ライフサイエンスコーパス: reprogramming

1 ry layer underlying MET to control efficient reprogramming.

2 s and unveils mechanisms of phospholipidomic reprogramming.

3 hways, but did not induce T(RM) cell lineage reprogramming.

4 function of TET proteins during somatic cell reprogramming.

5 derstanding of the role of TETs in chromatin reprogramming.

6 and licences T cell receptor driven proteome reprogramming.

7 aspects and the limitation sides of the OSKM reprogramming.

8 ssential characteristics of cancer metabolic reprogramming.

9 ate Oct4 in fibroblasts, leading to enhanced reprogramming.

10 verted in response to injury or experimental reprogramming.

11 nabling tumour progression through metabolic reprogramming.

12 and functions during genome-wide epigenetic reprogramming.

13 spond to OSKM induction underwent legitimate reprogramming.

14 he otherwise inefficient and stochastic OSKM reprogramming.

15 glial maturation that may prevent efficient reprogramming.

16 that enter a trophectoderm-like state during reprogramming.

17 Id1/2 as driver regulators of early stage of reprogramming.

18 ging is characterized by extensive metabolic reprogramming.

19 tory response that is dependent on metabolic reprogramming.

20 ormone coordinating systemic immunometabolic reprogramming.

21 at was closely involved in the initiation of reprogramming.

22 e tumours to targeted therapy via epigenetic reprogramming.

23 influence how NF-kappaB impacts Muller glia reprogramming.

24 al cells undergo substantial transcriptional reprogramming.

25 hanisms of hPGC specification and epigenetic reprogramming.

26 d increased chromatin accessibility later in reprogramming.

27 positioning, differentiation, and metabolic reprogramming.

28 fer into an oocyte, a process termed nuclear reprogramming.

29 venile hormone (JH), a hormone elevated upon reprogramming.

30 g-term epigenetic, metabolic, and functional reprogramming.

31 8) is expressed on iPSCs and is important in reprogramming, (2) sGRP78 promotes cellular functions in

32 An emerging concept of translational reprogramming addresses how to maintain the expression o

33 s miR-9/9(*) and miR-124 (miR-9/9(*)-124) as reprogramming agents that orchestrate direct conversion

34 ssion of constitutive heterochromatin during reprogramming and a non-repressive role for H3K9me3.

35 KLF10 as a component of this transcriptional reprogramming and a novel hepato-protective factor.

36 BCL6, leading to pre-memory transcriptional reprogramming and cell-fate bias.

37 me reorganization, which leads to epigenetic reprogramming and derepression of developmentally silenc

38 tational model to predict the progression of reprogramming and distinguish partially reprogrammed cel

39 he YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.

40 ion during DNA replication promotes germline reprogramming and epigenetic variation in plants propaga

41 Muller glia attractive targets for cellular reprogramming and highlighted the potential for curing d

42 LR4-induced glycolysis, macrophage metabolic reprogramming and inflammation.

43 In parallel, cellular reprogramming and organoid engineering are expanding the

44 netic modification, stem cell function, cell reprogramming and other processes.

45 se primordial germ cells (mPGCs), epigenetic reprogramming and pluripotency, but its role in the evol

46 cription factor (CoREST) is upregulated upon reprogramming and required for the epigenetic switch to

47 a valuable model for investigating cellular reprogramming and retinal regeneration.

48 ogic targeting of ILK reversed mitochondrial reprogramming and suppressed sEV-induced cell movements.

49 1A5 as an FTO target that promotes metabolic reprogramming and survival of VHL-deficient ccRCC cells.

50 on epigenetic trajectories, which implicates reprogramming and the pluripotency network as a central

51 human retinal epithelial cells leads to the reprogramming and transformation of these cells to neuro

52 ver of pancreatic cancer, promotes metabolic reprogramming and upregulates NRF2, a master regulator o

53 modifications, codon-dependent translational reprogramming, and induction of the unfolded protein res

54 autophagy, generation of hiPSCs via cellular reprogramming, and neuronal differentiation.

55 ential component of TCR-initiated T reg cell reprogramming, and Rag GTPase activities may be titrated

56 onic development, are essential for cellular reprogramming, and rewire gene networks in cancer cells.

