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1 on, including extremely widespread noncoding transcription.
2 view is that they can initiate bidirectional transcription.
3 t that predicted the initial wave of zygotic transcription.
4 tains an AD required for Rap1-dependent gene transcription.
5 breast cancer resistance protein (BCRP) gene transcription.
6 hesis as well as c-di-GMP-induced stalk gene transcription.
7 uence the pause-initiation limit to regulate transcription.
8 sis, and regulation of apoptosis and nuclear transcription.
9 cks repressor complexes to enable viral gene transcription.
10 by epigenetically activating Wnt target gene transcription.
11 aling via signal transducer and activator of transcription.
12 ating a positive feedback loop that sustains transcription.
13 o an intricate relationship between DSBs and transcription.
14 ivators contribute to the regulation of CCC1 transcription.
15 increased levels of sigma(F) -directed gene transcription.
16 sion, often mediated by global regulators of transcription.
17 activating H3K4-trimethyl marks promoting AR transcription.
18 single sigma factor to regulate chloroplast transcription.
19 o reveal the heterogeneity in IL-4-induced I transcription.
20 in, is critical for the eventual recovery of transcription.
21 level that cannot support productive reverse transcription.
22 hanges in chromatin states alter kinetics of transcription.
24 Jak2 and signal transducer and activator of transcription 3 phosphorylation and the expression of do
25 increased signal transducer and activator of transcription 3 phosphorylation, reduced IL-2 production
26 diated by signal transducer and activator of transcription 3 through an IL-23/acutely transforming re
27 sting platform relies on a defined exogenous transcription activator capable of binding a unique reco
29 ty map of promoters and enhancers, revealing transcription-activity-linked genomic interactions in th
31 inding of the repressor factor RE1-silencing transcription (also known as neuron-restrictive silencer
32 he oocyte-to-embryo transition by activating transcription, altering protein-coding sequences, produc
33 portance of RALY as an indirect regulator of transcription and cell cycle progression through the reg
34 bpA, show the effects of RbpA truncations on transcription and cell physiology, and indicate addition
35 crucial for cell identity by enhancing both transcription and Drosha/DGCR8-mediated primary miRNA (p
36 ons of genes is negatively regulated by gene transcription and may be modified by early-life experien
37 alpha (TNFalpha) selectively reduces BMPR-II transcription and mediates post-translational BMPR-II cl
40 rors the rapid and dynamic induction of DLL4 transcription and that this pathway is required for DLL4
43 remodeling complex is required for oncogenic transcription and tumor growth in non-small-cell lung ca
44 emonstrate a key role for HDAC1 in PU.1 gene transcription and, more importantly, uncover a novel mec
46 in modifications associated with euchromatic transcription, and couple RNAi-mediated transcript degra
49 either significantly increase T-box-mediated transcription antitermination, while other compounds cou
53 nase A pathway is potently inducing IL-1beta transcription, as well as boosting the ability of LPS to
55 segments, Rad21 or SMC3 (cohesin components),transcription at transcription start sites (TSS), and th
56 gulation such as the "hit-and-run" model and transcription bursting that could not be obtained by in
57 s, which resulted in a minimal impact on MYC transcription, but did not result in a statistically sig
58 histone phosphorylation, in turn, regulates transcription by attenuating the effect of local arginin
60 sults suggest that CTCF promotes HSV-1 lytic transcription by facilitating the elongation of RNA Pol
61 nique strategy for selectively targeting MYC transcription by pharmacological means as a potential tr
65 FOXO has been shown to interact with diverse transcription co-factors and integrate signals from mult
68 tween patients in XP subgroups with impaired transcription coupled nucleotide excision repair (TC-NER
69 ensatory roles for global-genome (XPC-1) and transcription-coupled (CSB-1) NER in ICL sensing were ex
71 repeat-encoding RNA (TERRA), but the role of transcription, CTCF, and TERRA in telomere replication i
72 suggest that in the absence of conventional transcription cycles, RBCs maintain a circadian rhythm i
75 as new regions of the genome become open for transcription during terminal differentiation, blocking
77 We found that several components of the PAF1 transcription elongation complex contribute to Chd1 recr
78 and CRISPR loci, Spt4/5 is recruited to the transcription elongation complex during early elongation
80 dition to serving as a histone chaperone and transcription elongation factor, Spt6 counteracts repres
81 ate of nascent transcripts is coordinated by transcription elongation factors (TEFs) such as polymera
84 cing expression of microphthalmia-associated transcription factor (MITF), and subsequent reductions i
87 cer associate domain (TEAD) and runt-related transcription factor 2 (RUNX2) transcription factors, re
90 ndently, and then simultaneously, mutating a transcription factor and the associated promoter it repr
92 rosophila, graded expression of the maternal transcription factor Bicoid (Bcd) provides positional in
93 attempted to determine the interplay between transcription factor binding motif evolution and GRN top
94 s by temporal expression pattern, identified transcription factor binding motifs enriched in each clu
96 on self-organizing maps with sequence-based transcription factor binding prediction led to the ident
97 < 1e-05) CpGs are significantly enriched for transcription factor binding sites of EBF1, EP300, and C
98 d a structure-based method for prediction of transcription factor binding sites using an integrative
99 of this fragment by promoting serum response transcription factor binding to a cryptic cis-element.
