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1 eir unique dual properties (self-renewal and multipotency).
2 em cell protein to regulate self-renewal and multipotency.
3 ecipients, confirming their self renewal and multipotency.
4 ciated and conserved function in maintaining multipotency.
5 F pathway, inhibited regeneration-induced BC multipotency.
6 uished by the properties of self-renewal and multipotency.
7  the intestinal crypt and their capacity for multipotency.
8 binding without effects on cell viability or multipotency.
9 ed a clear adipogenic ability with increased multipotency.
10 Oct4 that control stem cell self renewal and multipotency.
11 rve as an important mechanism to control HSC multipotency.
12 utes of stem cells, including quiescence and multipotency.
13 nction of this class of proteins to maintain multipotency.
14 tures of stem cells, namely self-renewal and multipotency.
15 s revealed the capacity for self-renewal and multipotency.
16 s biased; the remaining progenitors maintain multipotency.
17 h possess self-renewal ability and inducible multipotency.
18 progenitors to support their maintenance and multipotency.
19 pment, not least because of their remarkable multipotency.
20 ong-term self-renewal, clonal expansion, and multipotency.
21 neage bias while preserving self-renewal and multipotency.
22 d the immortalized FAPs (iFAPs) retain their multipotency.
23 dipocytes or fibroblasts demonstrating their multipotency.
24  Keap1, altered metabolism, and limited BMSC multipotency.
25 tor p63; eliminating DeltaNp63 unleashes HBC multipotency.
26 ct to self-replication, stemness traits, and multipotency.
27 ar cells is sufficient for HBC activation to multipotency.
28 ro-effector genes in MP cells, indicative of multipotency.
29  markers CD73, CD90 and CD105, and displayed multipotency.
30 twork that underpin NS cell self-renewal and multipotency.
31 nally activate Notch in daughters to control multipotency.
32 otype that maintain replicative capacity and multipotency.
33 ignature resulting in reprogramming cells to multipotency.
34  gene, protein, and functional signatures of multipotency.
35 ially enlarging the potential for pancreatic multipotency.
36 hematopoietic stem cell (HSC) quiescence and multipotency.
37 alysis can be applied to questions regarding multipotency.
38 uclear lamina, which thereby preserved their multipotency.
39  astrocytes and oligodendrocytes, indicating multipotency.
40                         Consistent with this multipotency, a significant portion of these tumor cells
41 e migrating neural crest cells that maintain multipotency and become transcriptionally primed towards
42 ystem occurs at mitotic exit when cells lose multipotency and begin to develop stable connections tha
43 elopment, including cell fate specification, multipotency and cell migration.
44 g cardiomyocytes or endocardium, they retain multipotency and contribute to different subsets of non-
45 materials chemistry in maintaining stem-cell multipotency and controlling differentiation.
46 ed decreased senescence and maintained their multipotency and differentiation potential until passage
47 come in response to ICB, suggesting that the multipotency and differentiation status of melanoma can
48  a process associated with loss of stem cell multipotency and engraftment potential.
49  rapid downregulation of genes that maintain multipotency and establish NPCs' neural identity.
50  crest-derived progenitors for self-renewal, multipotency and establishment of multiple neural crest-
51 s and mechanisms underlying cardiopharyngeal multipotency and heart versus head muscle fate choices r
52 udy was to determine their origin, degree of multipotency and heterogeneity, and contribution to vess
53 unknown whether they contribute to oncogenic multipotency and metastasis.
54  profile of transcription factors regulating multipotency and neural crest progenitor characteristics
55 the normally quiescent HBCs are activated to multipotency and proliferate when sustentacular cells ar
56 e phenotype with self-renewability, enhanced multipotency and proliferative capacity.
57   We show that FGF-MAPK signalling maintains multipotency and promotes the pharyngeal muscle fate, wh
58         We conclude that the balance between multipotency and selective neuropotency, which is charac
59  of cell types, yet molecules controlling NC multipotency and self-renewal and factors mediating cell
60               Itm2a+ P-SSCs displayed clonal multipotency and self-renewal and sat at the apex of the
61                Hematopoietic stem cell (HSC) multipotency and self-renewal are typically defined thro
62  cell characteristics such as clonogenicity, multipotency and self-renewal capacity.
63 ty to instructive signals, while maintaining multipotency and self-renewal capacity.
64  for regenerative therapies, but maintaining multipotency and self-renewal in cultured MSCs is especi
65 BCG2 expressing side population demonstrates multipotency and self-renewal properties indicating stem
66 n GABPbeta subunit, critically regulates HSC multipotency and self-renewal via controlling an essenti
67  and Foxg1 cooperation to maintenance of NSC multipotency and self-renewal, and establish a useful me
68 nic infection and cancer through quiescence, multipotency and self-renewal, hallmarks shared with mem
69 ly progenitors is not at the expense of full multipotency and support the current model of hematopoie
70 of cells that are endowed with self-renewal, multipotency, and a unique potential for tumor initiatio
71 al stromal cells, including self-renewal and multipotency, and asporin expression by reactive stromal
72 st strike a balance between self-renewal and multipotency, and differentiation.