57 the absence of individual enzymes can affect reprogramming, and thus the impact of mutations in cell

58 tion in isogenic PSCs generated by different reprogramming approaches, either somatic cell nuclear tr

59 nvironments to promote cell infiltration and reprogramming are discussed.

60 he factors used to induce differentiation or reprogramming are often identified by informed guesses b

61 vation leads to mitochondrial and glycolytic reprogramming are unknown.

62 nant of this process, establishing metabolic reprogramming as limiting for tumor initiation.

63 Indeed, near-complete DNA methylation reprogramming, as occurs during mammalian embryogenesis,

64 an important tool for inducing somatic cell reprogramming, as well as for dissecting the other biolo

65 Third, metabolic reprogramming assessed through real-time bioenergetic me

66 trate that rapid and extensive transcription reprogramming associated with hematopoietic differentiat

67 mphoma underwent substantial transcriptional reprogramming associated with increased lipid metabolism

68 ar the most comprehensive dataset for kinome reprogramming associated with melanoma progression, whic

69 ccessibility profiling uncovering epigenetic reprogramming at >1400 sites in neurons after prolonged

70 l epigenetic reprogramming windows: maternal reprogramming at fertilization, embryonic stem cell (ESC

71 romatin remodelling is essential for natural reprogramming at fertilization.

72 b.D mutants, suggesting that transcriptional reprogramming at this time point is not required for imm

73 tion of multicellular regulatory networks by reprogramming autoantigen-experienced CD4+ T cells into

74 h enhanced function, followed by progressive reprogramming away from TCR-dependent antibacterial resp

75 ellular metabolic, epigenetic and functional reprogramming, but how broadly trained immunity protects

76 ic acid metabolites and subject to metabolic reprogramming, but they have been neglected in N-ERD.

77 ivation and further promote cancer metabolic reprogramming by blocking the expression of the AKT inhi

78 nhibits mTOR activation and alters metabolic reprogramming by shifting glycolytic pathways and inhibi

79 Blocking metabolic reprogramming by tumor cells in obese mice improves anti

80 Recent evidence shows that transient reprogramming can ameliorate age-associated hallmarks an

81 Aberrant epithelial reprogramming can induce metaplastic differentiation at

82 ministic components in the microRNA-mediated reprogramming cascade.

83 recently showed that IL-1-induced glycolytic reprogramming contributes to allergic airway disease usi

84 This glycolytic reprogramming depends on Akt kinases, independent of mTO

85 olism in response to mutations, but how this reprogramming depends on the genetic context is not well

86 that earlier errors in germ-cell epigenetic reprogramming derail differentiation in cellular progeny

87 Expression reprogramming directed by transcription factors is a pri

88 intaining open chromatin for transcriptional reprogramming during adipogenic differentiation.

89 study not only unveils genome-wide plant AS reprogramming during infection but also establishes a no

90 d targeted proteomic method to assess kinome reprogramming during melanoma metastasis in three pairs

91 that AS is a distinct layer of transcriptome reprogramming during plant-pathogen interactions.

92 netic mark that contributes to transcriptome reprogramming during plant-pathogen interactions.

93 anisms that regulate autophagy and metabolic reprogramming during reactive oxygen species (ROS) gener

94 t HIV reactivation, indicating an epigenetic reprogramming effect of ZL0580 on HIV long terminal repe

95 tegies have been applied in order to improve reprogramming efficiency, mainly focused on removing rep

96 t correlated with rapid DNA demethylation at reprogramming enhancers and increased chromatin accessib

97 the deposition of H3.3 are paramount during reprogramming events that drive zygotic activation and t

98 ate stimuli and the epigenetic and metabolic reprogramming events that shape the induction of trained

99 also expanded, revealing the crucial role of reprogramming factors and chromatin remodelling.

