ライフサイエンスコーパス: cell plasticity

1 ppressor T-cell population, and limited Th17 cell plasticity.

2 oblems pertaining to tissue regeneration and cell plasticity.

3 netic modification may underlie regulatory T-cell plasticity.

4 well as a new strategy for controlling T reg cell plasticity.

5 ndings reveal a dramatic delay in inhibitory cell plasticity.

6 aggressive melanoma cells, causing melanoma cell plasticity.

7 nd phenotypic responses (outputs) underlying cell plasticity.

8 ve disputed the notion of hematopoietic stem cell plasticity.

9 ovascularization to test human hematopoietic cell plasticity.

10 t widely studied and debated example of stem cell plasticity.

11 ell biology including the phenomenon of stem cell plasticity.

12 gesting parity for inhibitory and excitatory cell plasticity.

13 ranscriptional programs governing nongenetic cell plasticity.

14 study cancer evolution, clonal mosaicism and cell plasticity.

15 ntains epigenome fidelity and embryonic stem cell plasticity.

16 e small intestine as a model system to study cell plasticity.

17 regulatory networks underlying Tgammadelta17 cell plasticity.

18 has provoked considerable debate about CD4 T cell plasticity.

19 ISC and the other calling for differentiated cell plasticity.

20 eatest challenges to cancer therapy is tumor cell plasticity.

21 on factor Snail1 by mechanisms of epithelial cell plasticity.

22 xploration of regulatory programs underlying cell plasticity.

23 ent mechanistic understanding of mesenchymal cell plasticity.

24 interplay between DNA repair, epigenome, and cell plasticity.

25 RNA splicing machinery and control of tumour cell plasticity.

26 ave been stymied by drug toxicity and tumour cell plasticity.

27 ts downstream signaling and regulated acinar cell plasticity.

28 A repair-induced chromatin changes influence cell plasticity.

29 that CPH acts as an epigenetic modulator of cell plasticity.

30 ms of endothelial and vascular smooth muscle cell plasticity.

31 e on the role of miR302 in the regulation of cell plasticity.

32 n the regulation of cell-cycle-mediated stem cell plasticity.

33 if the adjuvant used is one that supports T-cell plasticity.

34 AZA is also known to induce cell plasticity.

35 ation senses metabolic changes and modulates cell plasticity.

36 eterogeneity in cancer--clonal evolution and cell plasticity.

37 as a central regulator of pancreatic cancer cell plasticity.

38 lti-phenotypic cell population dynamics with cell plasticity.

39 nvestigators challenging the notion of these cells' plasticity.

40 The microenvironment-induced T-cell plasticity, a factor increasingly appreciated, may

41 Understanding tumor cell plasticity, a potential mechanism driving therapeut

42 icroenvironmental signals controlling cancer cell plasticity along EMT and suggests that hybrid and m

43 tic process and leverages entropy to measure cell plasticity along the trajectory.

44 e found that senescence does not alter alpha-cell plasticity: alpha-cells can reprogram to produce in

45 ative paradigm of CSC theory with reversible cell plasticity among cancer cells has received much att

46 udy provides a better appreciation of CD40-B cell plasticity and biology.

47 mmunotherapeutic target that regulates tumor cell plasticity and chemoresistance in ACC and supports

48 transcription factors, better captures T(H) cell plasticity and conversion as well as the breadth of

49 38 MAPK as an important regulator of Schwann cell plasticity and differentiation.

50 amming provides a powerful platform to study cell plasticity and dissect mechanisms underlying cell f

51 irections, particularly in addressing tumour cell plasticity and dynamic cell states.

52 tatic regulator that orchestrates both tumor cell plasticity and ECM remodeling, positioning ALK7 inh

53 d the highly dynamic mechanisms that control cell plasticity and fate.

54 nchecked oncogenic signaling to impaired AT2 cell plasticity and fibrogenesis.