73                             aBMSCs exhibited multipotency, and karyotypes were normal up to 30 PDs, w
74 eneration as a result of their self-renewal, multipotency, and paracrine capabilities.
75 relates with spatial segregation, exits from multipotency, and promotes the Krt8+ lineage, whereas Kr
76 ) T cells with improved in vivo persistence, multipotency, and tumor clearance.
77 ers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity following injection in
78             The deficits in self-renewal and multipotency are restored by expression of Notch1-ICD or
79      The hallmarks of HSCs, self-renewal and multipotency, are observed in in vitro assays and cell t
80 e TICs possess stem cell characteristics and multipotency as demonstrated by in vitro sphere-formatio
81                   They also maintained their multipotency, as evidenced by their ability to different
82 n in the absence of cell division, and their multipotency at the population level reflects collective
83 ted to provide a cellular memory to maintain multipotency but also stabilize cell fate decisions and
84                              NCDPs displayed multipotency by differentiating into microtubule-associa
85 tes hematopoietic stem cell self-renewal and multipotency by limiting stem cell proliferation and dif
86 at neural potential can be separated from NC multipotency by the action of a single gene, and establi
87  its ability to restore the self-renewal and multipotency defects of Ars2 knockout NSCs.
88 ic programs compatible with self-renewal and multipotency downstream of the HSC.
89 with as few as 200 cells, self-renewability, multipotency, drug resistance, metastatic potential, and
90 iscent of the genetic program that regulates multipotency during embryonic development(7).
91 fied in C. elegans, underlie progenitor cell multipotency during the development of diverse bilateria
92  occurring in human breast cancer, to induce multipotency during tumorigenesis in the mammary gland.
93 stabilizes lineage choice by suppressing the multipotency encoded in the genome via its interaction w
94 r signatures characterising pluripotency and multipotency exist, there is, as yet, no single quantita
95                                          The multipotency factor SOX2 was decreased during nitric oxi
96 ion (PDL) caused facultative reactivation of multipotency factors (Sox9 and Hnf1beta) in Ptf1a(+) aci
97 pressing the cell cycle and regulating other multipotency factors such as vasa.
98 eases the pool of PSCs, impairs their clonal multipotency for differentiation into osteoblasts and ch
99 -cell level, that self-renew without loss of multipotency for more than 140 population doublings and
100              Dnmt3a-null HSCs upregulate HSC multipotency genes and downregulate differentiation fact
101 F1 deficiency also reduced the expression of multipotency genes, including Slamf1, Mecom, Hoxa9, Hlf,
102          Furthermore, the cohort of germline multipotency genes, which are considered canonical neobl
103 possess stem cell characteristics, including multipotency, high proliferative potential, and their ca
104 sion is closely associated with pluripotency/multipotency in both mouse and human embryonic stem cell
105 m type I collagen-lineage cells and acquired multipotency in culture.
106  description of strategies that help promote multipotency in MSCs will be vital to future clinical us
107 t bidirectional Notch signaling may regulate multipotency in other systems.
108 lude that the acquisition and maintenance of multipotency in the small micromere lineage requires nan
109          Single-cell CITE-seq indicated that multipotency in the TdT(+) MPPs is associated with expre
110                              To assess their multipotency in vivo, periosteal cells were injected int
111 opulation-doubling rate, cell proliferation, multipotency, in vivo dentin regeneration, and immunosup
112 eterogeneous cells that expressed markers of multipotency, including Sox2, Sca1, and Rex1 (Zfp42).
113 MSCs to retain their stem-cell phenotype and multipotency, independent of differentiation-promoting m
114 d document the use of this methylation-based multipotency index for investigating human and mouse CD8
115 ysis and comparison to a CD8(+) T cell-based multipotency index showed that Tregs naturally exist in
116  established a DNA methylation-based T cell 'multipotency index' and found that beta cell-specific CD
117 r culture conditions favoring maintenance of multipotency, infection caused NPCs to quickly and abnor
118  GBC is a multipotent progenitor cell, whose multipotency is activated after destruction of both neur
119 and Ldb2, and promotes RPC proliferation and multipotency; it also controls specification of mammalia
120 l zone transcribe genes associated with both multipotency maintenance and neural differentiation, but
121 ss-repression and display unique features of multipotency (more open chromatin, complex gene regulato
122 y of cell behavior and identity owing to its multipotency, motility and ability to form a broad array
123 tion during embryonic development due to its multipotency, motility, and ability to form a broad arra
124                                Despite their multipotency, MPPs display poorly understood lineage bia
125 oth TSCM subpopulations exhibit considerable multipotency, no single population of TSCM cells has bot
126 f et al. (2014) demonstrate self-renewal and multipotency of a single CD62L(+) memory T cell across s
127 DNA-binding) genes maintain self-renewal and multipotency of adult neural stem cells.
128 , we evaluate evidence for the existence and multipotency of axial stem cells.