100 we show that transient expression of nuclear reprogramming factors, mediated by expression of mRNAs,

101 OSKM reprogramming were also observed in the reprogramming fibroblasts from a different individual.

102 In summary, the requirement of glycolytic reprogramming for proinflammatory cytokine production in

103 example, our method on Ascl1-induced direct reprogramming from fibroblast to neuron time course data

104 Metabolic reprogramming fulfils increased nutrient demands and reg

105 at prophase cohesin removal is a key step in reprogramming gene expression as cells transition from G

106 ions include metabolic manipulation, partial reprogramming, heterochronic parabiosis, pharmaceutical

107 Overexpression of Ascl1 is more effective in reprogramming immature MG, than mature MG, consistent wi

108 signaling, which in turn regulates metabolic reprogramming, immune suppression, resistance to apoptos

109 H3K9me2 by inhibiting EHMT1/2 during nuclear reprogramming impacts the levels of H3K9me3, 5mC, and 5h

110 Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to t

111 The beneficial effects of OSK-induced reprogramming in axon regeneration and vision require th

112 In female mice, we observed DNA methylation reprogramming in bone marrow-derived (BMD) monocytes as

113 Metabolic reprogramming in cancer cells, vs. non-cancer cells, ele

114 We review emerging concepts about metabolic reprogramming in cancer, with particular attention on wh

115 ) family enzymes is essential for epigenetic reprogramming in cell state transitions.

116 hat acute administration of cocaine triggers reprogramming in circadian gene expression in the striat

117 etylase (HDAC) inhibitors elicited metabolic reprogramming in concert with disruption of several Warb

118 Metabolic reprogramming in endothelial cells (ECs) thereby is cruc

119 Repression of cellular reprogramming in germ cells is critical to maintaining c

120 sphorylation independent eIF4E translational reprogramming in governing the protein synthesis of ERal

121 that requires epigenetic and transcriptional reprogramming in order to ultimately form ASC.

122 provide a rationale for exploiting metabolic reprogramming in pancreatic cancer cells to confer thera

123 life cycle during which the genome undergoes reprogramming in preparation for embryogenesis.

124 are separable from the preceding epigenetic reprogramming in primordial germ cells.

125 istone residues required for transcriptional reprogramming in response to heat and osmotic stress.

126 Neutrophils undergo immunometabolic reprogramming in severe COVID-19 illness.

127 This approach to track reprogramming in situ using micropatterned substrates co

128 ely to recruit KAP1 to imprinted loci during reprogramming in the absence of ZFP57.

129 ew studies have directly addressed metabolic reprogramming in the context of drug-resistant Mtb infec

130 y milieu in the breast as well as epigenetic reprogramming in the mammary gland, which can affect cel

131 Remarkably, transcriptional reprogramming includes a positive autoregulatory feedbac

132 Efferocytosis triggers cellular reprogramming, including the induction of mRNA transcrip

133 iation and pathogenicity depend on metabolic reprogramming inducing shifts toward glycolysis.

134 pecified by the endothelium is essential for reprogramming interstitial macrophages and dampening inf

135 fied a key role for smooth muscle cell (SMC) reprogramming into a mesenchymal stem cell (MSC)-like st

136 This revealed that reprogramming into primed and naive pluripotency follows

137 on, we show that MEKi leads to CD8(+) T cell reprogramming into T(SCM) that acts as a reservoir for e

138 cells react to their environment by flexibly reprogramming intracellular metabolic pathways that subs

139 Epigenetic reprogramming is a cancer hallmark, but how it unfolds d

140 Metabolic reprogramming is a hallmark of malignancy.

141 Oncogene-induced metabolic reprogramming is a hallmark of pancreatic cancer (PDAC),

142 Reprogramming is accomplished through the interplay of t

143 remains unclear how general DNA methylation reprogramming is across the tree of life.

144 PPARgamma reprogramming is altered in mice with cell-specific abla

145 studies have shown that global translational reprogramming is an early activation event in pattern-tr

146 Metabolism reprogramming is critical for both cancer progression an

147 Epigenetic reprogramming is involved in the response to heat acclim

148 Metabolic reprogramming is known to occur during the epithelial-me

149 te transport processes, indicating that host reprogramming is probably a common strategy in the NCLDV

150 Here we summarize how BCAA metabolic reprogramming is regulated in cancer cells and how it in

151 rm effects of EHS are mediated by epigenetic reprogramming is unknown.

152 and that induced by MYCN-mediated metabolic reprogramming, leads to synthetic lethality.

