戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 enerative proliferation, growth and regulate cellular plasticity.
2 cordingly, modulation of I(H) contributes to cellular plasticity.
3 nd may aid in identifying genes required for cellular plasticity.
4 s proposed to be important in the control of cellular plasticity.
5 her maternal cells transferred in utero have cellular plasticity.
6 flects aberrant neurodevelopment or impaired cellular plasticity.
7 ions of a single master regulator can induce cellular plasticity.
8 deling the cis-regulatory network underlying cellular plasticity.
9 transition (MET) are genetic determinants of cellular plasticity.
10 ivity of primary EnSC, indicative of loss of cellular plasticity.
11  discrete cellular populations with enhanced cellular plasticity.
12 asingly common clinical feature arising from cellular plasticity.
13 ring the circadian cycle as a cornerstone of cellular plasticity.
14 evant to neuroregeneration, and synaptic and cellular plasticity.
15 eny and heterogeneity, as well as functional cellular plasticity.
16  progenitor-like cells (NPC-like) that drive cellular plasticity.
17 ept may apply to other contexts of transient cellular plasticity.
18 assessing (A) agonism, (B) behavior, and (C) cellular plasticity.
19 c elements to finely tune activity-dependent cellular plasticity.
20  that affect cell fate decisions by altering cellular plasticity.
21 ance, other sources of variation result from cellular plasticity.
22 future enhancer and contribute to macrophage cellular plasticity.
23 f development, epigenetic reprogramming, and cellular plasticity.
24 ipocytes were growth-arrested and lost their cellular plasticity.
25 re extremely poor prognosis, may result from cellular plasticity.
26 ty is usually paralleled by a restriction of cellular plasticity.
27 se principles may apply to other contexts of cellular plasticity.
28 e identity specification with restriction of cellular plasticity.
29 atteries but also control the restriction of cellular plasticity.
30 oliferative two-step process while retaining cellular plasticity.
31 about the molecular basis of their intrinsic cellular plasticity.
32 on (EMT) is a dynamic process that relies on cellular plasticity.
33 rder to be successful, require extraordinary cellular plasticity.
34 ypomethylated sites, enhancer formation, and cellular plasticity.
35  SMAD signaling, which is a key regulator of cellular plasticity.
36 ators, including Fosl2, a key determinant of cellular plasticity.
37 thelial-mesenchymal-transition, stemness and cellular-plasticity.
38 tasis, particularly in tissues with inherent cellular plasticity(5).
39 EMT) is known to play roles in orchestrating cellular plasticity across many physiological and pathol
40                               This extensive cellular plasticity acts as a key mechanism to respond t
41 oss of secretory cells, however, may involve cellular plasticity, although the mechanism and extent o
42 n cells can, through contact guidance, alter cellular plasticity and accelerate the regeneration of c
43 vior, but the molecular substrates mediating cellular plasticity and activity in MSN subtypes in stre
44 uld facilitate the discovery of the basis of cellular plasticity and aid in the targeted programming
45 phila mushroom body neurons is necessary for cellular plasticity and associative memory formation.
46 in, inhibited ectopic transcription, limited cellular plasticity and caused multi-organ autoimmunity.
47                                              Cellular plasticity and de-differentiation are hallmarks
48 ular nucleotides to the development, growth, cellular plasticity and death of neural cells and the me
49 s emerging evidence that tumor cells exploit cellular plasticity and dedifferentiation programs to av
50 new insights into developmental hierarchies, cellular plasticity and diverse tissue microenvironments
51 on and development, which promotes increased cellular plasticity and enrichment of alternative cell f
52 d coculture models to investigate how innate cellular plasticity and external mesenchymal signals inf
53 ation resulting from genetic lesions unleash cellular plasticity and favor oncogenic cellular reprogr
54  LPC lines provide novel tools for models of cellular plasticity and hepatocarcinogenesis, as well as
55 tigating the molecular mechanisms underlying cellular plasticity and human neurodegenerative diseases
56                       Coordinated changes of cellular plasticity and identity are critical for plurip
57 des insights into the partitioned control of cellular plasticity and identity for both regenerative a
58 human atherosclerotic plaques and highlights cellular plasticity and intercellular communication at t
59 GFbeta-dependent regulatory loops conferring cellular plasticity and invasive behavior.
60 enhanced excitability is a characteristic of cellular plasticity and learning-dependent modifications
61 er cells via a mechanism involving increased cellular plasticity and lineage switching.
62 egulators of EMT, play a crucial role in the cellular plasticity and maintenance of the mesenchymal a
63 oles for TLR3 as a suppressor of hippocampal cellular plasticity and memory retention.
64 cogenic context-dependent manner can enhance cellular plasticity and motility, in part by using trans
65 stablishing the causal relationships between cellular plasticity and motor adaptation has remained a
66 gest noise has a crucial role in maintaining cellular plasticity and organizing the blastocyst.
