ライフサイエンスコーパス: gene expression program

1 export, which are central to the eukaryotic gene expression program.

2 ts as a major regulator of the TAL1 leukemic gene expression program.

3 26(N1ICD/+)) actively promotes a SC-specific gene expression program.

4 ription factors that represses the erythroid gene expression program.

5 ates Smad2/3 signaling and induces a complex gene expression program.

6 ctures intimately controls every step of the gene expression program.

7 estrate sequential deployment of the cardiac gene expression program.

8 positive transcriptional regulator of the PC gene expression program.

9 cess that requires the MRTF-dependent motile gene expression program.

10 as well as suppression of an injury-related gene expression program.

11 on of MRTFs and the activation of the motile gene expression program.

12 s to a block of the KLF1-dependent erythroid gene expression program.

13 at controls the Lgr5(+) intestinal stem cell gene expression program.

14 ividuals was associated with a distinct host gene expression program.

15 tes the canonical thermogenic and uncoupling gene expression program.

16 ure influences practically every step in the gene expression program.

17 entails a choreographic regulation of viral gene expression program.

18 of the normal terminal erythroid maturation gene expression program.

19 ent epidermal cells, initiating the follicle gene expression program.

20 transcriptionally represses a pro-metastatic gene expression program.

21 at induces an antimicrobial and inflammatory gene expression program.

22 ommitted to reactivation of the Th2 cytokine gene expression program.

23 tage-specific expression of the Lmo2-induced gene expression program.

24 , c-Myc amplifies the output of the existing gene expression program.

25 ased levels of transcripts within the cell's gene expression program.

26 e ESRPs in an epithelial posttranscriptional gene expression program.

27 the common regulator of the iron starvation gene expression program.

28 effect gene through regulation of the oocyte gene expression program.

29 a switch from an adaptive to an inflammatory gene expression program.

30 and triggering a vascular stability-related gene expression program.

31 l key transcription factors in the Th17 cell gene-expression program.

32 AF9- and Myb-dependent leukemia self-renewal gene-expression program.

33 erentiation and the fidelity of the TFH cell gene-expression program.

34 n expression of the MLL-AF6-driven oncogenic gene-expression program.

35 ne acetylation to activate a proregenerative gene-expression program.

36 with HOXA9 and modulates a HOXA9-controlled gene-expression program.

37 e been attributed to its ability to regulate gene expression programs.

38 organs and tissues generally have conserved gene expression programs.

39 for specialized cell-type and developmental gene expression programs.

40 sms by which cis-regulatory elements control gene expression programs.

41 ion process involving major modifications in gene expression programs.

42 opmentally appropriate expression and switch gene expression programs.

43 bryo development and regulating cellular and gene expression programs.

44 ck loop that contributes to the stability of gene expression programs.

45 e coactivators to execute stem cell-specific gene expression programs.

46 l hierarchical 'regulome' and the associated gene expression programs.

47 is-regulatory elements to establish specific gene expression programs.

48 space over time and is guided by coordinated gene expression programs.

49 encing of transposable elements rewires host gene expression programs.

50 owing for the initiation of lineage specific gene expression programs.

51 tors are required to control tissue-specific gene expression programs.

52 iple chromosomes and to modulate large-scale gene expression programs.

53 of NFkappaB activity and shapes CpG-induced gene expression programs.

54 cell populations rely on cell type-specific gene expression programs.

55 inant role for Ezh2 in the downregulation of gene expression programs.

56 riptional coactivators to maintain oncogenic gene expression programs.

57 many are now integral components of cellular gene expression programs.

58 e correlation between IFN-beta and IFN-gamma gene expression programs.

59 or the chromatin landscape for cell-specific gene expression programs.

60 germline and somatic variants to tumorigenic gene expression programs.

61 MaSCs by activating distinct autoregulatory gene expression programs.

62 3K27me3) epigenetic marks to silence ectopic gene expression programs.

63 grates multiple inputs and coordinates broad gene expression programs.

64 n factors more broadly involved in erythroid gene expression programs.

65 DNA sequences is critical for activation of gene expression programs.

66 rs as primary determinants of stage-specific gene expression programs.

67 Cell identity is determined by its gene expression programs.

68 nes, leading to the suppression of oncogenic gene expression programs.

69 rinciples for stochastic, mutually exclusive gene expression programs.

70 omplexes to establish and maintain oncogenic gene expression programs.

71 nd RNA-binding proteins (RBPs) can influence gene expression programs.

72 lator that antagonizes T and B cell-specific gene expression programs.