153 istone fraction resisting post-fertilisation reprogramming marks developmental genes whose expression

154 This suggests that epigenomic reprogramming may be a fundamental driver of glioma.

155 This transcriptional reprogramming may contribute to the beneficial effects o

156 y applicable strategy across tumor types for reprogramming MDSCs and TAMs into antitumorigenic immune

157 ogenitor cells (HSPCs) undergo translational reprogramming mediated by previously uncharacterized mec

158 These data suggest that reprogramming metabolism via activation of PKM2 is a nov

159 in cancer including angiogenesis, metabolic reprogramming, metastasis and DNA repair.

160 Preventing melanoma cell mechanical reprogramming might be a promising therapeutic strategy

161 Elevated MYCN levels promote metabolic reprogramming, mitochondrial dysfunction, reactive-oxyge

162 atment limit interpretation, we believe that reprogramming monocyte or macrophages by targeting immun

163 nowledge to research efforts directed toward reprogramming Muller glia in mammals.

164 and MC38 colorectal carcinoma mouse models, reprogramming nanoparticles in combination with checkpoi

165 alyses confirmed that locally delivered tAPC-reprogramming nanoparticles led to a significant cell-me

166 ncer illustrates the importance of metabolic reprogramming, necessary to synthesize the building bloc

167 Sox8 and Sox9 prevents ovarian-to-testicular reprogramming observed in XX Rspo1 loss-of-function mice

168 d that both osmotic adjustment and proteomic reprogramming occurred in these naturally desiccation-to

169 Extensive metabolic reprogramming occurs during tumour initiation and progre

170 informed characterization, manipulation, and reprogramming of activated cellular ensembles.

171 e microenvironment drives specific metabolic reprogramming of adipose tissue macrophages, contributin

172 egulated by NF-kappaB activation, leading to reprogramming of cell metabolism towards glycolysis and

173 es a profound transcriptional and epigenetic reprogramming of cells.

174 lation at T114 is associated with a striking reprogramming of cellular metabolism induced by a profou

175 tic regulation of gene transcription and the reprogramming of cellular metabolism.

176 ects the core clock mechanism but leads to a reprogramming of circadian gene expression in the liver

177 gakaryocytes consistent with CPI203-mediated reprogramming of cord blood hematopoietic stem and proge

178 We performed a non-integrative reprogramming of dermal fibroblasts obtained from two pa

179 ced upon activation and suppresses metabolic reprogramming of effector T cells.

180 g exit from the ESC state and in restricting reprogramming of EpiSCs.

181 Oplr16 was also able to enhance reprogramming of fibroblasts into pluripotent cells.

182 Chemical reprogramming of fibroblasts offers an opportunity to re

183 n of the stress hormone abscisic acid (ABA), reprogramming of gene expression, and altering of growth

184 Dynamic reprogramming of gene regulatory networks (GRNs) enables

185 of hyaluronic acid, which is enabled by the reprogramming of glucose metabolism.

186 Reprogramming of glycogen metabolism has recently been s

187 s) and smooth muscle cells (iSMCs) by direct reprogramming of healthy human fibroblasts from donors o

188 recise, large-scale analysis, selection, and reprogramming of heterogeneous cell populations.

189 impact of viruses, focusing on how metabolic reprogramming of host cells during lytic viral infection

190 D1 and NOD2 agonists induce early glycolytic reprogramming of human monocyte-derived macrophages (MDM

191 criptional level through distinct glycolytic reprogramming of human myeloid immune cells.

192 nfine cells into discrete islands during the reprogramming of human somatic cells from skin biopsies

193 Reprogramming of human somatic cells to induced pluripot

194 The reprogramming of human somatic cells to primed or naive

195 oadmap for the transcription-factor-mediated reprogramming of human somatic cells, indicate a role fo

196 Last, metabolic reprogramming of infected cells and viral lysis alter nu

197 s a RAS mutant tumor subset characterized by reprogramming of lipid metabolism, invasive and metastat

198 ic gonadotropin by TSC-derived ST reflects a reprogramming of macaque TSCs to an earlier pregnancy ph

199 r a proinflammatory metabolic and epigenetic reprogramming of macrophages in N-ERD.

200 Reprogramming of Majors upregulates Minor-biased genes a

201 growth and/or proliferation may require the reprogramming of metabolic pathways, whereby a switch fr

202 s of macrophage biology and demonstrate that reprogramming of metabolism should be considered a resul

203 ant metastatic sites and mediates epigenetic reprogramming of metastatic tumor cells.

