ライフサイエンスコーパス: platelet production

1 volved in megakaryocyte (MK) development and platelet production.

2 poptotic caspase cascade is not required for platelet production.

3 ide insights into the terminal mechanisms of platelet production.

4 platelet destruction and reduced bone marrow platelet production.

5 mbopoiesis during stress-induced accelerated platelet production.

6 in clinical development for cancer, affects platelet production.

7 ccelerated platelet destruction and impaired platelet production.

8 xtensions, which serve as assembly lines for platelet production.

9 mulates thrombopoiesis, leading to increased platelet production.

10 15d-PGJ(2)), increases Meg-01 maturation and platelet production.

11 lcysteine (NAC) attenuate 15d-PGJ(2)-induced platelet production.

12 celerated platelet destruction and decreased platelet production.

13 uding IFN-gamma, stimulate megakaryocyte and platelet production.

14 n, this mechanism may contribute to impaired platelet production.

15 s that regulate megakaryopoiesis and lead to platelet production.

16 dy-mediated platelet destruction and reduced platelet production.

17 n procoagulant activity, and does not effect platelet production.

18 aling induced apoptosis of MKs and increased platelet production.

19 Runx1 excision also resulted in inefficient platelet production.

20 il and discuss several disorders that affect platelet production.

21 ine regulating megakaryocyte development and platelet production.

22 Cs) promote thrombopoietin (TPO)-independent platelet production.

23 es suggest that autoantibody may also affect platelet production.

24 but may also contribute to the inhibition of platelet production.

25 mbopoietin (TPO) is the primary regulator of platelet production.

26 albumin-(serotonin)(6) conjugate during COAT-platelet production.

27 odel to study human megakaryocytopoiesis and platelet production.

28 es megakaryocyte proliferation and increased platelet production.

29 ITP patients there is an overall decrease in platelet production.

30 r regulator of megakaryocyte development and platelet production.

31 endothelial cell layers results in increased platelet production.

32 primary regulator of megakaryocyte (MK) and platelet production.

33 -linear increases in megakaryocytopiesis and platelet production.

34 equired for megakaryocyte differentiation or platelet production.

35 TA-1 influences megakaryocyte maturation and platelet production.

36 of single versus daily dosing in stimulating platelet production.

37 tegrins may have a role in MK maturation and platelet production.

38 is a primary regulator of megakaryocyte and platelet production.

39 ocytopenia is associated with suppression of platelet production.

40 ene could be important for the regulation of platelet production.

41 has profoundly changed our understanding of platelet production.

42 tors of all lineages and greatly accelerates platelet production.

43 as the major regulator of megakaryocyte and platelet production.

44 uration, should lead to an increased rate of platelet production.

45 hat TPO is not critical to the final step of platelet production.

46 11 (IL-11) is a growth factor that increases platelet production.

47 PO) is the physiologic Mpl-ligand regulating platelet production.

48 ncipal regulator of megakaryocytopoiesis and platelet production.

49 has been shown to be the major regulator of platelet production.

50 egakaryocyte proliferation, endomitosis, and platelet production.

51 een was a major site of megakaryopoiesis and platelet production.

52 atopoietic progenitor cells and is a site of platelet production.

53 ealing potential strategies toward enhancing platelet production.

54 g in the bone marrow and ensuring continuous platelet production.

55 ubstantial defect in human MK maturation and platelet production.

56 additional layer in parallel with canonical platelet production.

57 extensions, termed proplatelets, to control platelet production.

58 c of MKs primed for inflammation rather than platelet production.

59 has previously been dismissed as a source of platelet production.

60 , increased Mk survival, and higher rates of platelet production.

61 of hematopoiesis, megakaryocytopoiesis, and platelet production.

62 ll specifically amplified the MK lineage and platelet production.

63 e budding correlates with failure of in vivo platelet production.

64 and abnormal thrombopoiesis and for in vitro platelet production.

65 h clonal and nonclonal disorders of enhanced platelet production.

66 y promotes megakaryocyte differentiation and platelet production.

