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1 cells of specific daughter lineages (such as megakaryocytes).
2 therefore differentiation of stem cells into megakaryocytes.
3 pathway that has a low activity in polyploid megakaryocytes.
4 sive DNA methylation differences in maturing megakaryocytes.
5 rmation of multiple poles typically found in megakaryocytes.
6 ed by large polyploid precursor cells called megakaryocytes.
7 in synthesized in both endothelial cells and megakaryocytes.
8 re that are associated with modifications in megakaryocytes.
9 ion, and cytoskeletal dynamics in developing megakaryocytes.
10 bule sliding and proplatelet elongation from megakaryocytes.
11 ng in differentiation into erythroblasts and megakaryocytes.
12 erentiate into functional platelet-producing megakaryocytes.
13 a high level of protein expression in human megakaryocytes.
14 n and correction of surface alphaIIbbeta3 in megakaryocytes.
15 cks proplatelet formation in human and mouse megakaryocytes.
16 n significant amounts of TFPI-2 derived from megakaryocytes.
17 ecursors to differentiated erythroblasts and megakaryocytes.
18 take/storage of Fg in platelets and cultured megakaryocytes.
19 spleen, resulting in a four-fold increase in megakaryocytes.
20 lar features of adult-type cells on neonatal megakaryocytes.
21 ion also elicited adult features in neonatal megakaryocytes.
22 and progenitor cells (HSPCs) into functional megakaryocytes.
23 GATA1 effectively rescued maturation of PMF megakaryocytes.
24 s are physically proximal to Nbeal2 in human megakaryocytes.
25 timately lead to the production of polyploid megakaryocytes.
26 of the DMS from the surface membrane in rat megakaryocytes.
27 pon differentiation of HEL cells to adherent megakaryocytes.
28 s total cells 99-fold, erythrocytes 70-fold, megakaryocytes 0.5-fold, and CD34(+) stem/progenitor cel
29 plicated a platelet-independent role for the megakaryocyte, a Kit-dependent lineage that is selective
31 , we explored the functional implications of megakaryocyte accumulation in the femurs of mice after i
32 dentified populations of mature and immature megakaryocytes along with haematopoietic progenitors in
33 as normal, whereas we observed deficiency of megakaryocyte alpha-granule proteins and emperipolesis.
37 sability of proper chromosome segregation in megakaryocytes, an endomitotic SAC is activated in these
40 interacts with its cognate receptor c-MPL on megakaryocytes and bone marrow progenitor cells to promo
41 ctivation results in defective maturation of megakaryocytes and cell death, thus raising a note of ca
44 or GATA-1 generated mast cells, eosinophils, megakaryocytes and erythroid cells, and a pathway lackin
45 that have a higher basal RhoA activity than megakaryocytes and express both NMIIA and NMIIB at the c
46 with increased and morphologically abnormal megakaryocytes and increased numbers of phenotypically d
48 nally, iHPs generate acetylcholinesterase(+) megakaryocytes and phagocytic myeloid cells in vitro and
49 will focus on our understanding of committed megakaryocytes and platelet release in vivo and in vitro
50 rated mice selectively lacking Galpha(i2) in megakaryocytes and platelets (Gna(i2)(fl/fl)/PF4-Cre mic
51 transgenic mice expressing LOX in wild-type megakaryocytes and platelets (Pf4-Lox(tg/tg)) were gener
52 nt cellular composition, size, and function, megakaryocytes and platelets both depend on restraint of
53 (iPS) cells represent a potential source of megakaryocytes and platelets for transfusion therapies;
55 e stem cells for the efficient derivation of megakaryocytes and platelets have played a role in uncov
57 e may primarily reflect changes occurring in megakaryocytes and platelets, including the ability of t
63 nce mitochondrial biogenesis and activity in megakaryocytes and preserve mitochondrial functions in p
64 e that circRNAs are not enriched in cultured megakaryocytes, and demonstrate that linear RNAs decay m
65 evels by c-kit(+) hematopoietic progenitors, megakaryocytes, and Leptin Receptor(+) (LepR(+)) stromal
66 ncreased basal and thrombopoietin-stimulated megakaryocyte antigen expression, as well as basal level
67 atelets released by intrapulmonary-entrapped megakaryocytes appear more physiologic in nature and nea
70 shear, plateletlike particles generated from megakaryocytes are maximized at a shear stress typical o