204 Together, these findings show that while reprogramming of mitochondrial metabolism is a key facto

205 our current knowledge regarding spontaneous reprogramming of Muller glia in zebrafish and compares t

206 derstanding the mechanisms that suppress the reprogramming of Muller glia into neurogenic progenitors

207 mportant signaling 'hub' that suppresses the reprogramming of Muller glia into proliferating MGPCs an

208 itical regulator of inflammation, during the reprogramming of Muller glia into proliferating progenit

209 tes of daily neuronal remodeling through the reprogramming of neural development and assessed the eff

210 Therefore, during aging, sestrins induce the reprogramming of non-proliferative senescent-like CD27(-

211 plasts, a process that involves a concurrent reprogramming of nuclear gene expression and plastid mor

212 We assess the impact of transcriptional reprogramming of nuclear-encoded chloroplast genes durin

213 urposed to relieve autoimmunity by metabolic reprogramming of pathogenic Th17 cells.

214 l function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism,

215 romoted antiangiogenic and immunostimulatory reprogramming of Prox1-deficient tumors, destroyed tumor

216 rmone (JH) and ecdysone signaling during the reprogramming of social behavioral phenotypes in ants th

217 ring this process, and facilitate the direct reprogramming of somatic cells into induced trophoblast

218 mate metabolism explained by transcriptional reprogramming of specific structural genes of the pathwa

219 ation of Ptger4 misdirected the regenerative reprogramming of stem cells and prevented Sca-1(+) cell

220 was induced by transcriptomic and functional reprogramming of sugar beet tissue, resulting in a rever

221 muscle identity and requires transcriptional reprogramming of syncytial nuclei.

222 umor-initiating ETS translocations result in reprogramming of the AR cistrome.

223 t metabolic disruption was largely driven by reprogramming of the Early Growth Response 1 (EGR1) tran

224 n fewer lipid droplets, as well as metabolic reprogramming of the invasive cell phenotype, effectivel

225 factor receptor 2 (HER2) inhibitors involves reprogramming of the kinome through HER2/HER3 signaling

226 a diet high in carbohydrate, led to dramatic reprogramming of the liver transcriptional network.

227 We hypothesize that AH may lead to metabolic reprogramming of the liver, including dysregulation of g

228 reatment with gemcitabine leads to extensive reprogramming of the pancreatic tumor microenvironment a

229 ies, thus obscuring the true transcriptional reprogramming of the phagocyte.

230 Such early biased legitimate reprogramming of the responsive TFs aligns well with the

231 oposed that epigenetic factors accompany the reprogramming of the senescent genome; however, the mech

232 LPA and S1P, suggesting an LPA/S1P-mediated reprogramming of the TSC lipidome.

233 teomic screening, and identified substantial reprogramming of tumor metabolism involving oxidative ph

234 Metabolic reprogramming of tumor-specific T cells through enforced

235 Here, we show statistical reprogramming of two-dimensional (2D), noncompact self-a

236 This study depicted the reprogramming of WJ-MSC into rEC using unique transcript

237 Recent work has demonstrated that metabolic reprogramming, often mediated by inflammation, can lead

238 However, in the CNS, the impact of metabolic reprogramming on microglia, neuroinflammation, and subse

239 ication of primordial germ cells, epigenetic reprogramming or meiosis, and demonstrate that oocyte gr

240 This epigenomic reprogramming persists long after the initial exposure,

241 Metabolic reprogramming plays a central role in T cell activation

242 ent for oxidation to 5fC/5caC can rescue the reprogramming potential of Tet2-deficient mouse embryoni

243 and are also of paramount importance for the reprogramming process.

244 The molecular mechanism that underpins these reprogramming processes remains largely unexplored, whic

245 standing and limits rational improvements to reprogramming protocols.

246 Thus, direct reprogramming provides a platform to identify causes and

247 brain energy homeostasis and that metabolic reprogramming regulates microglial polarization, thereby

248 Thus, this mechanism of translation reprogramming regulates the cellular response to metabol

249 ntify, evaluate, and enrich for iPSCs during reprogramming relies on methods that fix, destroy, or si

250 e; however, the mechanism and extent of this reprogramming remain unknown.