100 enriched for histone-tail modifications and transcription factor binding with particular relevance f
101 indings demonstrate that during evolution, a transcription factor can act through multiple mechanisms
105 functions are transcriptionally regulated by transcription factor EB (TFEB) through the induction of
106 aloric restriction, is known to activate the transcription factor EB (TFEB), a master regulator of li
107 ranslocation of the lysosomal stress-sensing transcription factor EB and, eventually, cell death.
109 ate lymphoid cells (ILC2) share cytokine and transcription factor expression with CD4(+) Th2 cells, b
112 els promote the expression of the promitotic transcription factor FOXM1 (Forkhead box protein M1).
113 nodes in the metabolic network, the forkhead transcription factor FOXO has been shown to interact wit
114 suppress the induction of expression of the transcription factor Foxp3 in T cells, trans-presentatio
115 of structural variants, as they affect more transcription factor hubs in the tissue-specific network
116 cer located upstream of HLX (which encodes a transcription factor implicated in sprouting angiogenesi
117 Thus, two enhancers integrate combinatorial transcription factor input, feedback and redundancy to g
123 ver-enriched, endoplasmic reticulum-tethered transcription factor known to regulate the hepatic acute
124 -fructose diet in mice and that loss of this transcription factor leads to hepatic inflammation and e
125 nge from changes in protein conformation and transcription factor localization to chromosome reorgani
127 caused by mutations in the gene encoding the transcription factor Methyl CpG Binding Protein 2 (MECP2
129 contained the gene microphthalmia-associated transcription factor Mitf that has previously been assoc
130 e the Arabidopsis thaliana SG2-type R2R3-MYB transcription factor MYB15 as a regulator of defense-ind
131 NAc-modified proteins at the promoter of the transcription factor MYBL1, which was also characterized
132 owed that Tnc expression is repressed by the transcription factor Nkx2-1, a well-established suppress
133 lved in neural differentiation, and that the transcription factor OLIG2 is a central node in the affe
135 sed auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (P
136 Regulatory networks that include the Gata2 transcription factor play central roles in hematopoietic
138 rtly by intercellular communication, and the transcription factor PqsR is a necessary component in th
139 We now show that the homeodomain-containing transcription factor Prep1 is a repressor of adipogenic
140 At the 1q24 locus, we hypothesized that the transcription factor PRRX1 could be a strong candidate g
141 ecies Arabidopsis thaliana, the AP2-type AP2 transcription factor represents a major A-function prote
150 ing framework, we identify EOR-1 as a unique transcription factor that may regulate chromatin dynamic
151 YTOCHROME INTERACTING FACTOR 4 (PIF4), a key transcription factor that promotes hypocotyl growth.
152 this study, we describe the dual role of the transcription factor Xylanase promoter binding protein 1
155 vestigated whether variation in binding of a transcription factor, the vitamin D receptor (VDR), whos
156 ion of the SAM pointed domain-containing ETS transcription factor, which contributes to goblet cell h
157 eceptor (ADORA2A) promotes hypoxia-inducible transcription factor-1 (HIF-1)-dependent endothelial cel
159 lly through mechanisms other than changes in transcription factor-binding sites that drive patterning
160 variants, of which at least six (35%) alter transcription factor-DNA binding in neuroblastoma cells.