72 ecursors, and an elevation of mature CD41(+) megakaryocytes, as well as an increased number of polypl
73 monstrate a novel approach to studying human megakaryocyte biology as well as functional correction o
75 nvolving these TFs affect diverse aspects of megakaryocyte biology, and platelet production and funct
78 imura et al. show that platelet release from megakaryocytes can be induced by interleukin-1alpha (IL-
79 th GLP-1 receptor (GLP-1R) mRNA from a human megakaryocyte cell line (MEG-01), and found expression l
80 asses of assayable HPCs (colony-forming unit-megakaryocyte [CFU-MK], CFU-granulocyte/macrophage, burs
81 tion in mice, we show that a large number of megakaryocytes circulate through the lungs, where they d
82 differences: platelets derived from infused megakaryocytes closely resembled infused donor platelets
83 it-erythroid and reduced colony-forming unit-megakaryocyte colony formation driven by JAK2-V617F, but
85 hrombocytosis with a remarkable expansion of megakaryocyte-committed and multipotential progenitor ce
86 em cell (HSC) compartment contains stem-like megakaryocyte-committed progenitors (SL-MkPs), a cell po
87 and impaired differentiation were limited to megakaryocytes, consistent with a proproliferative effec
88 e, in contrast to other cell types examined, megakaryocytes continued DNA synthesis after loss of Aur
89 , recent advances in genetic manipulation of megakaryocytes could lead to new and improved therapies
95 g the internal membrane reserve structure of megakaryocytes (demarcation membrane system) and platele
98 crovessels close to these cells, and because megakaryocyte-derived supernatant fluid can reproduce th
100 human ontogenic master switch that restricts megakaryocyte development by modulating a lineage-specif
101 its requirement in normal hematopoiesis and megakaryocyte development has not been extensively chara
103 a GFI1B isoform that preferentially promotes megakaryocyte differentiation and platelet production.
105 a critical transcription factor (TF) during megakaryocyte differentiation, is among genes hemizygous
106 To clarify the cellular pathway in erythro-megakaryocyte differentiation, we correlate the surface
108 rric chloride injury and are attenuated with megakaryocyte-directed deletion of the cyclophilin D gen
109 ls with biased megakaryocyte potential, with megakaryocytes directly arising from HSCs under steady-s
111 esulted in age-dependent progressive anemia, megakaryocyte dysplasia and loss of hematopoietic stem c
112 ased slowly over 7 days, and originated from megakaryocyte endocytosis and intracellular processing o
114 supports a growing body of evidence that the megakaryocyte endomitotic cell cycle differs significant
115 asts, LepR+ cells, Nes-cre-expressing cells, megakaryocytes, endothelial cells or hematopoietic cells
117 uently, within the myeloid lineage, bipotent megakaryocyte-erythrocyte and granulocyte-macrophage pro
119 cell types, focusing on trajectories toward megakaryocyte-erythrocyte progenitors and lymphoid-prime
121 ly preleukemic expansion of a phenotypic pre-megakaryocyte/erythrocyte (Pre-Meg/E) progenitor populat
122 and CD71 within the previously defined human megakaryocyte/erythrocyte progenitor (hMEP; Lineage(-) C
123 ficient AML was characterized by an expanded megakaryocyte erythroid progenitor population that was a
124 itor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progenitor (MEP), and granulocyt
125 s differentiate from a shared precursor, the megakaryocyte-erythroid progenitor (MEP), which remains
126 ing cells, and, to a greater extent, CMP and megakaryocyte-erythroid progenitor development, and red
128 elopmentally arrested GATA1-deficient murine megakaryocyte-erythroid progenitors derived from murine
129 me granulocyte-macrophage progenitors and as megakaryocyte-erythroid progenitors differentiated to bo
130 tegy to exponentially expand ES cell-derived megakaryocyte-erythroid progenitors that have the capaci
131 dy clarifies the cellular hierarchy in human megakaryocyte/erythroid lineage commitment and highlight
134 ures, can differentiate into erythrocytes or megakaryocytes, exhibits very little expansion capacity,
138 t, the opposite changes in Rcor1/3 levels in megakaryocytes favor differentiation and likely maintain
139 the pathway contributes to the clearance of megakaryocytes following platelet shedding and constrain