67 n (TPO) mRNA and protein, thereby regulating platelet production.

68 d intermediate stage in the final process of platelet production.

69 the study of pathologic mechanisms of human platelet production.

70 MKs with low nuclear ploidy and to decreased platelet production.

71 did not interfere with MK differentiation or platelet production.

72 n megakaryocyte clones to examine effects on platelet production.

73 s is crucial for normal megakaryopoiesis and platelet production.

74 n live-cell microscopy and quantification of platelet production.

75 t is not clear how the proteasome influences platelet production.

76 reveal a profound role for Wnt signaling in platelet production.

77 -mediated platelet destruction and decreased platelet production.

78 othrombotic events associated with increased platelet production.

79 on megakaryocyte survival, development, and platelet production.

80 mbrane and cytoskeletal remodeling affecting platelet production.

81 ration and polyploidization are critical for platelet production; abnormalities in these processes ar

82 ombopoietin (TPO), the critical regulator of platelet production, acts by binding to its cell surface

83 le cellular and molecular targets to enhance platelet production after bone marrow transplantation or

84 rombopoietin (TPO), the primary regulator of platelet production, also plays an important role in hem

85 rrow has been proposed to be a major site of platelet production, although there is indirect evidence

86 hrombocytopenia (ITP) results from decreased platelet production and accelerated platelet destruction

87 Because abnormal platelet production and activation have been implicated

88 Enhanced platelet production and activation may predispose to art

89 Platelet production and activation were measured in B6-L

90 lin and a few other proteins that may impact platelet production and activation.

91 M)-containing receptor G6b-B is critical for platelet production and activation.

92 deficiency is associated with both increased platelet production and activation.

93 een identified in which tumors can stimulate platelet production and activation; activated platelets

94 that one or more Cdkn2a transcripts modulate platelet production and activity in the setting of hyper

95 tify the lungs as a primary site of terminal platelet production and an organ with considerable haema

96 tent stimulators of megakaryocyte growth and platelet production and are biologically active in reduc

97 Decreased platelet production and decreased half-life of platelets

98 015), demonstrating the relationship between platelet production and destruction.

99 function as a chaperon for TGF-beta1 during platelet production and does not activate significant qu

100 cus may identify a gene product that affects platelet production and function and contributes to the

101 cyte growth and development factor regulates platelet production and function by stimulating endoredu

102 me (BCS), treatment directed toward altering platelet production and function may be more rational an

103 Changes in platelet production and function produced by PEG-rHuMGDF

104 define the regulatory role of Mpl ligand on platelet production and function we measured the effects

105 iverse aspects of megakaryocyte biology, and platelet production and function, culminating in thrombo

106 To establish the role of caspases in platelet production and function, we generated mice lack

107 , suggesting a major role of this isozyme in platelet production and function.

108 in cytoskeleton is a prerequisite for proper platelet production and function.

109 al glycosylation of key proteins involved in platelet production and function.

110 critical for megakaryocytopoiesis and normal platelet production and function.

111 ac1 and Cdc42 possess redundant functions in platelet production and function.

112 sulted in a defect in the terminal stages of platelet production and had a mild effect on platelet fu

113 s support a novel role for TrkA signaling in platelet production and highlight its potential as thera

114 Consistent with this, we found an elevated platelet production and increase in megakaryocytes in th

115 n and is caused by immune-mediated decreased platelet production and increased platelet destruction.

116 e insights into the mechanisms that regulate platelet production and may aid in the development of st

117 system (DMS) provides a membrane reserve for platelet production and muscle transverse (T) tubules fa

118 here are fundamental changes in the sites of platelet production and phenotypes of resultant platelet

119 nown link between hyperglycemia and enhanced platelet production and reactivity.

120 specifically stimulates megakaryopoiesis and platelet production and reduces the severity of thromboc

121 Mechanisms of platelet production and release by mammalian megakaryocy

122 The tight regulation of platelet production and removal from the blood circulati

123 Multifaceted and complex mechanisms control platelet production and removal in physiological and pat

124 ed on megakaryocyte (Mk) differentiation and platelet production and signaling.

