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1 into activator and repressor E2Fs, regulates cell cycle genes.
2 al network able to control the expression of cell cycle genes.
3 e full function of NF-Y in activation of the cell cycle genes.
4 in MYC binding to the promoters of selected cell cycle genes.
5 are underrepresented in both early and late cell cycle genes.
6 t role in transcriptional regulation of late cell cycle genes.
7 ents have several limitations in identifying cell cycle genes.
8 ctors to discriminate cell cycle against non-cell cycle genes.
9 ll cycle by controlling the transcription of cell cycle genes.
10 s characterized by the altered regulation of cell cycle genes.
11 BrdU uptake in vivo and actively transcribed cell cycle genes.
12 rm cells through translational regulation of cell cycle genes.
13 and does not govern expression of canonical cell cycle genes.
14 ing E2F1 binding to the promoters of various cell cycle genes.
15 tion, as well as E2F-dependent expression of cell cycle genes.
16 gibbon genome by disrupting transcription of cell cycle genes.
17 feration by coordinately regulating numerous cell cycle genes.
18 ption factors, reversing their repression of cell cycle genes.
19 ic coregulator complexes to the promoters of cell cycle genes.
20 l mechanism by which nuclear IRS-1 activates cell cycle genes.
21 sion presumably through the control of early cell cycle genes.
22 and represses transcription of E2F-regulated cell cycle genes.
23 ing a role for DREAM and RB in repression of cell cycle genes.
24 modulating the periodic expression of early cell cycle genes.
25 of expression exhibited by these three G(1) cell cycle genes.
26 nly partially required for the expression of cell cycle genes.
27 ation of PKC and modulation of cell survival/cell cycle genes.
28 ion and mitosis by stimulating expression of cell cycle genes.
29 eins required for transcription of essential cell cycle genes.
30 -DREAM in p53 and p21 mediated repression of cell cycle genes.
31 n Autism Research Initiative), synaptic, and cell cycle genes.
32 cell cycle regulatory genes relative to non-cell cycle genes.
33 approach based on Boolean logic to identify cell cycle genes.
34 al activator that promotes the expression of cell cycle genes.
35 inger (ZF) transcriptional regulator of many cell cycle genes.
36 , whereas miR-294 suppresses, the phasing of cell cycle genes.
37 ntiation and activation of pro-proliferative cell cycle genes.
38 on of at least a subset of pro-proliferative cell cycle genes.
39 endent repression of important E2F-dependent cell-cycle genes.
40 sitory surge of pro-apoptotic components and cell-cycle genes.
41 lf-renewal, such as stem cell fate genes and cell-cycle genes.
42 ent LIN37 results in a reduced repression of cell-cycle genes.
43 ted to the expression of immune response and cell-cycle genes.
44 feration with concomitant modulation of some cell cycle genes, (2) augmented the NRF2-mediated antiox
45 ession pattern almost entirely consisting of cell cycle genes (5-year odds ratio of metastasis, 24.0;
46 In addition to highlighting conservation of cell cycle genes across large evolutionary distances, th
47 accessibility at a small subset of critical cell cycle genes act to enforce cell cycle exit during t
49 (targeting PIK3CA alterations), palbociclib (cell cycle gene alterations), AZD4547 (FGFR alteration),
50 fter RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MI
51 nhibitor CR8 after SCI significantly reduced cell cycle gene and protein expression, microglial activ
52 ased histone acetylation at the promoters of cell cycle genes and E2F targets upon loss of E2F4 in RB
54 e abnormalities, we observe dysregulation of cell cycle genes and increased apoptosis in neural crest
55 enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low bin
56 hylase PHF8 transcriptionally regulates many cell cycle genes and is therefore predicted to play key
57 pression analysis reveals a dysregulation of cell cycle genes and markers of differentiation in the C
58 l pro-tumorigenic genetic programs including cell cycle genes and Myc-regulated genes before the indu
59 in keratinocytes results in up-regulation of cell cycle genes and repression of many epidermal differ
61 These changes ensure basal transcription of cell-cycle genes and are critical for their re-activatio
62 F2A or -D also resulted in the activation of cell-cycle genes and down-regulation of markers of termi
63 nalysis demonstrated that miR-34a suppresses cell-cycle genes and induces several neural-related gene
65 rial depolarization, decreased expression of cell-cycle genes and reduced tumor size in xenograft and
66 ng pathway to downregulate a large number of cell-cycle genes and to arrest the cell cycle at the G1/
67 pression was associated with upregulation of cell-cycling genes and co-downregulation of genes implic
68 nd the cis- motif features are predictive of cell cycle genes, and a combination of the two types of
69 eficiency led to an increase in E2F targets, cell cycle genes, and DNA replication and a decrease in
70 Additionally, modulation of cardiac genes, cell cycle genes, and pluripotency markers were analyzed
71 BR pathway, does not have a direct effect on cell cycle genes, and promoter analysis suggests a disti
72 H is required for the expression of multiple cell cycle genes, and the gene expression signature resu
73 crucial role of plant GBPs in the control of cell cycle genes, and thus, in cell fate maintenance.