165 ion by increasing expression of two cellular transcription factors (KLF4 and BLIMP1) which cooperativ
166 criptional dysregulation induced by aberrant transcription factors (TF) is a key feature of cancer, b
168 ith the adipogenic cocktail, which activates transcription factors (TFs) glucocorticoid receptor (GR)
169 Characterizing the binding specificities of transcription factors (TFs) is crucial to the study of g
173 are cognate binding sites for the identified transcription factors and are necessary and sufficient f
174 cells expressed reduced levels of B-lineage transcription factors and B cell receptor (BCR)/pre-BCR-
175 me-wide functional screen to interrogate the transcription factors and cofactors in thermogenic gene
177 ) cell functional subsets are defined by key transcription factors and output of cytokines, such as I
178 underlying redox-regulation of AP-1 Fos/Jun transcription factors and provide structural insight for
179 lterations in the RB-regulated E2F family of transcription factors are infrequent, casting doubt on a
181 PSC-CMs) were transduced with the neurogenic transcription factors Brn2, Ascl1, Myt1l and NeuroD.
182 egulatory Factor (MyRF) is one of the master transcription factors controlling myelin formation and d
183 ctor 1 (EBF1) and paired box 5, two critical transcription factors directing B cell lineage specifica
184 ntification and characterization of 175 bHLH transcription factors from apple (Malus x domestica).
185 in vitro Furthermore, SRC-2 coactivated the transcription factors GATA-binding protein 4 (GATA-4) an
186 xperiments revealed a critical role for FOXO transcription factors in mediating these proliferative v
188 the present work we examine three dimers of transcription factors in the NFkappaB family: p50p50, p5
189 tly targeted Smad4, Hif1a, and Rora, all key transcription factors in the Th17 cell gene-expression p
190 ptual framework for how different classes of transcription factors interact to select and activate re
191 that the differentiation-dependent cellular transcription factors KLF4 and BLIMP1 induce lytic EBV r
193 e, the phosphate starvation (PHO) responsive transcription factors Pho4 and Pho2 are required for gen
197 creted proteins controlled by a group of MYB transcription factors that are required for sperm releas
198 and promoters, which is mediated by pioneer transcription factors that recruit activating chromatin
199 iral proteins EBNA3A, EBNA3B, and EBNA3C are transcription factors that regulate a multitude of cellu
200 istinguishing features such as gene sets and transcription factors that show different activities amo
201 YTOCHROME INTERACTING FACTOR (PIF) family of transcription factors which have been shown to be involv
202 min A, acts as a ligand for nuclear receptor transcription factors with more than 500 known target ge
203 ulation of two basic helix-loop-helix (bHLH) transcription factors with predicted effector binding el
204 swap-minus (dsm) mutations are functional as transcription factors yet are defective in replication o
205 cosanoid-forming enzymes as well as relevant transcription factors, allowing us to better understand
206 f p38 and JNK, phosphorylation of downstream transcription factors, and overexpression of IFN-beta mR
207 periments on cells depleted for the Forkhead transcription factors, Fkh1 and Fkh2, previously associa
208 tors of gene expression, including other AP2 transcription factors, histone-modifying enzymes, and re
209 andidate genes, including cell type-specific transcription factors, neurotransmitter-synthesizing enz
210 rrelated with the expression of multiple ETS transcription factors, particularly in SDHD promoter wil
212 reduced expression of Th1 and Th2 associated transcription factors, Tbet and GATA3, and reduced produ
213 with non-sex-specific terminal selector-type transcription factors, whereas the sex specificity of dm
220 ot activate interferon-stimulated gene (ISG) transcription following treatment with the noncanonical
221 ification for DNase-seq, analysis of nascent transcription from Global-Run On (GRO-seq) data, and cha
222 tly, HMBA has also been shown to trigger HIV transcription from latently infected cells, via a CDK9/H
224 ed viral-mediated gene transfer to block the transcription function of CREB, SRF, and MEF2 in the vis
226 eeper understanding of the evolution of gene transcription in and between plant species, we performed
230 ar barrier function through a non-canonical, transcription-independent signalling mechanism that driv