125 biologically important for MK maturation and platelet production and support the importance of MT reg

126 thrombocytopenias due primarily to impaired platelet production and those due to acceleration of ran

127 ion preferentially activate STAT1, promoting platelet production and thrombocythemia, whereas homozyg

128 In this study, neonatal platelet production and turnover were investigated in ne

129 se observations improve our understanding of platelet production and validate the study of proplatele

130 Whether hyperglycemia promotes platelet production and whether enhanced platelet produc

131 hat the past and present have revealed about platelet production and whether mature blood platelets m

132 Inefficient platelet production and/or defective platelet function r

133 icial for ex vivo gene editing, for enhanced platelet production, and for the improved usage of cord

134 jor regulators of megakaryocyte development, platelet production, and function.

135 F on pharmacokinetics, megakaryocytopoiesis, platelet production, and platelet function were characte

136 Megakaryopoiesis, platelet production, and platelet lifespan were unpertur

137 poietic stimulation on megakaryocytopoiesis, platelet production, and platelet viability and function

138 the hemostatic response to injury, promotes platelet production, and prolongs platelet survival.

139 Megakaryocyte mass, reflected in the rate of platelet production, appears to be the major determinant

140 topoiesis, the exact mechanisms and sites of platelet production are unknown.

141 ted changes have functional consequences for platelet production, as the movement of MKs away from th

142 e marrow subjected to static or microfluidic platelet production assays had a higher capacity for pro

143 , JAK2-mutant mice and WT controls increased platelet production at the expense of erythrocytes.

144 t ABCG4, a close relative of ABCG1, controls platelet production, atherosclerosis, and thrombosis.

145 "barbell shapes" of the penultimate stage in platelet production, because addition of the tetramer-di

146 Platelet production begins with the extension of large p

147 row-derived MKs is not the only mechanism of platelet production, but that it may also occur through

148 thrombopoietin receptor agonist, stimulates platelet production by a similar mechanism to endogenous

149 oned and shown to regulate megakaryocyte and platelet production by activating the cytokine receptor

150 We hypothesized that CCL5 could regulate platelet production by binding to its receptor, CCR5, on

151 transplantation and may underlie inefficient platelet production by megakaryocytes derived from pluri

152 vers a dual role for Vps34 as a regulator of platelet production by MKs and as an unexpected regulato

153 Thus, Scl and Lyl1 share functional roles in platelet production by regulating expression of partner

154 Stimulation of platelet production by romiplostim may provide a new the

155 Stimulation of platelet production by thrombopoietin-receptor agonists

156 in platelet RNA processing, and differential platelet production by tumor-educated megakaryocytes are

157 Megakaryocytopoiesis and platelet production can be assessed with reasonable accu

158 ereas quantitative or qualitative defects in platelet production can lead to inherited platelet disor

159 t survival, and that subsequently, increased platelet production compensated for ongoing platelet des

160 tes platelet production and whether enhanced platelet production contributes to enhanced atherothromb

161 ts may open new avenues for the treatment of platelet production disorders and help to explain the th

162 lood levels of TPO in patients with impaired platelet production due to aplastic anemia (AA) and with

163 ytopenic Purpura) and decreased upon reduced platelet production due to chemotherapy-induced bone mar

164 ombopoietin (TPO) increases myeloid cell and platelet production during antibody-mediated chronic kid

165 increased in pathologies involving increased platelet production (Essential Thrombocythemia, Idiopath

166 ying impaired fetal megakaryocytopoiesis and platelet production following pregnancy complications ch

167 nt in facilitating proplatelet formation and platelet production from cultured megakaryocytes.

168 Frank with having proposed defective platelet production from megakaryocytes in ITP in 1915.

169 Platelet production from precursor cells called megakary

170 Indeed, FLNa mutations alter platelet production from their bone marrow precursors, t

171 Thrombopoietin affects nearly all aspects of platelet production, from self-renewal and expansion of

172 The role of specific molecules in platelet production has been elucidated in greater detai

173 between altered cholesterol homeostasis and platelet production has not been explored.