129 how that the ablation of LCs reactivates the multipotency of BSCs from multiple epithelia both in viv
130 ely dependent on the ability to maintain the multipotency of cells and control their differentiation.
131 generation immunotherapies by preserving the multipotency of effector cells rather than enhancing the
132  is the full manifestation of the pluri- and multipotency of embryonic and adult stem cells, thus the
133 are orchestrated to regulate maintenance and multipotency of HSCs.
134 e, we investigated self-renewal capacity and multipotency of individual memory lymphocytes by in vivo
135          In this way, Mbd3/NuRD protects the multipotency of lymphoid progenitors, preventing B cell-
136  Our results suggest that MBD1 maintains the multipotency of NSCs by restraining the onset of differe
137                 Our results suggest that the multipotency of progenitor cells is defined by the exist
138 VPCs) offer a paradigm for investigating how multipotency of progenitor cells is maintained during pe
139  as floating cultures, thereby revealing the multipotency of RPCs generated from integration-free hiP
140                              Considering the multipotency of SCPs in development, we suggest that the
141                          Our findings reveal multipotency of SCPs, providing a developmental link bet
142 e mechanisms that establish and maintain the multipotency of stem cells are poorly understood.
143 into how epigenetic regulation preserves the multipotency of stem cells for subsequent differentiatio
144 esolution and demonstrated clonogenicity and multipotency of the Gli1-expressing progenitors.
145 ated from human PPE cells, demonstrating the multipotency of the human ES-derived PPE cells.
146                              We suggest that multipotency of the nerve-associated progenitors lasting
147                                              Multipotency of these cells was demonstrated by their ca
148                                              Multipotency of these cells was demonstrated by their ca
149 fication of surfaces that allow retention of multipotency of this key regenerative cell type have rem
150  demonstrated the proliferative capacity and multipotency of this population.
151     Furthermore, reconstitution activity and multipotency of UM171-treated HSCs are specifically comp
152  reprogramming-like event that preserves the multipotency of vulval precursor cells (VPCs), allowing
153 is little definitive information about their multipotency or extent of contribution to the axis.
154  lineage tracing, allowing the definition of multipotency potential to be achieved with high confiden
155 lies the existence of an underlying germline multipotency program in these cell types that has a prev
156 monstrate that this epigenetically regulated multipotency program is firmly coupled to the clinical o
157 that are hallmark characters of the germline multipotency program.
158  signals organize epigenetic marks to confer multipotency remain to be uncovered.
159 an aortic endothelial cells in vitro acquire multipotency rendering the cells susceptible to osteoind
160 avior including self-renewal, expansion, and multipotency, resulting in the eradication of large meta
161 8(+) T cells retained a stem-like epigenetic multipotency score.
162               Stemness, as "self-renewal and multipotency," seems not to be limited to a particular c
163 he key properties of a stem cell population: multipotency, self-renewal and clonal longevity.
164 multiple histologic phenotypes indicative of multipotency suggests a stem cell-like etiology of ovari
165 arked by cytokeratin K14 and Axin2 undergo a multipotency switch, they do not make a significant cont
166                          They exhibit clonal multipotency that can give rise to myogenic, melanocytic
167 hysical property robustly predicts stem cell multipotency, there exists a unique and minimal set of t
168 ect reprogramming to maintain or reestablish multipotency; they acquire an active block to signal tra
169 as a stem cell niche to maintain prohemocyte multipotency through Hedgehog and JAK/STAT signaling.
170 ization that neural crest cells retain broad multipotency throughout migration and even in post-migra
171 ld be expanded extensively while maintaining multipotency to differentiate into cardiomyocytes, smoot
172   Adipose-derived stem cells (ADSCs) possess multipotency to differentiate into various lineages, inc
173 e time and place in which cells transit from multipotency to one of several differentiated lineages.
174 s, we show that only some progenitors regain multipotency to produce de novo ductal and glandular str
175 th the ability of long-term self-renewal and multipotency to reconstitute all blood lineages.
176 ch T cell precursors progress from primitive multipotency to T lineage commitment.
177 s successfully negotiate the transition from multipotency to unipotency, including the loss of self-r
178 activities, promoting cell proliferation and multipotency under maintenance conditions and osteogenes
179 gests that an active mechanism restricts BSC multipotency under normal physiological conditions, alth
180 at TNF-which is secreted by LCs-restricts BC multipotency under normal physiological conditions.
181 However, adult unipotent BSCs can reactivate multipotency under regenerative conditions and upon onco
182                      Here we investigated MG multipotency using injury paradigms that target differen
183 rity was assessed by flow cytometry and TMSC multipotency was examined by induction of neural cells,
184                                              Multipotency was required for Th17 cell-mediated tumor e
185                                              Multipotency was verified via further differentiation to
186 izing a transient radiation-induced state of multipotency, we used the adenylcyclase activator forsko
187   Neural stem cells proliferate and maintain multipotency when cultured in the presence of FGF2, but
188                  Some of these cells exhibit multipotency, whereas others do not.
189 othesises that migrating cells maintain full multipotency, whilst progressive fate restriction envisa

 
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