67 unravels some of the molecular mechanisms of cellular plasticity and reprogramming, and demonstrates
68  glucocorticoids and chronic stress regulate cellular plasticity and resilience and to inform the fut
69 ducible ISCs, extending our understanding of cellular plasticity and stemness.
70  addressed the role of RIM1alpha in aberrant cellular plasticity and structural reorganization after
71   Our data suggest that fork speed regulates cellular plasticity and that remodeling of replication f
72 tional repression of Nestin by p53 restricts cellular plasticity and tumorigenesis in liver cancer.
73 r the control of gene expression regulation, cellular plasticity, and behavior.
74 ts significant intra-tumoural heterogeneity, cellular plasticity, and complex TME, appreciating and u
75 lex interactions between signaling programs, cellular plasticity, and immune programs that characteri
76 ctor implicated in epigenetic reprogramming, cellular plasticity, and rapid growth as well as tumorig
77 These findings demonstrate that REPs possess cellular plasticity, and suggest that the phenotypic tra
78        During therapy, adaptations driven by cellular plasticity are partly responsible for driving t
79 onstrated appearance of de novo CSCs through cellular plasticity at a multicellular stage.
80 eractions between the cerebellar circuit and cellular plasticity at different sites.
81 elements underlying synaptic integration and cellular plasticity, but many features of these importan
82 y, these findings suggest that TAK1 supports cellular plasticity by suppressing spontaneous PCD activ
83 -independent mitophagy, also participates in cellular plasticity by sustaining oxidative bioenergetic
84         Our results indicate that modulating cellular plasticity can alter cell fate decisions and ma
85 circuit-specific, drug-induced molecular and cellular plasticity can have distributed effects on the
86 nal studies reveal that tumor initiation and cellular plasticity can initiate from multiple lineage s
87 IN and provides mechanistic insight into how cellular plasticity can lead to genomic changes that dri
88 P proteins are involved in the regulation of cellular plasticity cells and melanoma drug resistance a
89 dington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast "land
90 ll number of observations, while reproducing cellular plasticity commonly observed during development
91 that adult fish osteoblasts display elevated cellular plasticity compared with mammalian bone-forming
92 ion, cancer cells are endowed with increased cellular plasticity compared with their normal counterpa
93             The role of Chi3l1 in regulating cellular plasticity confers a targetable vulnerability t
94                  Intrinsic heterogeneity and cellular plasticity contribute to its rapid progression
95                                              Cellular plasticity contributes to intra-tumoral heterog
96                                              Cellular plasticity contributes to intratumoral heteroge
97                                              Cellular plasticity contributes to the regenerative capa
98 ors, PKA, and PKC is a flexible mechanism of cellular plasticity controlling the firing behavior of c
99 rtate (NMDA) receptors mediate mechanisms of cellular plasticity critical for spatial learning in rat
100 -associated ribosome biogenesis program with cellular plasticity, de-differentiation, cancer progress
101                                              Cellular plasticity describes the ability of cells to tr
102 tween microenvironment, genetic lesions, and cellular plasticity drives the metastatic cascade and re
103 icate interplay between clonal evolution and cellular plasticity driving metastatic seeding and point
104                                              Cellular plasticity during cancer metastasis is a major
105 ants are essential players in the control of cellular plasticity during development and in the adult
106  development share many properties including cellular plasticity, dynamic cell motility, and integral
107 esponse to ENR, there are lasting effects on cellular plasticity even after the discontinuation of EN
108     Here, we show that reduced levels of the cellular plasticity factor ZEB1 in macrophages increase
109 pus, fate specification may act as a form of cellular plasticity for adapting to environmental change
110 lity that young mice might retain sufficient cellular plasticity for mitotic hair cell regeneration.
111          We also discuss the implications of cellular plasticity for regenerative medicine and for ca
112         These data suggest a higher level of cellular plasticity for the intact spinal cord than has
113                                              Cellular 'plasticity' further enables cells to alter the
114               Intratumoral heterogeneity and cellular plasticity have emerged as hallmarks of cancer,
115 and provide a potential strategy to modulate cellular plasticity in a regenerative setting.
116                                              Cellular plasticity in adult multicellular organisms is
117                                              Cellular plasticity in adult organs is involved in both
118                     While the acquisition of cellular plasticity in adult stem cells is essential for
119 uscle is among the most striking examples of cellular plasticity in animal tissue development, and wh
120 nd the part played by chromatin structure in cellular plasticity in both development and cancer.
121 , network entropy predicts a higher level of cellular plasticity in cancer stem cell populations comp
122  a model in which the epigenome can modulate cellular plasticity in development and disease by regula
123 ification that regulates gene expression and cellular plasticity in development and disease.