174 The process of platelet production has so far been understood to be a 2

175 an megakaryopoiesis, hereditary disorders of platelet production have confirmed contributions from th

176 the specific roles of these proteins during platelet production have not been established.

177 als using thrombopoietic agents to stimulate platelet production have shown favorable outcomes in ITP

178 te the transcriptional programs required for platelet production, how chromatin regulators control th

179 eutrophil-megakaryocyte interactions promote platelet production in a humanized bioreactor and myelof

180 in nonhuman primates, PEG-rHuMGDF increases platelet production in a linear log-dose-dependent manne

181 mbinant thrombopoietins (TPOs) could enhance platelet production in a variety of thrombocytopenic sta

182 dependent kinase phosphorylation and reduced platelet production in bone marrow chimeras.

183 ve been shown to be effective stimulators of platelet production in cancer patients.

184 gle dose, is a potent stimulus for prolonged platelet production in humans.

185 single intravenous dose potently stimulates platelet production in mice, challenging the need for it

186 activity that enhances megakaryopoiesis and platelet production in mice.

187 n-based membrane skeleton in proplatelet and platelet production in murine megakaryocytes.

188 ditionally was able to effectively stimulate platelet production in normal mice.

189 akaryocytopoiesis and the means to stimulate platelet production in numerous clinical situations.

190 MGDF has potent stimulatory effects on platelet production in patients with chemotherapy-induce

191 hesis that G-CSF contributes to the residual platelet production in T(-) mice.

192 d as reduced platelet counts, lower rates of platelet production in the immune model of thrombocytope

193 nd most likely only marginally contribute to platelet production in the steady state.

194 terleukin-6 (IL-6) and IL-11, did not induce platelet production in thrombocytopenic, TPO-deficient (

195 ith platelet overproduction, contributing to platelet production in vitro and in vivo.

196 ploidy of megakaryocyte progenitor cells and platelet production in vitro and in vivo.

197 Analysis of platelet production in vitro reveals that FlnA-null MKs

198 tor that stimulates megakaryocytopoiesis and platelet production in vivo and promotes the development

199 alterations in megakaryocyte development or platelet production in vivo or in colony assays.

200 ed cells provided only delayed and transient platelet production in vivo, and no CFU-MK developed in

201 e bone marrow environment, thereby enhancing platelet production in vivo.

202 stimulates megakaryocytopoiesis in vitro and platelet production in vivo.

203 to be dispensable for mouse PPF in vitro and platelet production in vivo.

204 although the eltrombopag-induced increase in platelet production in WAS/XLT is less than in ITP, eltr

205 let mass turnover, a steady-state measure of platelet production, increased fivefold (P < 10(-4)).

206 y a significant acceleration and increase of platelet production, indicating that hGH may exert a com

207 nsible for normal megakaryocyte function and platelet production is altered in MLL3/4-deficient megak

208 bout the role of miRs in normal human MK and platelet production is limited.

209 tly increased and a compensatory increase in platelet production is not effective in many patients.

210 cell levels of all lineages are reduced, and platelet production is profoundly impaired.

211 emained unsatisfactory, particularly because platelet production is rarely observed.

212 destruction, and in a significant proportion platelet production is suboptimal.

213 Platelet production is tightly regulated to avoid bleedi

214 iological effect on megakaryocytopoiesis and platelet production is unknown.

215 l myeloproliferative neoplasm with excessive platelet production, is associated with an increased ris

216 rombopoietin (TPO), the primary regulator of platelet production, is composed of an amino-terminal 15

217 being the primary physiological regulator of platelet production, it is now apparent that TPO also ac

218 gnaling in megakaryocytes is dispensable for platelet production; its key role in control of platelet

219 t CDKN2A deficiency predisposes to increased platelet production, leading to increased platelet activ

220 Platelet production, maintenance, and clearance are tigh

221 Stimulation of platelet production may be an effective treatment for th

222 el pathway by which megakaryocytopoiesis and platelet production may be regulated.