73 re transcription factors that drive specific gene expression programs.

74 lance between proapoptotic and antiapoptotic gene expression programs.

75 kappaB and MAPK pathways allow dose-specific gene expression programs.

76 sible to preferentially induce four distinct gene expression programs.

77 hancer activity is important for controlling gene expression programs.

78 adaptive changes in cellular physiology and gene expression programs.

79 it chromatin machinery to activate oncogenic gene expression programs.

80 hromatin remodeling and regulate tumorigenic gene expression programs.

81 es residing in different organs have diverse gene-expression programs.

82 ions of IRF4 and IRF8 in regulating distinct gene-expression programs.

83 eristics, which are a reflection of distinct gene-expression programs.

84 y needs to be inhibited to make the PrE-like gene expression program accessible for activation by GAT

85 erations to the corresponding changes in the gene expression program across the cell cycle and in dif

86 ing next-generation sequencing to define the gene expression programs active in regeneration-permissi

87 appears to simply add to the tissue-specific gene expression programs already established in other ce

88 otypic outcomes and divergent alterations in gene expression programs among different tumors, despite

89 lation caused the loss of the BPDCN-specific gene expression program and apoptosis.

90 1 (Gfi1) orchestrates the fidelity of the DP gene expression program and developmental maturation int

91 nscription of a key set of genes within this gene expression program and might therefore be exception

92 oping can override a stringent developmental gene expression program and suggest a novel approach to

93 lar processes ensure timely execution of the gene expression program and survival under conditions of

94 sential for the complete shutdown of the ESC gene expression program and the transition to new cell s

95 of neurogenesis to fully repress the neural gene expression program and to promote glial gene expres

96 hy tumor-specific MYC levels induce specific gene expression programs and alter defined biological pr

97 genetic regulatory networks that orchestrate gene expression programs and direct cell fate decisions

98 Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic abili

99 CtBP modulates oncogenic gene expression programs and is an emerging drug target,

100 cessive activation and silencing of specific gene expression programs and is driven by tissue-specifi

101 ng protein, thereby mediating stage-specific gene expression programs and post-meiotic chromatin reor

102 eceptor family member signaling in postnatal gene expression programs and select ontogeny-specific ph

103 e the participation of HvVP1 in antagonistic gene expression programs and support its central role as

104 opmental stage-specific enhancers determines gene expression programs and temporal regulation of tran

105 redict enhancers that regulate cell-specific gene expression programs and the cell-to-cell variations

106 d requires characterizing cell-type-specific gene expression programs and their regulation during reg

107 omatin-remodeling SWI/SNF complex determines gene expression programs and, consequently, contributes

108 hat controlled an iNKT-cell lineage-specific gene-expression program and epigenetic landscape in a de

109 ctivated a major portion of the TEC-specific gene-expression program and suppressed the MPC-specific

110 n, regulation of an E2F-dependent cell-cycle gene expression program, and estrogen-dependent mitogeni

111 BAP1 and PBRM1 regulate seemingly different gene expression programs, and BAP1 loss was associated w

112 m of a regulatory switch controlling crucial gene expression programs, and provide a framework for un

113 y reversed reprogrammed chromatin, malignant gene expression programs, and tumorigenesis.

114 owever, the mechanisms driving such atypical gene expression programs are incompletely understood.

115 We find that while tissue-specific gene expression programs are largely conserved, alternat

116 cultures using nitrogen-limited chemostats, gene expression programs are strikingly similar regardle

117 or cyclin A2-CDK activity to restrict its IE gene expression program as a unique level of self-limita

118 transcription factor (TF) binding and global gene expression programs as multipotent cells differenti

119 d/or PMA on Jurkat T cells, we show that the gene expression program associated with activation of TC

120 is and is linked to a previously unexplained gene expression program associated with anti-PD-1 immuno

121 ion quantification ("3-seq") to discover the gene expression program associated with human photoaging

122 n brown adipose tissue controls antagonistic gene expression programs associated with energy balance

123 s HDACs and enhances histone acetylation and gene expression programs associated with memory and lear

124 therapeutic targets for modulating aberrant gene expression programs associated with MLL-fusion leuk

125 as cells enter G0, their survival and global gene expression programs become increasingly dependent o

126 these mRNA populations revealed the diverged gene expression programs between filial and maternal com

127 data provide molecular support for distinct gene expression programs between the AC-type SAMs of Sel

128 tazoan cells requires execution of different gene expression programs but recent single-cell transcri

129 KSHV replicates actively, via a controlled gene expression program, but can also remain latent.

130 is an ovarian cancer oncogene that regulates gene expression program by modulating HDAC activity.