55 sing stress resistance, while also enhancing cell plasticity and functionality.

56 n summary, our study reveals that adaptive T cell plasticity and genomic alterations determine respon

57 e major underlying processes enabling cancer cell plasticity and greatly facilitates these major caus

58 in the expression of critical genes promotes cell plasticity and has a critical role in accurately or

59 Accordingly, tumor cell plasticity and how it affects disease progression h

60 n animal models and clinically, is that of T-cell plasticity and how lymphocytic responses are determ

61 t CRACD depletion drives neuroendocrine (NE) cell plasticity and immune evasion in SCLC.

62 CRACD as a tumor suppressor that constrains cell plasticity and immune evasion, highlighting the CRA

63 and local microenvironments that impact stem cell plasticity and impair regenerative capacity.

64 ransfer can regulate the maintenance of stem cell plasticity and induce beneficial cell phenotype mod

65 , via the viral protein Tax, exploits CD4+ T cell plasticity and induces transcriptional changes in i

66 s identify that FRA1 is a mediator of acinar cell plasticity and is critical for acinar cell de-diffe

67 EMT) is a dynamic process that drives cancer cell plasticity and is thought to play a major role in m

68 In addition, we discuss T(H)17 cell plasticity and its incorporation into the current u

69 The ontogeny of AT2 cell plasticity and its transcriptional and epigenetic m

70 ting several pathways involved in epithelial cell plasticity and luminal-to-basal conversion.

71 The tumor microenvironment drives cancer cell plasticity and metastasis, and unraveling the under

72 epigenetic regulators in determining cancer cell plasticity and metastatic progression.

73 lies that refinement of the concepts of stem cell plasticity and of the stem cell niche is warranted.

74 , we studied the role of Hes1 in both acinar cell plasticity and pancreatic regeneration after caerul

75 te intrinsic signals that promote epithelial cell plasticity and paracrine signals that induce basal-

76 nt studies suggesting the existence of tumor cell plasticity and phenotypic switching between subtype

77 Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking c

78 The switch in cell plasticity and protein expression was confirmed by

79 m by which thermal stress induces progenitor cell plasticity and recruits a distinct form of thermoge

80 nforcing specialized lineages and regulating cell plasticity and regeneration.

81 Our findings suggest that cell plasticity and remodeling responses such as deforma

82 demyelinated adult CNS, which has decreased cell plasticity and scarring.

83 ed function of succinate in enhancing cancer cell plasticity and stemness.

84 generative response through the induction of cell plasticity and stemness.

85 erarchical signaling network regulating PDAC cell plasticity and suggest that the molecular decision

86 ignant properties that affect both the tumor cell plasticity and the endothelial cell behavior.

87 systems to study the markers of cancer stem cell plasticity and their evolution during metastatic gr

88 Itacitinib promoted CD8 T cell plasticity and therapeutic responses of exhausted a

89 nd beneficial role for the SASP in promoting cell plasticity and tissue regeneration and introduces t

90 X2 and TGFbeta signaling affects lung cancer cell plasticity and TKI tolerance.

91 ng the molecular mechanisms underlying plant cell plasticity and totipotency.

92 division but also acts as a driver of cancer cell plasticity and treatment resistance.

93 ine/autocrine axis instigating breast cancer cell plasticity and triggering metastasis.

94 Thus, PRC2-targeted therapy may reduce tumor cell plasticity and tumor heterogeneity, offering a new

95 t Nodal signaling has a key role in melanoma cell plasticity and tumorigenicity, thereby providing a

96 he molecular mechanisms that control Schwann cell plasticity and underlie nerve pathology, including

97 the central role of copper as a regulator of cell plasticity and unveils a therapeutic strategy based

98 resolve long-standing questions about CD4 T cell plasticity, and propose alternative differentiation

99 ithelial traits, an increase in stemness and cell plasticity, and the acquisition of more aggressive

100 ampered by their intrinsic autofluorescence, cell plasticity, and the complexities of monocyte-MPhi c

101 erative potential, the demonstration of stem cell plasticity, and the creation of human embryonic ste

102 s a link between Bmal1, Myh9, mouse melanoma cell plasticity, and tumor immunity.