223 an important underlying cause for defects in platelet production, morphology, and function.

224 The primary physiologic regulator of platelet production, Mpl ligand, has recently been clone

225 Platelet production must be regulated to avoid spontaneo

226 Platelet production occurs after the formation of MK pro

227 ion, migration, and maturation of MKs before platelet production occurs.

228 ses) to determine the effects of stimulating platelet production on peripheral platelet concentration

229 l, accounting for approximately 50% of total platelet production or 10 million platelets per hour.

230 ormal platelet counts using drugs to promote platelet production or by interfering with mechanisms re

231 might be indicated in patients with impaired platelet production or increased platelet destruction, i

232 Platelet production, or thrombopoiesis, is a critical pr

233 ined action of Rac1 and Cdc42 is crucial for platelet production, particularly by regulating microtub

234 s a suitable therapeutic strategy to support platelet production, particularly during the early phase

235 ired for normal megakaryocyte maturation and platelet production partly because of regulation of cyto

236 DENV in modulating the megakaryopoiesis and platelet production process.

237 Both hypercholesterolemia and increased platelet production promote atherothrombosis; however, a

238 hanisms through which thrombopoietin affects platelet production provide new insights into the interp

239 umption, lifespan dependent consumption, and platelet production rate may have caused the thrombocyto

240 first such interval defining the equilibrium platelet production rate.

241 owed that newborn and adult mice had similar platelet production rates, but neonatal platelets surviv

242 esponses, but the events that lead to mature platelet production remain incompletely understood.

243 its role in MK development and regulation of platelet production remained elusive.

244 le to insufficient compensatory expansion in platelet production resulting from HIV-impaired delivery

245 ecoding the pathways of megakaryopoiesis and platelet production should help revolutionize the manage

246 rculating platelets, results from inadequate platelet production, splenic platelet sequestration, or

247 Receptors linked to granulocyte or platelet production supported complete erythroid develop

248 To more definitively substantiate that platelet production takes place in the lungs, megakaryoc

249 indirect, noncytocidal suppressive effect on platelet production, the mechanism of which is unknown.

250 on, (b) identify a new intermediate stage in platelet production, the preplatelet, (c) delineate the

251 Although microtubules are known to regulate platelet production, the underlying mechanism of proplat

252 hese results demonstrate that NO facilitates platelet production, thereby establishing the essential

253 e mechanisms regulating megakaryopoiesis and platelet production (thrombopoiesis) are still incomplet

254 limit hypercholesterolemia-driven excessive platelet production, thrombosis, and atherogenesis, as o

255 m platelets is sufficient to drive increased platelet production through MK CCR5.

256 Here we used an in vitro model of murine platelet production to investigate a potential role for

257 urther confirm the role of TrkA signaling in platelet production, TrkA deficient DAMI cells were gene

258 as MK maturation, proplatelet formation, and platelet production under in vitro conditions were unaff

259 is equally, or more, effective at promoting platelet production under these experimental conditions.

260 developmental process critical for efficient platelet production via unknown mechanisms.

261 takes place in the lungs, megakaryocyte and platelet production was accelerated in mice by phlebotom

262 The idea that platelet production was defective in ITP was superseded

263 Moreover, platelet production was impaired in MKs in which down-re

264 Platelet production was maintained and platelet autoanti

265 Until recently, platelet production was the least understood aspect of b

266 association between NO-induced apoptosis and platelet production, we exposed Meg-01 cells to S-nitros

267 hich GPIbalpha-filamin interactions regulate platelet production, we manipulated the expression level

268 ocess of intravasation facilitates efficient platelet production while maintaining the megakaryocyte

269 anding of the specific mechanisms regulating platelet production will yield strategies to treat patie

270 ed a marked stimulation of megakaryocyte and platelet production with no apparent adverse effects.

271 ion, driving a bias for megakaryopoiesis and platelet production without causing significant HSC expa

272 el PEGylated TPO mimetic peptide, stimulates platelet production without developing neutralizing anti

273 lopment of safe, small, molecules to enhance platelet production would be advantageous for the treatm