140 The demarcation membrane system (DMS) in megakaryocytes forms the plasma membrane (PM) of future
141 These results demonstrate that cultured megakaryocytes from GPS patients provide a valuable mode
142 We report the first analysis of cultured megakaryocytes from GPS patients with NBEAL2 mutations.
148 stromal cells in the bone marrow: promoting megakaryocyte growth and proplatelet formation by intera
153 induced-pluripotent stem cell (iPSC)-derived megakaryocytes (iMegs) to better understand these clinic
155 ow that genomic abnormalities are present in megakaryocytes in MPNs and that these appear to be assoc
157 inical specimens, we observed an increase in megakaryocytes in the bone marrow of 6/8 patients with m
159 By contrast, BDNF is undetectable in mouse megakaryocytes, in line with the absence of BDNF in mous
160 ed myeloid:erythroid ratio of 5:1, increased megakaryocytes including micromegakaryocytes in the abse
161 Wang et al report that ex vivo-derived human megakaryocytes infused into mice are trapped in the pulm
162 We showed that ex vivo-generated murine megakaryocytes infused into mice release platelets withi
163 iche may have been created by relocating the megakaryocytes into the spleen, thereby allowing normal
165 purpura (ITP), production of platelets from megakaryocytes is defective, even while marrow megakaryo
166 m localization; thus, cytokinesis failure in megakaryocytes is the consequence of both the absence of
167 0 genes associated with myeloid neoplasms on megakaryocytes isolated from aspirated bone marrow.
170 re restricted, being highly expressed in the megakaryocyte lineage but downregulated during erythropo
171 mice with selective p110beta deletion in the megakaryocyte lineage is thrombus instability at a high
174 e previously shown that SRF is essential for megakaryocyte maturation and platelet formation and func
177 s Aurora kinases or Cdk1 are dispensable for megakaryocyte maturation, and inhibition of mitotic kina
178 Genetic ablation of miR-142 caused impaired megakaryocyte maturation, inhibition of polyploidization
179 we identify Pak2 as an essential effector of megakaryocyte maturation, polyploidization, and proplate
184 In support of the hypothesis that reducing megakaryocytes may reduce metastasis, we found that thro
186 occur during development of primary cultured megakaryocytes (MEG) and primary erythroblasts (ERY) fro
187 t in vitro, still retained bipotency for the megakaryocyte (MegK) and erythrocyte (E) lineages, altho
188 s such as the bone marrow; we observed large megakaryocytes migrating out of the bone marrow space.
190 onstrate that from embryonic day (E) 8.5 all megakaryocyte (MK) colony-forming cells belong to the co
191 ar membrane invaginations reminiscent of the megakaryocyte (MK) demarcation membrane system (DMS), wh
195 myeloproliferative neoplasm characterized by megakaryocyte (MK) hyperplasia, bone marrow fibrosis, an
198 in primary maturing mammalian erythroid and megakaryocyte (MK) lineages as well as their common prog
203 ontent of organelles is transported from the megakaryocyte (MK) to the nascent platelets along microt
208 ion, the mechanisms controlling [Mg(2+)]i in megakaryocytes (MKs) and platelets are largely unknown.