103 y in melanoma progression, metastasis, tumor cell plasticity, and tumor therapeutic resistance.

104 nical forces regulate biochemical signaling, cell plasticity, and vascular disease.

105 of plasticity; (2) epigenomic regulation of cell plasticity; and (3) conserved mechanisms governing

106 However, data supporting stem cell plasticity are extensive and cannot be easily dismi

107 the molecular mechanisms underpinning cancer cell plasticity are incompletely understood.

108 The mechanisms that mediate epithelial cell plasticity are only beginning to be understood.

109 gulatory mechanisms that restrict or promote cell plasticity are poorly understood.

110 Taken together, these results support cell plasticity as a driver of BPH progression and thera

111 t be used to characterize T cell phenotype/T cell plasticity as a function of seasonality, or as a re

112 and show that PDGFRalpha targets progenitor cell plasticity as a profibrotic mechanism.

113 k for a mechanistic understanding of in situ cell plasticity as a treatment for diabetes and other de

114 invasion and migration in addition to tumor cell plasticity as shown by vasculogenic mimicry.

115 is capable of discovering adaptive forms of cell plasticity associated with complex logical function

116 ciated link between Keap1-Nrf2 signaling and cell plasticity at early tumorigenesis.

117 f the PCLAF-DREAM axis in promoting alveolar cell plasticity, beyond cell proliferation control, prop

118 bolic reprogramming not only promotes cancer cell plasticity, but also provides novel insights for tr

119 tion is underpinned by dedifferentiation and cell plasticity, but the signaling pathways that regulat

120 rovide insights into the regulation of tumor cell plasticity by an embryonic milieu, which may hold s

121 SL2 that controls V(gamma)6(+) Tgammadelta17 cell plasticity by stabilizing type 3 identity and restr

122 amming by a FUNDC1-LonP1 axis controls tumor cell plasticity by switching between proliferative and i

123 results suggest an avenue for promoting stem cell plasticity by targeting barriers of latent lineage

124 issue homeostasis, demonstrating that tumour cell plasticity can be differentially targeted.

125 Pancreatic exocrine cell plasticity can be observed during development, panc

126 lls in human autoimmunity and show that Treg cell plasticity can be tissue specific.

127 Cell plasticity, changes in cell fate, is crucial for ti

128 basis of the tumour immune microenvironment, cell plasticity, circulating tumour cells and the develo

129 conceivable that changes in stem/progenitor cell plasticity contribute to the loss of this capacity,

130 T helper 17 (Th17) cell plasticity contributes to both immunity and autoimm

131 Tumor cell plasticity contributes to functional and morphologi

132 Such tumor cell plasticity contributes to immunotherapy resistance;

133 Cancer cell plasticity contributes to therapy resistance and me

134 scriptional events that determine epithelial cell plasticity controlled by TGF-beta.

135 Therefore, we investigated whether liver cell plasticity could contribute to IHBD regeneration in

136 This endocrine cell plasticity could have implications for islet develo

137 nal predictions, support the idea that Golgi cell plasticity could play a crucial role in controlling

138 Deregulated cell plasticity could result in the development of debil

139 est that genetics, cell of origin, and tumor cell plasticity determine SCLC subtype.

140 ion immunotherapy strategies to reduce tumor cell plasticity-driven resistance in cancer.

141 etween the tumor microenvironment and cancer cell plasticity drives intratumor phenotypic heterogenei

142 ys a major role in the control of epithelial cell plasticity during cancer progression.

143 However, the mechanisms governing alveolar cell plasticity during lung repair remain elusive.

144 are an essential manifestation of epithelial cell plasticity during morphogenesis, wound healing, and

145 r regulating the scaling of cell numbers and cell plasticity during mouse development and following i

146 players establishing epithelial-mesenchymal cell plasticity during reversible and irreversible EMT.

