis progression, and FAK s

157 higher in ConA-treated control mice than in HSC-depleted mice.

158 se (LAL/Lipa) inhibitor on LD degradation in HSCs during activation in vitro The LAL inhibitor increa

159 hondrial mass has been reported to be low in HSCs.

160 al turnover capacity is comparatively low in HSCs.

161 tivates inflammasome and fibrosis markers in HSCs and that neutralizing antibody to CCL5 inhibited ac

162 invoked to explain low mitochondrial mass in HSCs, we observed that mitochondrial turnover capacity i

163 ed effects of AKT signaling and migration in HSCs.

164 and inheritable transcriptional programs in HSCs and is reinforced over cell division by recursive i

165 ion of both cell cycle and Jak2 signaling in HSCs.

166 tefactually low fluorescence specifically in HSCs because of dye efflux.

167 Depletion of TANGO1 in HSCs blocked collagen I secretion without affecting othe

168 r Kit(W-sh) mice injected with MCs increased HSC activation, which decreased with supernatants from B

169 stemic ascorbate depletion in mice increased HSC frequency and function, in part by reducing the func

170 Triggering of PGE2 receptors increases HSC survival in part via the PKA-mediated induction of t

171 nd identified 21 small molecules that induce HSC inactivation.

172 Del-1-induced HSC proliferation and myeloid lineage commitment were me

173 estradiol increases during pregnancy induced HSC proliferation in the bone marrow but not HSC mobiliz

174 As G-CSF treatment also induces HSC proliferation, we sought to examine whether G-CSF-me

175 herefore, we hypothesize that TB4 influences HSC activation through hedgehog (Hh) pathway.

176 Treatment of irradiated HSCs with Dkk1 in vitro increased the recovery of both l

177 arker) and collagen 1 in both WT and TLR4-KO HSCs.

178 f cytokines and chemokines in WT and TLR4-KO HSCs.

179 mice had significantly reduced 27HC levels, HSC mobilization, and EMH during pregnancy but normal bo

180 amic, nitric oxide (NO) bioavailability, LF, HSC activation, and microthrombosis were evaluated in CC

181 reduced liver:lymph S1P gradient and limited HSC egress from the liver.

182 Cs to promote Tet activity in vivo, limiting HSC frequency and suppressing leukaemogenesis.

183 We show that ex vivo-matured and fetal liver HSCs express programmed death ligand 1 (PD-L1).

184 -HSCs, HSCs matured ex vivo, and fetal liver HSCs.

185 ice maintained on a vitamin A-free diet lose HSCs and show a disrupted re-entry into dormancy after e

186 Hdac8-deficient LT-HSCs displayed hyperactivation of p53 and increased apop

187 vide evidence of a multipotent lymphomyeloid HSC origin of SF3B1 mutations in MDS-RS patients and pro

188 are major enforcers of quiescence, maintain HSC homeostasis by positively regulating thrombopoietin

189 dicate a critical role of DDT in maintaining HSCs and progenitor cells, and in preventing premature a

190 miR-99 maintains HSC long-term reconstitution activity by inhibiting diff

191 Integrin beta3 signaling maintains HSCs within the niche.

192 progenitors into the cell cycle; cycling MB-HSCs fail to revert into quiescence in the absence of hi

193 logic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors marked by histidine d

194 amine, which activates the H2 receptor on MB-HSCs to promote their quiescence and self-renewal.

195 iological demands to intrinsically primed MB-HSCs to enforce homeostasis.

196 r depletion, while an H2 agonist protects MB-HSCs from depletion after sepsis.

197 ide (LPS) treatment specifically recruits MB-HSCs and progenitors into the cell cycle; cycling MB-HSC

198 ells lie in close anatomical proximity to MB-HSCs and produce histamine, which activates the H2 recep

199 ntion in the ER, which promotes UPR-mediated HSC apoptosis.

200 anismal viability in evolution and in modern HSC transplantation approaches.

201 Human and mouse HSCs had unusually high levels of ascorbate, which decre

202 lesteryl ester, and RE in both rat and mouse HSCs.

203 th muscle actin (alpha-SMA) in rat and mouse HSCs.

