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1 , whereas miR-294 suppresses, the phasing of cell cycle genes.
2 ctors to discriminate cell cycle against non-cell cycle genes.
3 ll cycle by controlling the transcription of cell cycle genes.
4 s characterized by the altered regulation of cell cycle genes.
5 BrdU uptake in vivo and actively transcribed cell cycle genes.
6 rm cells through translational regulation of cell cycle genes.
7 and does not govern expression of canonical cell cycle genes.
8 ing E2F1 binding to the promoters of various cell cycle genes.
9 ntiation and activation of pro-proliferative cell cycle genes.
10 tion, as well as E2F-dependent expression of cell cycle genes.
11 feration by coordinately regulating numerous cell cycle genes.
12 ption factors, reversing their repression of cell cycle genes.
13 ic coregulator complexes to the promoters of cell cycle genes.
14 l mechanism by which nuclear IRS-1 activates cell cycle genes.
15 sion presumably through the control of early cell cycle genes.
16 and represses transcription of E2F-regulated cell cycle genes.
17 modulating the periodic expression of early cell cycle genes.
18 of expression exhibited by these three G(1) cell cycle genes.
19 on of at least a subset of pro-proliferative cell cycle genes.
20 ation of PKC and modulation of cell survival/cell cycle genes.
21 ion and mitosis by stimulating expression of cell cycle genes.
22 eins required for transcription of essential cell cycle genes.
23 a direct role for brlA in the regulation of cell cycle genes.
24 tations in cyclin A, string (cdc25), and new cell cycle genes.
25 minant inhibitory effect on transcription of cell cycle genes.
26 into activator and repressor E2Fs, regulates cell cycle genes.
27 al network able to control the expression of cell cycle genes.
28 e full function of NF-Y in activation of the cell cycle genes.
29 in MYC binding to the promoters of selected cell cycle genes.
30 are underrepresented in both early and late cell cycle genes.
31 t role in transcriptional regulation of late cell cycle genes.
32 inger (ZF) transcriptional regulator of many cell cycle genes.
33 ents have several limitations in identifying cell cycle genes.
34 endent repression of important E2F-dependent cell-cycle genes.
35 sitory surge of pro-apoptotic components and cell-cycle genes.
36 lf-renewal, such as stem cell fate genes and cell-cycle genes.
37 ted to the expression of immune response and cell-cycle genes.
38 feration with concomitant modulation of some cell cycle genes, (2) augmented the NRF2-mediated antiox
39 ession pattern almost entirely consisting of cell cycle genes (5-year odds ratio of metastasis, 24.0;
41 fter RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MI
42 nhibitor CR8 after SCI significantly reduced cell cycle gene and protein expression, microglial activ
44 e abnormalities, we observe dysregulation of cell cycle genes and increased apoptosis in neural crest
45 enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low bin
46 hylase PHF8 transcriptionally regulates many cell cycle genes and is therefore predicted to play key
47 pression analysis reveals a dysregulation of cell cycle genes and markers of differentiation in the C
48 l pro-tumorigenic genetic programs including cell cycle genes and Myc-regulated genes before the indu
50 oral expression of fliQ, ccrM, and other key cell cycle genes and ultimately the regulation of the ce
51 F2A or -D also resulted in the activation of cell-cycle genes and down-regulation of markers of termi
52 nalysis demonstrated that miR-34a suppresses cell-cycle genes and induces several neural-related gene
54 pression was associated with upregulation of cell-cycling genes and co-downregulation of genes implic
55 nd the cis- motif features are predictive of cell cycle genes, and a combination of the two types of
56 BR pathway, does not have a direct effect on cell cycle genes, and promoter analysis suggests a disti
57 H is required for the expression of multiple cell cycle genes, and the gene expression signature resu
58 ion and margins are associated with the late cell-cycle genes, and a metagene that represents the EGF
59 ed cell proliferation, altered expression of cell-cycle genes, and decreased amounts of nuclear, but
60 ave altered expression of a select number of cell-cycle genes, and we identified the mRNA of cyclin-d
62 e sequencing has revealed many C. crescentus cell cycle genes are conserved in other Alphaproteobacte
66 analysis of p53-dependent repression of the cell cycle genes B-MYB (MYBL2), BUB1, CCNA2, CCNB1, CHEK
67 opose a computational model to predict human cell cycle genes based on transcription factor (TF) bind
69 ough inhibition of neointimal hyperplasia by cell cycle gene blockade therapy results in improved end
71 x controls cellular quiescence by repressing cell cycle genes, but its mechanism of action is poorly
72 -LIP releases E2F.Rb-dependent repression of cell cycle genes by a disruption of E2F1.Rb complexes an
73 WT1 proteins facilitate expression of these cell cycle genes by antagonizing transcriptional repress
74 hat Rb can actively repress transcription of cell cycle genes by binding and inactivating transcripti
76 keletal genes keratin-18 and beta-actin, the cell cycle gene C-MOS, and housekeeping genes GAPDH and
77 Subsequent to its activation, hundreds of cell-cycle genes can then be expressed, including the cy
78 pathways by up-regulating the expression of cell cycle genes cdc2, PRC1 and PCNA, and the transcript