124 ent reprogramming factors that can stimulate cellular plasticity in differentiated cells; however, th
125 t RNAs provide a mechanism for modulation of cellular plasticity in diverse cell types in the PDAC mi
126 monstrates that DNA methylation is a mark of cellular plasticity in HSCs.
127 c injury creates an environment that induces cellular plasticity in human organs, and understanding t
128  as some glial cells, providing evidence for cellular plasticity in individual cell types.
129 nvestigate the causes underlying the lack of cellular plasticity in mammalian cells, we examined the
130         Environmental cues profoundly affect cellular plasticity in multicellular organisms.
131 ovo formation of acini involves induction of cellular plasticity in multiple non-acinar cell populati
132                                   Functional cellular plasticity in neurons from the medial prefronta
133 pon injury adult tissues can exhibit massive cellular plasticity in order to achieve proper tissue re
134 t that XIST loss leads to CSC enrichment and cellular plasticity in ovarian cancer, pointing to poten
135 s study identifies SRRM3 as a key inducer of cellular plasticity in prostate cancer with neuroendocri
136 st Keystone Symposium devoted exclusively to cellular plasticity in regeneration and tumorigenesis wa
137 iscuss potential therapeutic implications of cellular plasticity in regenerative medicine and cancer.
138  to identify transcriptional fingerprints of cellular plasticity in response to altered GABAergic inh
139  Identification of the mechanisms underlying cellular plasticity in salamander cells is important bec
140 y shows rare cell heterogeneity and confirms cellular plasticity in SCLC providing a valuable resourc
141                                        Thus, cellular plasticity in seeds protects against perturbati
142                               In this review cellular plasticity in the adult liver and stomach will
143 s and better understanding the mechanisms of cellular plasticity in the adult salivary gland, such st
144  provide evidence for a remarkable degree of cellular plasticity in the aged human retina.
145 olecular mechanism underlying behavioral and cellular plasticity in the brain following cocaine self-
146 lysine acetyltransferase (KAT) enzymes drive cellular plasticity in the context of somatic cell repro
147 this review, we will discuss the evidence on cellular plasticity in the liver, focusing our attention
148 e overturned dogma, provoked reevaluation of cellular plasticity in the mature brain and raised hopes
149 nAChR-mediated fast synaptic transmission to cellular plasticity in the neural circuits underlying ol
150  population, highlighting the criticality of cellular plasticity in therapeutic response.
151 n the mouse embryo has underscored important cellular plasticity in this embryonic territory(6).
152             Phenotype switching is a form of cellular plasticity in which cancer cells reversibly mov
153 chanistically, we found that Atoh8 restrains cellular plasticity, independent of cellular identity, b
154 rtuins as key mediators of the molecular and cellular plasticity induced by drugs of abuse in NAc, an
155 the mechanotransduction pathways controlling cellular plasticity, inflammation, and, ultimately, vess
156 transition (EMT), a biological phenomenon of cellular plasticity initially reported in embryonic deve
157 y which adult ductal-committed cells acquire cellular plasticity, initiate organoids and regenerate t
158                     Silencing KRCC1 inhibits cellular plasticity, invasive properties, and potentiate
159 eneration, representing the remarkable plant cellular plasticity, involves reconstitution of stem cel
160                                              Cellular plasticity is a key facet of cellular homeostas
161                                              Cellular plasticity is a principal feature of vertebrate
162                                              Cellular plasticity is a state in which cancer cells exi
163                                        Thus, cellular plasticity is a temporally acquired trait of th
164        Coincident with the emergence of such cellular plasticity is an altered response to transformi
165                                         This cellular plasticity is associated with cancer progressio
166                                              Cellular plasticity is crucial for adapting to ever-chan
167                                              Cellular plasticity is mediated by loss of ARID1A-depend
168 ell fate decisions in developmental systems, cellular plasticity is now emerging as a general theme i
169 en together, these findings demonstrate that cellular plasticity is regulated epigenetically, and tha
170                                              Cellular plasticity is represented by position shift alo
171  complex biological pathway that facilitates cellular plasticity, is used by tumor cells to enable me
172 rtex by measuring both the thickness of, and cellular plasticity markers in, the AI with magnetic res
173                                         This cellular plasticity may indicate a possible endogenous r
174                                      Two key cellular plasticity mechanisms -Epithelial-to-Mesenchyma
175 d eye to activate cortex, but the underlying cellular plasticity mechanisms are incompletely understo
176 re arguably two of the most widely discussed cellular plasticity mechanisms for learning and memory.
177 ing suggests that behavioral training alters cellular plasticity mechanisms such that NMDARs are not
178 ransition from the pre-CP to the CP, but the cellular plasticity mechanisms that underlie this change
179 s in memory are caused by the development of cellular plasticity mechanisms within the brain's memory
180 rain is made possible by a huge diversity of cellular plasticity mechanisms.