74 ion and margins are associated with the late cell-cycle genes, and a metagene that represents the EGF
75 ed cell proliferation, altered expression of cell-cycle genes, and decreased amounts of nuclear, but
76 ave altered expression of a select number of cell-cycle genes, and we identified the mRNA of cyclin-d
78 e sequencing has revealed many C. crescentus cell cycle genes are conserved in other Alphaproteobacte
81 on the phase-specific causal interaction of cell cycle genes, as well as temporal interdependencies
83 analysis of p53-dependent repression of the cell cycle genes B-MYB (MYBL2), BUB1, CCNA2, CCNB1, CHEK
84 cycle, pioneering microarray studies defined cell cycle genes based on cyclic variation in their expr
85 opose a computational model to predict human cell cycle genes based on transcription factor (TF) bind
87 ough inhibition of neointimal hyperplasia by cell cycle gene blockade therapy results in improved end
88 of FBL17 leads not only to misregulation of cell cycle genes, but also to a strong upregulation of g
90 sidered to be a transcriptional activator of cell cycle genes, but its function during development re
91 x controls cellular quiescence by repressing cell cycle genes, but its mechanism of action is poorly
92 -LIP releases E2F.Rb-dependent repression of cell cycle genes by a disruption of E2F1.Rb complexes an
93 WT1 proteins facilitate expression of these cell cycle genes by antagonizing transcriptional repress
95 keletal genes keratin-18 and beta-actin, the cell cycle gene C-MOS, and housekeeping genes GAPDH and
96 Subsequent to its activation, hundreds of cell-cycle genes can then be expressed, including the cy
97 pathways by up-regulating the expression of cell cycle genes cdc2, PRC1 and PCNA, and the transcript
101 hose expression was altered by GLI1 included cell cycle genes, cell adhesion genes, signal transducti
103 es the detection of previously characterized cell-cycle genes compared to approaches that do not acco
104 d by AGN194,204 required PPARalpha including cell-cycle genes, consistent with AGN-induced hepatocyte
106 ed cytokines and the downregulation of tumor cell-cycle genes correlated with NCR2 expression and gre
107 strate that FoxM1 regulates transcription of cell cycle genes critical for progression into S-phase a
109 , the auxin transporter PIN-FORMED1, and the cell cycle genes CYCLIN A2;1 and PROLIFERATING CELL NUCL
110 Expression of NF-YA1 and the G2/M transition cell cycle genes Cyclin B and Cell Division Cycle2 was r
114 odulation of the beta-catenin/TCF responsive cell cycle genes, cyclin D1 and p21, we inhibited beta-c
115 dimerizing partner, DP1 and E2F-upregulated cell cycle genes (cyclins E, A, B and D3) and enhanced t
117 MOS1 and TCP15 both affect the expression of cell-cycle genes D-type CYCLIN 3;1 (CYCD3;1), which may
118 -phase TFs decreases expression of many late cell cycle genes, delays mitotic progression, and reduce
120 olled in Total Therapy II, overexpression of cell cycle genes distinguished CA from no CA, especially
122 ike, E2F4 and MuvB) cooperate to repress all cell cycle genes during G1 and inhibit entry into the ce
128 rtaken a genome-wide characterization of the cell cycle genes encoded by Chlamydomonas reinhardtii, a
129 Our studies demonstrate that two other G(1) cell cycle genes, encoding cyclin D and CDK4/6, have sim
130 of RNA processing, chromatin remodeling and cell-cycle genes enriched for promoter binding by Chd8,
131 transcription factor regulates expression of cell cycle genes essential for DNA replication and mitos
132 ident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA repl
134 tions, irrespective of type, associates with cell cycle gene expression and adverse outcome, whereas