209 ass III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs) and platelets, we created a mouse m
211 telet-forming cells of the conceptus are not megakaryocytes (MKs) but diploid platelet-forming cells
215 where low MPL levels on platelets and mature megakaryocytes (MKs) lead to high serum THPO levels, whe
216 act of Jak2 deletion in platelets (PLTs) and megakaryocytes (MKs) on blood counts, stem/progenitor ce
217 lear cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity b
220 s is due to their loss from platelets/mature megakaryocytes (MKs), and not by initial impaired format
221 only Tmod isoform detected in platelets and megakaryocytes (MKs), caps actin filament (F-actin) poin
222 d by large bone marrow (BM) precursor cells, megakaryocytes (MKs), which extend cytoplasmic protrusio
229 understanding of the complex processes that megakaryocytes must undergo to generate platelets both i
230 d not yet fully understood interaction among megakaryocytes, myeloid cells, fibroblasts, and endothel
231 d electron microscopy and show that although megakaryocyte numbers are normal in bone marrow and sple
232 r, our results suggested that an increase in megakaryocytes occurring in response to metastatic cells
234 1(+/-) iMegs replicate many of the described megakaryocyte/platelet features, including a decrease in
236 g a murine MPS I model, we demonstrated that megakaryocyte/platelets were capable of producing, packa
242 t HSCs contain a subset of cells with biased megakaryocyte potential, with megakaryocytes directly ar
243 ntified a CID-dependent bipotent erythrocyte-megakaryocyte precursor (PEM) population, and a CID-inde
244 heme has been challenged, with the origin of megakaryocyte precursors being one of the most debated s
245 yocyte ultrastructure, increased bone marrow megakaryocyte precursors, and an elevation of mature CD4
248 ripotent stem cells to generate immortalized megakaryocyte progenitor cell lines that can be cryopres
249 ntegrity and stability of mRNAs derived from megakaryocyte progenitor cells remain poorly quantified
251 pulations: "Pre-MEP," enriched for erythroid/megakaryocyte progenitors but with residual myeloid diff
257 tion, SL-MkPs become activated, resulting in megakaryocyte protein production from pre-existing trans
258 epletion of GNB1 (encoding Gbeta1) in murine megakaryocytes reduced protease-activated receptor 4, ac
262 ufficient TPM4 expression in human and mouse megakaryocytes resulted in a defect in the terminal stag
263 ndomitosis, and ablation of the Plk1 gene in megakaryocytes results in defective polyploidization acc
265 curs in a cell-autonomous manner as shown by megakaryocyte-specific (Pf4-Cre) double-knockout mice.
266 s similar to those noted with other critical megakaryocyte-specific TFs; however, unlike those TFs, F
267 erythroid-specific genes are upregulated and megakaryocyte-specific transcripts are downregulated.
271 n of proliferating, developmentally arrested megakaryocytes, suggesting that GATA1 suppression in ES
272 s with PMF contain large numbers of atypical megakaryocytes that are postulated to contribute to fibr
273 are anucleate cytoplasmic discs derived from megakaryocytes that circulate in the blood and have majo
275 en of the 12 patients had genomic defects in megakaryocytes that were not present in nonmegakaryocyti
276 aluronan within their bone marrow and within megakaryocytes, the cells responsible for platelet gener
277 haematopoietic progenitor cells give rise to megakaryocytes, the giant bone marrow cells that in turn
279 latelets, we established primary cultures of megakaryocytes, the progenitors of platelets, and we fou
280 s and establish an unanticipated capacity of megakaryocytes to mediate IL-1-driven systemic inflammat
284 sociated with macrothrombocytopenia, altered megakaryocyte ultrastructure, increased bone marrow mega
287 Proplatelet formation by Hyal-2 knockout megakaryocytes was disrupted because of abnormal formati
289 demonstrated that platelet formation by GPS megakaryocytes was severely affected, a defect which mig
293 therapy because they can differentiate into megakaryocytes which are capable of forming several thou
294 re red blood cells; increased and persistent megakaryocytes which release high levels of platelets fo
295 nd BM of patients harbor atypical, clustered megakaryocytes, which contribute to the disease by secre
297 oted polyploidization and differentiation of megakaryocytes with PMF-associated mutations and had pot
298 ve the capacity to differentiate into mature megakaryocytes with the ability to produce functional pl
299 tiated HEL cells and those differentiated to megakaryocytes, with a shift to more N-linked sialoglyco
300 nt mice exhibited a 90% relative decrease in megakaryocytes, yet they developed more aggressive metas
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