147 tivation of BMP signaling governs epithelial cell plasticity, EMT, and tumorigenicity during breast c

148 Cancer cell plasticity enables the acquisition of new phenotypi

149 ZEB1 is also a key determinant of cell plasticity, endowing cells with the capacity to wit

150 g logical functions, making the evolution of cell plasticity equivalent to a simple categorisation le

151 Here, we discuss the definition of cell plasticity, evaluate state-of-the-art model systems

152 Tumor cell plasticity exhibited as an epithelial-mesenchymal t

153 nd featured a workshop on terminology in the cell plasticity field.

154 will we be able to fully harness adult stem cell plasticity for clinical purposes.

155 dicating how difficult it will be to exploit cell plasticity for therapeutic purposes.

156 Thus, gut T cell plasticity generates atypical, potent T(FH) cells p

157 In the past few years, cell plasticity has emerged as a mode of targeted therap

158 A rush of papers proclaiming adult stem cell plasticity has fostered the notion that there is es

159 led to clinical trials in humans, true stem cell plasticity has not rigorously been established in m

160 er deciphering the molecular basis of tumour cell plasticity has the potential to contribute to new t

161 This concept of stem-cell "plasticity" has helped to galvanize research on st

162 ng helper T cell and group 3 innate lymphoid cell plasticity have been extensively studied, the mecha

163 al evidence supporting the existence of stem-cell plasticity have been refuted because stem cells hav

164 The molecular mechanisms governing pituitary cell plasticity have not been fully elucidated.

165 We now understand that cell plasticity, i.e., cells adaptively changing differe

166 molecular and cellular mechanisms of cancer cell plasticity in a conditional oncogenic Kras mouse mo

167 demonstrate that LIN28B promotes supporting cell plasticity in an mTORC1-dependent manner.

168 ion (EMT) plays a major role in facilitating cell plasticity in cancer and allows cancer cells to esc

169 expression contribute markedly to epithelial cell plasticity in colorectal carcinogenesis.

170 tes the in vivo study of stem and progenitor cell plasticity in disease and regeneration.

171 k for a statistically robust study of cancer cell plasticity in diverse tissue microenvironments.

172 en immune cells, metal metabolism, and tumor cell plasticity in driving metastasis and anemia.

173 ) that regulates cholesterol homeostasis and cell plasticity in endodermal-derived tissues.

174 e-cell genomic analysis confirmed the cancer cell plasticity in every rare cell group harboring clona

175 hnologies to obtain functional insights into cell plasticity in healthy and diseased tissues.

176 as development, might exert in programming B-cell plasticity in later life is a poorly studied area.

177 data thus indicate a key function of T(H)17 cell plasticity in maintaining immune homeostasis, and d

178 e investigated the time course of inhibitory cell plasticity in mouse primary visual cortex by using

179 nce of such mechanisms that drive epithelial cell plasticity in multiple diseases associated with con

180 LCC-12 interferes with cell plasticity in other settings and reduces inflammati

181 cells may be a common theme underlying adult cell plasticity in regenerative vertebrates.

182 Cancer cell plasticity in response to evolutionary pressures is

183 set of development also has implications for cell plasticity in somatic cell nuclear transfer, genomi

184 Our findings also provide insights into cell plasticity in the adult mammalian brain, which has

185 the endocardium reveal extensive endothelial cell plasticity in the infarct zone and identify the end

186 ce that the developmental drop in supporting cell plasticity in the mammalian cochlea is, at least in

187 nscription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung.

188 The molecular mechanisms regulating Schwann cell plasticity in the PNS remain to be elucidated.

189 hese studies and provide evidence for single-cell plasticity in the primary motor cortex of primates.