251 Injury-induced transcriptional reprogramming requires ATF3, a transcription factor that

252 A methylation that is resistant to embryonic reprogramming, resulting in parental origin-specific mon

253 rs on enhancers trigger genome-wide enhancer reprogramming, resulting in transcriptional transitions

254 gether, unbiased analysis of transcriptional reprogramming revealed a significant degree of negative

255 Genome-wide profiling during reprogramming reveals CoREST represses expression of enz

256 We found that after reprogramming SCAP-O or subclone SCAP-O(BCOR-mut) into i

257 the complex interactions between these plant-reprogramming sedentary endoparasites and their infected

258 ed at the initial programming visit and each reprogramming session.

259 fic chromatin network is a critical event in reprogramming somatic cells into pluripotent status.

260 alysis of genomic loci bound by GATA3 during reprogramming suggests a correlation of recognition moti

261 ment of curative interventions, for example, reprogramming T cell defects during the period of asympt

262 Reprogramming T cells to express a gain-of-function EZH2

263 c-MET inhibition causes profound metabolic reprogramming that can be targeted by drug combination t

264 n and consequently to elicit transcriptional reprogramming that can endow cancer cells with aggressiv

265 ying efficiencies depending on the method of reprogramming that created them.

266 ne interleukin-13 in orchestrating metabolic reprogramming that drives adaptation to endurance exerci

267 he tissue-of-origin in shaping the metabolic reprogramming that enables tumour growth.

268 life span across species, leads to metabolic reprogramming that enhances utilisation of fatty acids f

269 sing muscle, where it orchestrates metabolic reprogramming that preserves glycogen in favor of fatty

270 ributes in the cancer cell while dynamically reprogramming the function of innate and adaptive immune

271 otherapies, due in part to the difficulty of reprogramming the highly immunosuppressive tumor microen

272 an instructive role of tumor cell lineage in reprogramming the stromal microenvironment.

273 utic potential of targeting this pathway for reprogramming the TME.

274 overy and development of drugs for metabolic reprogramming, their associated challenges, and their ut

275 while simultaneously facilitating epigenetic reprogramming through a glucose-fueled histone hyperacet

276 These findings suggest that reprogramming to a stable naive human pluripotent stem c

277 d unlock metabolically restricted epigenetic reprogramming to drive metabolic dysfunction.

278 ire alpha-ketoglutarate-dependent epigenetic reprogramming to elicit anti-inflammatory gene expressio

279 vours mitochondrial biogenesis and metabolic reprogramming to ensure energy production and cellular a

280 We harnessed the power of reprogramming to examine GRP78, a chaperone protein gene

281 mice, revealing the sufficiency of metabolic reprogramming to influence immune cell functions during

282 Here, we utilize reprogramming to investigate natural behavioral specific

283 s important both for lineage commitment, and reprogramming to naive pluripotency.

284 5caC has roles distinct from 5hmC in somatic reprogramming to pluripotency.

285 ested a strategy of pharmacologic macrophage reprogramming to rescue HSPC mobilization.

286 e through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation

287 cognate receptors, T cells undergo metabolic reprogramming to support their activation, differentiati

288 vation (ZGA), the quiescent genome undergoes reprogramming to transition into the transcriptionally a

289 ic rewiring of granulopoiesis and neutrophil reprogramming toward an anti-tumor phenotype; this proce

290 Currently, the molecular mechanisms by which reprogramming transcription factors and miRNAs coordinat

291 nt to a dedifferentiation mechanism by which reprogramming transcription factors Oct4 and Sox2 drive

292 The results also suggest that reprogramming tumor cells toward non-pathological fates

293 d to deoxycytidine to deoxyuridine metabolic reprogramming upon ER stress induction.

294 Notably, this metabolic reprogramming was also associated with an accumulation o

295 This metabolic reprogramming was required to generate a number of proin

296 ate transcriptional responses of TFs to OSKM reprogramming were also observed in the reprogramming fi

297 ts in compromised development and epigenetic reprogramming, which demonstrates that heterochromatin r

298 last rejuvenation through laterally confined reprogramming, which has important implications in regen

299 methylation during three crucial epigenetic reprogramming windows: maternal reprogramming at fertili

300 lymphoid composition, and underwent partial reprogramming with acquisition of CD68/CD206 on MNPs and