80 gene Nkx 3.1, the AR coactivator ARA-70, and cell cycle genes Cdk1 and Cdk2 were androgen regulated i
83 hose expression was altered by GLI1 included cell cycle genes, cell adhesion genes, signal transducti
85 es the detection of previously characterized cell-cycle genes compared to approaches that do not acco
86 d by AGN194,204 required PPARalpha including cell-cycle genes, consistent with AGN-induced hepatocyte
87 can also repress transcription of endogenous cell cycle genes containing E2F sites through recruitmen
88 ed cytokines and the downregulation of tumor cell-cycle genes correlated with NCR2 expression and gre
89 strate that FoxM1 regulates transcription of cell cycle genes critical for progression into S-phase a
91 , the auxin transporter PIN-FORMED1, and the cell cycle genes CYCLIN A2;1 and PROLIFERATING CELL NUCL
92 Expression of NF-YA1 and the G2/M transition cell cycle genes Cyclin B and Cell Division Cycle2 was r
96 odulation of the beta-catenin/TCF responsive cell cycle genes, cyclin D1 and p21, we inhibited beta-c
97 dimerizing partner, DP1 and E2F-upregulated cell cycle genes (cyclins E, A, B and D3) and enhanced t
99 MOS1 and TCP15 both affect the expression of cell-cycle genes D-type CYCLIN 3;1 (CYCD3;1), which may
100 -phase TFs decreases expression of many late cell cycle genes, delays mitotic progression, and reduce
102 olled in Total Therapy II, overexpression of cell cycle genes distinguished CA from no CA, especially
103 sing antisense oligodeoxynucleotides against cell cycle genes, double-stranded oligodeoxynucleotides
110 rtaken a genome-wide characterization of the cell cycle genes encoded by Chlamydomonas reinhardtii, a
111 Our studies demonstrate that two other G(1) cell cycle genes, encoding cyclin D and CDK4/6, have sim
112 of RNA processing, chromatin remodeling and cell-cycle genes enriched for promoter binding by Chd8,
113 transcription factor regulates expression of cell cycle genes essential for DNA replication and mitos
114 ident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA repl
116 tions, irrespective of type, associates with cell cycle gene expression and adverse outcome, whereas
117 lysine 14 (H3K14ac) and is required for key cell cycle gene expression and cancer cell proliferation
118 chanism for E2F factors in the regulation of cell cycle gene expression and cell cycle progression un
119 n recruiting B-Myb and FoxM1 to promote late cell cycle gene expression and in regulating cell cycle
120 ors required for DNA replication, while late cell cycle gene expression begins during G2 to prepare f
121 by clustering the yeast genes based on their cell cycle gene expression data and the human genes base
123 y, an application of our method to different cell cycle gene expression datasets suggests that our me
124 cell cycle gene expression and in regulating cell cycle gene expression from quiescence through mitos
125 with the importance of stromal response and cell cycle gene expression in colon tumor recurrence.
126 he effect of all-trans-retinoic acid (RA) on cell cycle gene expression in RA sensitive CA-OV3 and RA
130 analysis was used to determine how the yeast cell cycle gene expression program is regulated by each
131 signaling on progenitor cell regulation and cell cycle gene expression, and loss of epithelial Pygo2
132 ative assay integrating stromal response and cell cycle gene expression, in tumor specimens from pati
133 F1R, appears to have an amplifying effect on cell cycle gene expression, thus providing a molecular e
134 plex remains bound to FoxM1 during peak late cell cycle gene expression, while B-Myb binding is lost
137 ellular and physiologic processes, including cell cycle, gene expression, cell viability, stress resp
138 sion patterns resulting from manipulation of cell-cycle gene expression alter the physiology of the o
140 d alpha6(hi)beta1(hi)CD34(hi) CSCs differ in cell-cycle gene expression and proliferation characteris
141 s on two public datasets: the Stanford yeast cell-cycle gene expression data, and a gene expression d
143 o determine whether the observed patterns in cell-cycle gene expression in Clock mutants resulted in
144 low-error-rate classification for both yeast cell-cycle gene expression profiles and Dictyostelium ce
145 roliferation, regulation of an E2F-dependent cell-cycle gene expression program, and estrogen-depende
154 ession profiling studies suggested that core cell-cycle genes functioning during the G1/S, S, and G2/
155 ell cycle-dependent elements (CDEs), and one cell cycle gene homology region (CHR), typically found i
156 ical, Sp1-like, cell cycle-dependent element/cell cycle gene homology region, and p53-binding sites.
160 ified CDE-CHR (Cell cycle-Dependent Elements-Cell cycle genes Homology Region) region of cyclin A pro
161 uencing in mouse and rat OPCs, we identified cell cycle genes (i.e., Cdc2) and chromatin components (
165 ssociated with significant downregulation of cell cycle genes in both OE21 (P<0.0001) and OE33 (P=0.0
167 To explore the mechanism of repression of cell cycle genes in cervical carcinoma cells following E
168 n contrast, expression was lower in 40 of 44 cell cycle genes in eNOS-KO mice, in association with im
172 rofluidic device, we tracked the dynamics of cell cycle genes in single yeast with subminute exposure
173 the expression of several growth factors and cell cycle genes in the aromatase transgenic mammary gla
174 in transcript abundance of cell division and cell cycle genes in the drought-stressed ovary only.