190 tumor cellular heterogeneity and non-genetic cell plasticity in tumors pose a recently recognized cha

191 ithelial-to-mesenchymal transition (EMT) and cell plasticity in tumour heterogeneity and clonal evolu

192 el permits comprehensive study of human stem cell plasticity in vivo.

193 The discovery of Th17 cell plasticity, in which CD4(+) IL-17-producing Th17 ce

194 he high potential of utilizing the increased cell plasticity inherent to invasive cancer cells for tr

195 Cell plasticity is a core biological process underlying

196 Cell plasticity is a crucial trait for cancer progressio

197 e models, we show that alveolar type 1 (AT1) cell plasticity is a major and unappreciated mechanism t

198 Tumour cell plasticity is a major barrier to the efficacy of ta

199 We conclude that stem-cell plasticity is a true characteristic of NSCs and tha

200 hing and provide proof that targeting tumour cell plasticity is a viable therapeutic opportunity.

201 Th17 cell plasticity is associated with pathogenicity in chro

202 We conclude that liver cell plasticity is competent for regeneration of IHBDs i

203 Smooth muscle cell plasticity is considered a prerequisite for atheros

204 Th17 cell plasticity is crucial for development of autoinflam

205 The observed cell plasticity is dependent on ZEB1, a key regulator of

206 This mitral cell plasticity is odor specific, recovers gradually ove

207 This cell plasticity is particularly prominent in more regene

208 accepted that dynamic and reversible tumour cell plasticity is required for metastasis, however, in

209 The evidence for and against stem-cell plasticity is reviewed here as well as some of the

210 essel co-option, perivascular niche, and GBM cell plasticity jointly drive resistance to therapy duri

211 cell heterogeneity in tissues and of T(H)17 cell plasticity leading to alternative T cell states and

212 lead to a disturbance of later events in Th cell plasticity, leading to autoimmune diseases or other

213 regeneration results from diminished Schwann cell plasticity, leading to slower myelin clearance.

214 s therapeutic strategy could suppress cancer cell plasticity, limit metastasis, and activate antitumo

215 vitro and in vivo, a function known as "stem cell plasticity", makes them an appealing cell source fo

216 Immune cell plasticity may augment suppression of Th2 cells by

217 heses regarding the mechanisms by which Th17-cell plasticity may be controlled in vivo.

218 This novel mechanism for CNS cell plasticity may operate in wider contexts.

219 Modulation of basal cell plasticity may represent a relevant target for ther

220 Additional Purkinje cell plasticity mechanisms may also contribute to eyebli

221 Thus, it is unknown whether Th17 cell plasticity merely reflects change in expression of

222 g the coming-of-age of the regenerative stem cell plasticity model.

223 ntigen 1 (FRA-1) as a central node in tumour cell plasticity networks, and discuss mechanisms regulat

224 We hypothesized that AZA-induced cell plasticity occurs via a transient multipotent cell

225 onal consequences of this mode of epithelial cell plasticity on targeted cell lysis by cytotoxic T ly

226 Small molecules that can interfere with cell plasticity or kill cells in a cell state-dependent

227 ractile force as a determinant of epithelial cell plasticity, particularly in cancer cells that can s

228 ear events could be shared between different cell plasticity phenomena across phyla.

229 Cell plasticity plays a key role in embryos by maintaini

230 alysis of our model, it is found that cancer cell plasticity plays an essential role in maintaining t

231 r model reveals that the delay in inhibitory cell plasticity potently accelerates Hebbian plasticity

232 REAM transcriptional signature increases AT2 cell plasticity, preventing lung fibrosis in organoids a

233 asing evidence supports the idea that cancer cell plasticity promotes metastasis and tumor recurrence

234 This high degree of stem cell plasticity prompted us to test whether dead myocard

235 se findings provide insights into how cancer cell plasticity regulated by SOX2 and TGFbeta signaling

236 in EGFR-mutant lung cancer, as SOX2-mediated cell plasticity regulated by TGFbeta stimulation and epi

237 rns HSPG biosynthesis and its role in cancer cell plasticity remain elusive.