131 dual roles for JMJD6 in promoting adipogenic gene expression program by post-transcriptional regulati

132 ated process that requires tightly regulated gene expression programmed by transcription factors and

133 Misregulation of these gene expression programs can cause a broad range of dise

134 Importantly, DNMT3A(R882H)-induced gene-expression programs can be repressed through Dot1l

135 the soluble nucleoplasmic pool over time as gene expression programs change during development or di

136 e in the establishment of cell-type specific gene expression programs characteristic of different cel

137 events is the acquisition of a mature T-cell gene expression program characterized by the induction o

138 es are driven by an evolutionarily conserved gene expression program comprising dozens of microRNAs a

139 s known to be important in the regulation of gene expression programs conferring cellular identities.

140 A comparison of the gene expression programs controlled by AG and the B func

141 lement other regulatory mechanisms to ensure gene expression programs controlling MG reprogramming ar

142 ncomitant loss of E2f3a normalized placental gene expression programs, corrected placental defects, a

143 reveal the existence of a unique herpesviral gene expression program corresponding to neither canonic

144 r calcium flux with activation of an anergic gene-expression program dependent on the transcription f

145 egulates developmentally and tissue-specific gene expression programs, disruption of which have been

146 factors ETS1 and ETS2 mediate activation of gene expression programs downstream of RAS/MAPK signalin

147 To characterize gene expression programs driving lineage choice, we sequ

148 rate that, rather than controlling essential gene expression programs, Drosophila JmjC proteins gener

149 n cancers, but how they influence the cancer gene expression program during cancer initiation and pro

150 We show that RUNX1 represses the erythroid gene expression program during megakaryocytic differenti

151 esults provide a global view of the changing gene expression program during this key period, defining

152 regulatory mechanism driving spatiotemporal gene expression programs during animal development.

153 essential for establishing lineage-specific gene expression programs during cell differentiation.

154 chromatin remodeling establishes coordinated gene expression programs during development, yet importa

155 ematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differenti

156 on of chromatin states is thought to control gene expression programs during lineage specification.

157 chanisms play a major role in the control of gene expression programs during normal development and a

158 n by different splicing factors to fine tune gene expression programs during these physiological and

159 le in orchestrating spatiotemporally precise gene-expression programs during development.

160 or post-translational modification to induce gene expression programs essential in tumorigenicity.

161 A highly orchestrated gene expression program establishes the properties that

162 rotein level but provide novel insights into gene expression programs expected to define different T

163 ch is thought to induce different downstream gene expression programs (Figure 1A).

164 rovide a powerful way to construct synthetic gene expression programs for a wide range of application

165 PRDM13 inhibits gene expression programs for excitatory neuronal lineage

166 nthetic systems, and the faculty to engineer gene expression programs from a minimal set of first pri

167 Following injury, keratinocytes switch gene expression programs from the one that promotes diff

168 at androgen-independent AR binding directs a gene expression program in CRPC, which is necessary for

169 n arrest, suggesting that the injury-related gene expression program in Dgcr8 cKOs cannot be attribut

170 ption factors (TFs) dominates control of the gene expression program in embryonic stem cells and othe

171 o-regulated genes, thereby altering the host gene expression program in favor of viral persistence.

172 eukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells.

173 Therefore, ETS1 regulates a broad gene expression program in NK cells that promotes target

174 ETS1 and ETS2 can regulate a cell migration gene expression program in opposite directions, and prov

175 emia that is strictly dependent on a defined gene expression program in the cell of origin, which inc

176 In contrast, the gene expression program in the deletion mutant of dosR,

177 dent mechanism to restrict the smooth muscle gene expression program in the developing mesothelium an

178 as important targets mediating p63-regulated gene expression program in the epidermis.

179 th in vivo and shifted the immunosuppressive gene expression program in tumor-associated macrophages

180 Overall, the metabolic gene expression program in tumors is similar to that in

181 -coding genes to maintain cell-type-specific gene expression programs in all human cells is a fundame

182 ptional regulators can orchestrate oncogenic gene expression programs in cancer.

183 environment required for proper execution of gene expression programs in differentiating KCs, and pro

184 Cell fate is established through coordinated gene expression programs in individual cells.

185 Preexisting gene expression programs in LSCs can be used to assess t

186 -binding proteins (RBPs) critically regulate gene expression programs in mammalian cells by modulatin

187 Thus, Rfx2 coordinates multiple, distinct gene expression programs in MCCs, regulating genes that

188 to elucidate the regulatory logic of global gene expression programs in mouse embryonic stem (ES) ce

189 sus H3K4) to differentially control specific gene expression programs in neurons.