204 In mouse HSCs, Pot1a knockdown increases DNA damage response (DDR

205 Here, the authors show in murine HSCs that the telomere binding protein POT1a inhibited t

206 re found in the SDT group, while p53-mutated HSC-3 cells did not show such increase.

207 This population of somatically mutated HSC, which initiates and sustains MPNs, is termed MPN st

208 NOD HSCs were held in their niche by excess expression of CX

209 n the setting of allogeneic nonmyeloablative HSC transplants (HSCTs), stable mixed chimerism is suffi

210 erentially target MPN stem cells over normal HSC.

211 a-dependent HSC mobilization and EMH but not HSC division in the bone marrow.

212 HSC proliferation in the bone marrow but not HSC mobilization.

213 rcellular communication in the activation of HSC for liver fibrosis in HCV infection.IMPORTANCE HCV-a

214 predicted effects of FOXP3 in the biology of HSC and may provide new tools to manipulate primitive fe

215 nd revealed new insights into the biology of HSC recovery after HSCT.

216 We hypothesized that coordination of HSC specification with vessel patterning might involve m

217 inical bone-marrow recovery within 5 days of HSC infusion, which was up to 20 days before engraftment

218 a pronounced lineage skewing, a hallmark of HSC ageing.

219 The indifference of HSC to nutrient sensing through RagA contributes to thei

220 differentiation in vitro, with rapid loss of HSC-enriched LSK cells.

221 suggest that FOXO3 serves as a protector of HSC genomic stability and health.

222 ese results uncover long-range regulation of HSC migration emerging from the brain.

223 ntify BMPER as a novel positive regulator of HSC development.

224 y Sin3B as a novel and critical regulator of HSC functions.

225 To identify novel secreted regulators of HSC maturation, we performed RNA sequencing over these s

226 ents offered RI services, though only 61% of HSCs did so.

227 Ablation of HSCs impaired tolerance to allogeneic islet transplants

228 irs the competitive repopulation capacity of HSCs.

229 Analysis of the composition of HSCs and HSC-derived multipotent progenitors (MPPs) reve

230 models that recapitulated differentiation of HSCs into progenitor cell types, focusing on trajectorie

231 likely owing to increased differentiation of HSCs toward myeloid/erythroid-associated MPP2s.

232 as the result of a gradual disappearance of HSCs in livers of Lipa(-/-) mice.

233 oiesis as well as for the normal function of HSCs.

234 ow it affects the long-term functionality of HSCs and the blood system as a whole.

235 s, it will be necessary to refine markers of HSCs matured ex vivo.

236 ) revealed a significantly reduced number of HSCs, likely owing to increased differentiation of HSCs

237 with HSCs had increased hepatic retention of HSCs (1697 +/- 247 cells in mice given FTY720 vs 982 +/-

238 duce SIP signaling and increase retention of HSCs in the liver could increase their antifibrotic acti

239 s activation, proliferation, and survival of HSCs and protects from liver fibrogenesis.

240 respiratory capacity of MPPs exceeds that of HSCs.

241 Indeed, TCA treatment of HSCs promoted accumulation of ceramide through inhibitio

242 thrombin-cleaved OPN attenuates aging of old HSCs, resulting in increased engraftment, decreased HSC

243 R fails to reproduce the effects of UM171 on HSC activity, its expression is required for the repopul

244 varoxaban (RVXB), a direct antifactor Xa, on HSC phenotype, liver fibrosis (LF), liver microthrombosi

245 ConA was administered i.v. to control or HSC-depleted mice; hepatic histopathology and cytokines/

246 th muscle actin and mRNA expression of other HSC activation markers.

247 and to produce a higher number of phenotypic HSCs and fewer progenitors.

248 Across phyla, HSCs arise from hemogenic endothelium in the ventral flo

249 ified and compared the transcriptomes of pre-HSCs, HSCs matured ex vivo, and fetal liver HSCs.

250 In BDL Kit(W-sh) mice, IBDM, proliferation, HSC activation/fibrosis, and TGF-beta1 expression/secret

251 ysiological levels of corticosterone promote HSC migration via the GC receptor Nr3c1-dependent signal

252 ic effects of repeated infusions of purified HSCs.