238 Mechanisms underlying tumor cell plasticity remain poorly understood.

239 porting the notion that clonal selection and cell plasticity represent two sides of the same coin.

240 l-to-mesenchymal transitions (EMTs) underlie cell plasticity required in embryonic development and fr

241 gulators might endorse cancer cells with the cell plasticity required to conduct dynamic changes in c

242 ts and, therefore, may have consequences for cell plasticity, resilience, and survival in patients wi

243 revealed a remarkable dichotomy in RS and IB cell plasticity; spared whisker potentiation occurred in

244 bens GABA neurons are well studied, VTA GABA cell plasticity, specifically inhibitory inputs to VTA G

245 In truth, stem cell plasticity, strictly defined, has yet to be rigorou

246 licate genome-reprogramming studies and stem-cell plasticity studies, but could also reveal clues abo

247 umor microenvironments (TMEs) induce stromal cell plasticity that affects tumorigenesis.

248 n the pituitary display remarkable levels of cell plasticity that allow remodeling of the relative pr

249 s, and may provide new perspectives on tumor cell plasticity that could be exploited for novel therap

250 /STAT3 axis as a central regulator of cancer cell plasticity that directly links proteoglycan synthes

251 hus, the GLI2-OPN circuit is a driver of PDA cell plasticity that establishes and maintains an aggres

252 ature of the disease and to recapitulate the cell plasticity that is observed in this disease context

253 ly a dynamic and reversible phenotypic tumor cell plasticity that renders a proportion of cells both

254 Cell plasticity, the ability of differentiated cells to

255 microenvironment (TME) contributes to cancer cell plasticity, the specific TME factors most actively

256 levant aspect in intratumor heterogeneity is cell plasticity-the ability of a cell to switch to new i

257 Cell plasticity theoretically extends to all possible ce

258 In addition to the changes in cell plasticity, these studies demonstrated that chronic

259 ts that CRC tumours leverage intestinal stem cell plasticity to both proliferate (via proCSCs) when u

260 Human B cells exploit CD4(+) T-cell plasticity to create flexibility in the effector T-

261 ored a novel strategy leveraging endothelial cell plasticity to enhance reprogramming efficiency.

262 k a tightrope', retaining adequate levels of cell plasticity to generate and maintain tissues while a

263 Translating the promise inherent in tumor cell plasticity to the clinical arena remains a major ch

264 hyper-activated immune system and epithelial cell plasticity underlies colon cancer development.

265 lysis can assist in further understanding of cell plasticity underlying angiogenesis and other comple

266 esents a basic morphogenetic process of high cell plasticity underlying embryogenesis, wound healing,

267 Thus, innate cytokine signals regulate T(H)1 cell plasticity via an individual cell-intrinsic rheosta

268 fore each mating session; thus, VTA dopamine cell plasticity was dependent on action of endogenous op

269 To characterize mechanisms of beta-cell plasticity, we studied a model of severe insulin re

270 In an in vivo mouse model promoting T(REG) cells plasticity, we found that USP11 protein was expres

271 transcriptional patterns that support cancer cell plasticity, where KDM5B depleted cancer cells exhib

272 Cell plasticity, which includes transdifferentiation and

273 egulation by PRC2 is a key mediator of tumor cell plasticity, which is required for the adaptation of

274 of the PAF-Wnt signalling axis in modulating cell plasticity, which is required for the maintenance o

275 notypic heterogeneity is the result of tumor cell plasticity, which-together with the genetic backgro

276 multi-phenotypic cancer model by integrating cell plasticity with the conventional hierarchical struc

277 there has been increasing evidence of T(FH) cell plasticity, with some T(FH) cells expressing genes

278 focus on the mechanisms that regulate cancer cell plasticity within a tumor, and explore the concept