235 RNA sequencing confirmed that Hh-mediated transcription is increased in B-lineage cells from Gli3-
236 an be rapidly suppressed by IL-10 even after transcription is initiated, and this is associated with
238 ct of genetic variation on the regulation of transcription, isoform usage, and allele-specific expres
239 lts show that TCF19 interacts with an active transcription mark and recruits a co-repressor complex t
240 regulation raises the intriguing notion that transcription of an mRNA, despite carrying a canonical c
241 nstrated that mTORC1-S6K1 signaling controls transcription of CHK1 via Rb-E2F by upregulating cyclin
242 Additionally, we observed an increase in transcription of dipeptidylpeptidase 4, as well as a pla
243 The epigenetic mechanisms that (dys)regulate transcription of Dlg4/PSD95, or other plasticity genes,
245 gatively affects its ability to activate the transcription of downstream genes and promote cell proli
246 r, arising from a mutation that disrupts the transcription of Fragile X Mental Retardation Protein (F
248 radient is established in response to graded transcription of glycolytic enzymes downstream of fibrob
249 3 and BR signaling converge to influence the transcription of hypocotyl growth-promoting SAUR19 subfa
253 ufC and sufD (sufD*), resulting in decreased transcription of sufSUB Consistent with the transcriptio
255 for > 94% of all transcripts, with increased transcription of the entire locus driving Flt1 upregulat
258 and Mus musculus) showed a human-like mtDNA transcription pattern, the invertebrate pattern (Drosoph
260 early changes in HCV-specific CD8(+) T cell transcription preceded the overt establishment of T cell
261 its human tRNA(Lys3) to serve as the reverse transcription primer via an interaction between lysyl-tR
262 thesis.IMPORTANCE The fates of HIV-1 reverse transcription products within infected cells are not wel
263 ng are largely independent of alterations in transcription rate during the early stages of stress res
265 support grows for the notion that the act of transcription rather than the RNA product itself is func
266 transcript isoforms with opposite effects on transcription recovery after UV-induced DNA damage.
267 understanding of the molecular mechanism of transcription regulation on cellular stress and reveal f
270 tified locations of elongation complexes and transcription-repair coupling events in genes throughout
271 s that encode the E2 protein, which controls transcription, replication, and genome maintenance in in
273 es advantage of characteristic bidirectional transcription signatures at active TSSs in GRO/PRO-seq d
274 arly elongation within 500 base pairs of the transcription start site and akin to its bacterial homol
276 r SMC3 (cohesin components),transcription at transcription start sites (TSS), and the number of CCCTC
277 's enrichment or biased distribution towards transcription start sites in the promoters of co-express
278 ongly enriched in repressed regions and near transcription start sites, whereas the genetically regul
280 of HMGA1 to stimulate beta-catenin-dependent transcription, suggesting that interactions between ORF2
281 eletion resulted in additive effects on CCC1 transcription, suggesting that other activators contribu
282 -catenin signaling elicits context-dependent transcription switches that determine normal development
283 studied nuclear, bacterial, or bacteriophage transcription systems but that similarities are found on
284 Here we report that PTCL are sensitive to transcription-targeting drugs, and, in particular, to TH
287 e recruitment of FACT (facilitates chromatin transcription that enhances the engagement of Pol II int
288 identified for their role in modulating CREB transcription, the past 5 years has seen an expansion in
289 ogen receptor alpha (ERalpha) regulates gene transcription through two activation functions (ERalpha-
291 f cancer cell identity and promote oncogenic transcription to which cancer cells become highly addict
294 transcription start site on the majority of transcription units, while on a subset of genes, includi
295 ction in CLL cells, stimulating PKCbeta gene transcription via increased association of SP1 and decre
297 ntrol pancreatic and beta-cell type-specific transcription, which are found within areas I (bp -2694
298 ed nucleotide is incorporated during reverse transcription, which greatly facilitates the protocol by
299 anscriptional chromatin modifications during transcription, which is affected by the strength of hist
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