253 erized by trans-differentiation of quiescent HSCs to HSC myofibroblasts, which secrete extracellular

254 rEC-HSCs have a transcriptome and long-term self-renewal cap

255 lial cells to haematopoietic stem cells (rEC-HSCs) through transient expression of the transcription-

256 to infection, and excessive exposure reduces HSC repopulation capacity.

257 1 in the CNS, but not the periphery, reduces HSC mobilization.

258 bone marrow niche is required to regenerate HSCs and leukemic cells with functional ability to rearr

259 ted cell-autonomously to negatively regulate HSC function and myelopoiesis through Tet2-dependent and

260 from the sympathetic nervous system regulate HSC egress via its niche, but how the brain communicates

261 st has emerged in how inflammation regulates HSC fate and how it affects the long-term functionality

262 eficient mice revealed that ZFP521 regulates HSC self-renewal and differentiation.

263 the recovery of both long-term repopulating HSCs and progenitor cells, and systemic administration o

264 N-acetylcysteine reduces ROS levels, rescues HSC cycling defects, and partially mitigates HSPC DNA da

265 e deferoxamine or a genetic approach rescues HSCs loss, promotes chemotherapeutic efficacy, and enhan

266 ng factors elaborated by BM ECs that restore HSC function and the immune repertoire in aged mice.

267 immune-deficient mice, SF3B1 mutated MDS-RS HSCs differentiated into characteristic ring sideroblast

268 Prostaglandin E2 (PGE2) stimulates HSC renewal and engraftment through, for example, induct

269 t the S1P antagonist FTY720; we then studied HSC mobilization and localization.

270 e marrow (BM) microenvironment in supporting HSC function may prove to be beneficial in treating age-

271 these results show that Pot1a/POT1 sustains HSC activity and can be used to expand HSC numbers ex vi

272 ase in engraftment, an increase in long-term HSC frequency and loss of stem cell polarity.

273 We found that HSC maturation in vivo or ex vivo is accompanied by the

274 The HSC and MPP phenotypes are reminiscent of premature agin

275 through the BPHS program, especially at the HSC level.

276 s, the regulatory pathways implicated in the HSC DNA damage response have not been fully elucidated.

277 This hitherto unknown Del-1 function in the HSC niche represents a juxtacrine homeostatic adaptation

278 w that obesity alters the composition of the HSC compartment and its activity in response to hematopo

279 interrogating the complex composition of the HSC niche and dissecting the niche remodeling processes

280 in Del-1 as a component and regulator of the HSC niche.

281 Overall, these findings indicate that the HSC compartment plays an underrecognized role in the est

282 stead, we find that proliferation within the HSC compartment is restricted to CD41-expressing cells t

283 ited regenerative potential found within the HSC compartment.

284 refore ultimately requires approaching those HSCs that are functionally affected by age.

285 , integrin alphavbeta3, is activated through HSC adhesion to extracellular matrix and niche cells.

286 the molecular mechanisms that contribute to HSC aging.

287 y trans-differentiation of quiescent HSCs to HSC myofibroblasts, which secrete extracellular matrix p

288 ts demonstrated that HCV-exo internalized to HSC and increased the expression of profibrotic markers.

289 ession of CXCR4, which, when blocked, led to HSC mobilization and prolonged islet allograft survival.

290 xt overlapped a 122-gene signature unique to HSCs with a list of 160 genes encoding proteins that are

291 to demonstrate that, after transplantation, HSCs are very asymmetrically distributed and uncover a t

292 mation of stress fibers in TGF-beta1 treated HSCs.

293 advantage when cotransplanted with wild-type HSCs.

294 Compared with other facility types, HSCs were less likely to have adequate stock of vaccines

295 isms, we conducted in vitro experiments with HSCs infected with adenoviral vectors encoding LacZ, Dyn

296 Mice given the S1P antagonist (FTY720) with HSCs had increased hepatic retention of HSCs (1697 +/- 2

297 Ascorbate therefore accumulates within HSCs to promote Tet activity in vivo, limiting HSC frequ

298 rive hematopoietic aging phenotypes in young HSCs.

299 Cs impair the repopulating activity of young HSCs and impart a myeloid bias.

300 Exposure of young HSCs to an OPN knockout niche results in a decrease in e