181                                              Cellular plasticity mediates tissue development as well
182 ng dissemination and colonization, including cellular plasticity, metabolic reprogramming, the abilit
183 remodeled during development, might underlie cellular plasticity more generally.
184 etwork for singing and may point to sites of cellular plasticity necessary for song maintenance.
185 -tumoral heterogeneity and the potential for cellular plasticity occurring during disease development
186 ation of HSCs and their niche depends on the cellular plasticity of bone marrow adipocytes.
187 netic program controlling the phenotypic and cellular plasticity of EMT remains unclear, one contribu
188              Our study demonstrates that the cellular plasticity of mammalian cardiomyocytes is the r
189                     To better understand the cellular plasticity of neuroblastoma in chemoresistance,
190                                          The cellular plasticity of neuroblastoma is defined by a mix
191  identifying the organization, function, and cellular plasticity of the ventral tegmental area (VTA)
192 reatic ductal adenocarcinoma (PDAC) involves cellular plasticity, particularly the epithelial-to-mese
193  offers an alternative means to the study of cellular plasticity, possibly in the context of drug scr
194 -mesenchymal transition (EMT) is a classical cellular plasticity process induced by various cell-intr
195 ia signaling to the epigenetic machinery and cellular plasticity processes.
196                                              Cellular plasticity progressively declines with developm
197                            Here, we used the cellular plasticity-regulating process of epithelial-to-
198 ver, the ability of drugs to induce forms of cellular plasticity related to behavioral sensitization
199 uce EMT, the complex process underlying such cellular plasticity remains poorly understood.
200 rly after peripheral nerve injury confer the cellular plasticity required for sensory neurons to tran
201  Increasing data suggest that impairments of cellular plasticity/resilience underlie the pathophysiol
202 t the TF Tfap2e can reprogram VSNs bypassing cellular plasticity restrictions, and that it directly c
203 n exposure to the SASP, cancer cells undergo cellular plasticity resulting in increased proliferation
204 conds, endowing neurons with a novel form of cellular plasticity shaping synaptic integration, dendri
205 salamander myofibers in numbers suitable for cellular plasticity studies.
206 behavioral outcomes caused by differences in cellular plasticity, subcellular signaling pathways, and
207 ould be involved in functional mechanisms of cellular plasticity such as synaptic depression that rep
208          Behavioural learning is mediated by cellular plasticity, such as changes in the strength of
209  Firing rate potentiation is a novel form of cellular plasticity that could contribute to motor learn
210                            Understanding the cellular plasticity that enables urodeles to regenerate
211 tern of immune infiltration and a program of cellular plasticity that involves loss of NE traits.
212 s, even when cancer cells acquire a state of cellular plasticity that may no longer support the expre
213 ndocrine therapy results from an increase in cellular plasticity that permits the emergence of a horm
214 ies therefore delineate how to transform the cellular plasticity that underlies drug resistance into
215 ressor genes can create a state of increased cellular plasticity that, when challenged with antiandro
216 ons in gene expression to support growth and cellular plasticity through incompletely understood mech
217                                 Manipulating cellular plasticity through inhibition of DOT1L before t
218 ggests a new design principle in controlling cellular plasticity through multiple intermediate cell f
219 instem circuits provide a means for relating cellular plasticity to behavioral gain control.
220  utilization, preTCR-pMHC interactions limit cellular plasticity to facilitate normal thymocyte diffe
221 itment and unleashed an unexpected degree of cellular plasticity towards the liver and duodenum fates
222                     Here, we report that the cellular plasticity transcription factors ZEB1 and ZEB2
223  Increasing data suggest that impairments of cellular plasticity underlie the pathophysiology of bipo
224 or epilepsy-susceptibility variants modulate cellular plasticity via Ras and Akt signaling.
225 ether, these data suggest that IKCs modulate cellular plasticity via Ras and Akt signaling.
226 n is necessary to maintain cell identity and cellular plasticity via the regulation of transcription
227    In many songbirds, vocal learning-related cellular plasticity was thought to end following a devel
228                                  To quantify cellular plasticity, we developed Transcompp (Transition
229               While explicitly acknowledging cellular plasticity, we propose categorizing these cell
230 However, boundaries can also sharpen through cellular plasticity, with cell fate changes driven by up
231 ic factors plasmin(ogen) and fibrin(ogen) in cellular plasticity within adult tissues of the digestiv
232                                    Increased cellular plasticity within the neoplastic compartment of
233  after inhibition of BMP6 signaling suggests cellular plasticity within the salivary gland and a poss
234 ing that BMP signaling may govern aspects of cellular plasticity within tumor hierarchies.

 
Page Top