190 ferentiate into macrophages and adopt unique gene expression programs in response to environmental cu

191 d as key regulatory molecules of immune cell gene expression programs in response to microbial and ti

192 omputational normalization to compare global gene expression programs in steady-state and dynamic con

193 site sampling frequency and impair critical gene expression programs in striatal neurons.

194 stinct Polycomb components in the control of gene expression programs in the disorders of epidermal d

195 croRNAs (miRNAs) are important regulators of gene expression programs in the pancreas; however, littl

196 tivation of CDK4 represses the gluconeogenic gene-expression program in vitro and in vivo.

197 incident with activation and differentiation gene-expression programs in a cell-division-dependent ma

198 We found here that Hes1 constrained myeloid gene-expression programs in T cell progenitor cells, as

199 h Th1 and Th17 cells, but also have a unique gene expression program, including genes associated with

200 g cells abrogated the cell of origin-derived gene expression program, including the expression of Hox

201 ion by partially restoring the EGFR-promoted gene expression program, including the sustained express

202 egulation of cell differentiation-associated gene expression programs, including an accessibility of

203 7 signaling in AML cells activates stem cell gene expression programs, including the Wnt pathway, and

204 ed upon inhibition, resulting in an abnormal gene expression program influencing the glial lineage.

205 sence of a transcriptional partner induces a gene expression program involved in T cell exhaustion.

206 hare core aspects of a memory cell precursor gene expression program involving Bcl6, and a strong rel

207 Additionally, expression of a novel gene expression program involving sonic hedgehog (Shh),

208 es revealed that a rapidly-induced antiviral gene expression program is active against disparate huma

209 This gene expression program is dependent on the disruptor of

210 epression of pre-existing ES cell-associated gene expression program is followed by activation of TS

211 Dysregulation of the normal gene expression program is the cause of a broad range of

212 y wounding, indicating that a common initial gene expression program is triggered regardless of missi

213 Epigenetic control of gene expression programs is essential for normal organis

214 together, induction of liver STAT3-dependent gene expression programs is essential to countering the

215 An outstanding issue in understanding T cell gene expression programs is whether RUNX1 and ETS1 have

216 els in adulthood, with particular focus on a gene expression program known as the conserved transcrip

217 other transcription factors involved in seed gene expression programs, like BPBF.

218 During latent infection, a restricted gene expression program limits immune targeting and cis-

219 atin structure play a role in regulating the gene expression program linked to memory formation.

220 Blocking Snail and/or its associated gene expression program may provide an additional tool t

221 Thus, FOXC2 or its associated gene expression program may provide an effective target

222 iversity is governed in part by differential gene expression programs mediated by transcription facto

223 ve to other genes, suggesting how changes in gene expression programs might be accomplished during de

224 Disease development involves a gene expression program mimicking virus-induced diabetes

225 anisms by which SOX10 guides the appropriate gene expression programs necessary to promote the melano

226 n to repress the ability of HSF1 to activate gene-expression programs necessary for cancer survival.

227 differentiation- and development-associated gene expression program of ESCs.

228 melanoma cells become pigmented and enact a gene expression program of melanocyte differentiation.

229 To gain deeper insight into the gene expression program of murine HSCs, we combined sing

230 Activation induces extensive changes in the gene expression program of naive CD4(+) T cells, promoti

231 and recruit Mediator to activate much of the gene expression program of pluripotent embryonic stem ce

232 erations to the corresponding changes in the gene expression program of these malignant cancer cells.

233 Correct gene expression programming of the cardiomyocyte underli

234 ional activators, concurrently activates the gene expression programs of several domains.

235 vide the structural framework for the global gene expression programs of the individual chromosomes.