176 rough transcriptional regulation of specific cell-cycle genes in a cell-type- and developmental-stage
177 nt cells, AR selectively upregulates M-phase cell-cycle genes in androgen-independent cells, includin
180 ing genes, there was increased expression of cell cycle genes including an A-type cyclin and a subuni
181 ma cells in the levels of expression of many cell cycle genes including cyclin A, B and E, cdk 2,4 an
182 -195 regulates the expression of a number of cell cycle genes, including checkpoint kinase 1 (Chek1),
183 88 target the upstream regions especially of cell cycle genes, including cyclins, cyclin-dependent ki
184 nfection results in dysregulation of several cell cycle genes, including inhibition of cyclin A trans
185 amming in this setting activated a subset of cell-cycle genes, including CENPE, a centromere binding
187 ered expression of developmental factors and cell cycle genes is associated with a higher degree of e
191 ndividual REST target ribosome biogenesis or cell cycle genes is sufficient to induce activation of Q
192 t increase and the expression of an array of cell cycle genes is virtually unchanged in Dp1-deficient
193 t while Chd8 stimulates the transcription of cell cycle genes, it also precludes the induction of neu
194 revealed downregulation of ion transport and cell cycle genes, leading to altered calcium handling an
195 arly G2 had increased RNA levels, while core cell cycle genes linked to early G1 and late G2 had redu
196 selectively regulating H3K9 demethylation at cell cycle gene loci, thereby representing a key player
198 LL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression o
200 ne expression studies point to regulation of cell cycle genes, muscle myosins, NotchR and Wnt pathway
202 he KEN box as a template, we have identified cell cycle genes Nek2 and B99 as additional Cdh1-APC sub
205 is encoded within the promoter region of the cell cycle gene POLR3D in the antisense orientation.
206 ow broadly CMV alters the regulation of host cell cycle gene products and highlight the establishment
207 immortalized rat-1 fibroblasts by monitoring cell-cycle gene promoter-driven luciferase activity.
208 kdown, p107 compensated for p130 loss at all cell cycle gene promoters examined, allowing cells to re
209 r the DREAM complex finds that a set of core cell cycle genes regulated in both U2OS and HeLa cells a
212 is critical for regulating the expression of cell cycle genes required for hepatocyte proliferation.
215 hanges in alternative polyadenylation (APA), cell cycle genes showed mostly alternative splicing (AS)
216 gous neonatal hearts identified a network of cell cycle genes significantly up-regulated and down-reg
217 nd that, rapidly after BET displacement, key cell-cycle genes (SKP2, ERK1, and c-MYC) were downregula
219 inhibited the E2-induced expression of early cell cycle genes such as cyclins D1, D3, E1, E2, and B2.
220 ding p38 MAPK-regulated or ERK-1/2-regulated cell-cycle genes such as FOS, MAPK8, MYC, various cyclin
223 er many cells), some, but not all, canonical cell cycle genes tend to be co-expressed in groups in si
226 right ventricle, and we identified numerous cell cycle genes that are dependent on Gata4 by microarr
227 n of transcriptional, signalling, growth and cell cycle genes that probably play a role in the atroph
228 patocyte proliferation through expression of cell cycle genes that stimulate cyclin-dependent kinase
229 DBF2 belongs to a group of budding yeast cell cycle genes that when mutated prevent cyclin degrad
230 s transcription of the CCNB2, KIF23 and PLK4 cell cycle genes through the recently discovered p53-p21
232 of expression of transcriptionally regulated cell cycle genes to an accuracy of 2 min (approximately
233 g hepatocyte proliferation and expression of cell cycle genes to levels found in young regenerating m
234 density array that tiles the promoters of 56 cell-cycle genes to interrogate 108 samples representing
235 e promoters, interfering with progression of cell cycle, gene transcription, initiation of apoptotic
237 eta/SMAD signaling, which directly regulates cell-cycle gene transcription to control a reversible G1
239 oherence of the relative activation times of cell-cycling genes under different experimental conditio
242 ed expression of miR-221, expression of many cell cycle genes was altered and pathways promoting epit
243 our data showed that expression of the core cell-cycle genes was coordinately regulated during polli
245 wed a decrease in total heterochromatin, and cell cycle genes were derepressed, leading to proliferat
247 onfirmed at the protein level, revealed that cell cycle genes were upregulated in trkB.T1(+/+) but no
248 GSIS), and expression of differentiation and cell-cycle genes were analyzed in human islets transduce
249 feration, survival, and induction of several cell cycle genes, whereas expression of antisense TR3 ab
250 fibroblasts and decreased binding to target cell cycle genes, while a phosphomimetic substitution (S
251 only a practical tool for identifying novel cell cycle genes with high accuracy, but also new insigh
252 a distinct expression signature enriched for cell-cycle genes without requiring the presence of AR-FL
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