236 neage priming, activation, and repression of gene expression programs) provides insight into fundamen

237 Here, we identify the gene expression program regulated by FoxP1 in both human

238 Thus, the ETS/AP-1 sequence defines a unique gene expression program regulated by the relative levels

239 Pathway analysis revealed that gene expression programs regulated by synovial fibroblas

240 ZFP36L1 controlled a gene-expression program related to signaling, cell adhes

241 find that these organoid cortical cells use gene expression programs remarkably similar to those of

242 Disruption of the intricate gene expression program represents one of major driving

243 unter environmental stresses that regulate a gene expression program required for adaptation and surv

244 anglia periodically reactivate, initiating a gene expression program required for productive replicat

245 Gene expression programs required for differentiation de

246 s from which CSB is depleted show defects in gene expression programs required for neuronal different

247 LXR-cofactor complexes activate the gene expression program responsible for cholesterol effl

248 a fusion oncoprotein that drives an aberrant gene expression program responsible for the development

249 How the meiotic gene expression program temporally restricts kinetochore

250 Unfolding of the gene expression program that converts precursor cells to

251 that ES7c is cleaved at early stages of the gene expression program that enables cells to successful

252 ed to fully initiate an interferon-regulated gene expression program that included the Irf8 target ge

253 -modified germline transcripts to maintain a gene expression program that is conducive for progressio

254 Alk1 signaling to promote a flow-responsive gene expression program that limits nascent arterial cal

255 strate that FOXO3A is critical to maintain a gene expression program that poises HSCs for rapid induc

256 Notch induces a broad antiapoptotic gene expression program that protects against intrinsic,

257 The gene expression program that results from FOXA1 overexpr

258 These results highlight specific cellular gene expression programs that are responsive to distinct

259 ver, the roles for alpha3beta1 in regulating gene expression programs that control the behaviors of i

260 However, the gene expression programs that depend upon sustained MYC

261 suggest that LIN28 may regulate splicing and gene expression programs that drive breast cancer subtyp

262 ernative splicing (AS) is a key component of gene expression programs that drive cellular differentia

263 matopoietic stem cells (HSCs) possess unique gene expression programs that enforce their identity and

264 The gene expression programs that establish and maintain spe

265 The p53 transcription factor modulates gene expression programs that induce cell cycle arrest,

266 se distinct cell fates are driven by massive gene expression programs that promote the necessary chan

267 DNA methylation and histone modifications on gene expression programs that promote this malignancy.

268 Gene expression programs that regulate the abundance of

269 specific properties are encoded by selective gene expression programs that shape molecular repertoire

270 erentiation is driven by the reactivation of gene expression programs that share many characteristics

271 However, the gene expression programs that stabilize blood vessels ar

272 Heritable epigenetic mechanisms then lock in gene-expression programs that define lineage identity.

273 allel, activation initiates context-specific gene-expression programs that drive effector functions a

274 Neuronal gene expression programs therefore fall into two fundame

275 ption factors are essential for implementing gene expression programs, they do not function in isolat

276 1 plays a role in transmitting hematopoietic gene expression programs through mitosis when transcript

277 knowledge of how transcription factors drive gene expression programs through their interactions with

278 nvironmental signals with activation-induced gene-expression programs through modulation of the epige

279 distinct and specific roles in regulation of gene-expression programs throughout postnatal developmen

280 required to fully execute the rpoS-dependent gene expression program to allow E. coli to adapt to sus

281 ivates an elaborate and tightly orchestrated gene expression program to induce critical antimicrobial

282 Gene expression programs undergo constant regulation to

283 histone H1 dynamics for the establishment of gene expression programs underlying cerebellar morphogen

284 chromatin remodeling activities to regulate gene expression programs underlying cIN development.

285 has the potential to foster precision in the gene expression programs underlying development.

286 ome analysis indicated that Tsc1 coordinated gene expression programs underlying immune function, tra

287 amily of transcription factors that regulate gene expression programs underlying key immunological pr

288 that Dgcr8 is responsible for modulation of gene expression programs underlying myelin formation and

289 icroenvironment to generate lineage-specific gene expression programs upon differentiation.

290 is required in ESCs to initiate appropriate gene expression programs upon somatic multi-lineage diff

291 g sites, while a common macrophage-adipocyte gene expression program was retained.

292 f identifying new regulators of this massive gene expression program, we have used a GFP-based protei

293 bsynaptic muscle nuclei with their selective gene expression programs were all reduced.

294 hy AC has a highly expressed skeletal muscle gene expression program, which is switched off during ma

295 cytes exhibited a predominantly latent viral gene expression program with some lytic or abortive repl

296 onal regulatory modules (TRMs) that regulate gene expression programs with spatiotemporal specificity

297 that AC chondrocytes share a high-abundance gene-expression program with skeletal muscle.

298 hanistically distinct, senescence-associated gene expression programs, with altered expression of dis

299 a recently discovered feature of eukaryotic gene expression programs, yet its function remains large

300 post-mitotic cell transitions and modulates gene expression programs, yet the mechanisms are poorly