135 lysine 14 (H3K14ac) and is required for key cell cycle gene expression and cancer cell proliferation
136 chanism for E2F factors in the regulation of cell cycle gene expression and cell cycle progression un
137 The retinoblastoma protein (RB) restricts cell cycle gene expression and entry into the cell cycle
138 n recruiting B-Myb and FoxM1 to promote late cell cycle gene expression and in regulating cell cycle
139 scriptional regulators sits at the center of cell cycle gene expression and plays vital roles in norm
140 revealed that T antigen knockdown inhibited cell cycle gene expression and reduced expression of key
141 hearts by single cell RNA-seq and identified cell cycle gene expression as a major determinant of tra
142 ors required for DNA replication, while late cell cycle gene expression begins during G2 to prepare f
143 usually initiated through the repression of cell cycle gene expression by formation of a transcripti
144 by clustering the yeast genes based on their cell cycle gene expression data and the human genes base
146 y, an application of our method to different cell cycle gene expression datasets suggests that our me
147 cell cycle gene expression and in regulating cell cycle gene expression from quiescence through mitos
148 with the importance of stromal response and cell cycle gene expression in colon tumor recurrence.
149 of both p130 and RB yielded higher levels of cell cycle gene expression in G0 and G1 cells compared t
150 he effect of all-trans-retinoic acid (RA) on cell cycle gene expression in RA sensitive CA-OV3 and RA
155 analysis was used to determine how the yeast cell cycle gene expression program is regulated by each
156 es of human biopsies and identified a strong cell cycle gene expression signature in OAC compared to
157 signaling on progenitor cell regulation and cell cycle gene expression, and loss of epithelial Pygo2
158 ative assay integrating stromal response and cell cycle gene expression, in tumor specimens from pati
159 F1R, appears to have an amplifying effect on cell cycle gene expression, thus providing a molecular e
160 plex remains bound to FoxM1 during peak late cell cycle gene expression, while B-Myb binding is lost
163 ellular and physiologic processes, including cell cycle, gene expression, cell viability, stress resp
164 sion patterns resulting from manipulation of cell-cycle gene expression alter the physiology of the o
165 show that as breast TIC form, a decrease in cell-cycle gene expression and increase in self-renewal
166 d alpha6(hi)beta1(hi)CD34(hi) CSCs differ in cell-cycle gene expression and proliferation characteris
167 4E accumulation and significantly diminished cell-cycle gene expression and tumor volume of A431-deri
168 s on two public datasets: the Stanford yeast cell-cycle gene expression data, and a gene expression d
170 how that GCN5 is an essential coactivator of cell-cycle gene expression driven by MYC overexpression
171 o determine whether the observed patterns in cell-cycle gene expression in Clock mutants resulted in
173 low-error-rate classification for both yeast cell-cycle gene expression profiles and Dictyostelium ce
174 roliferation, regulation of an E2F-dependent cell-cycle gene expression program, and estrogen-depende
175 tion of GBM tumors based on a DNA repair and cell-cycle gene expression signature exposes vulnerabili
176 , knowledge of the changes in DNA repair and cell-cycle gene expression that occur during tumor devel
185 ession profiling studies suggested that core cell-cycle genes functioning during the G1/S, S, and G2/
186 ical, Sp1-like, cell cycle-dependent element/cell cycle gene homology region, and p53-binding sites.
190 ified CDE-CHR (Cell cycle-Dependent Elements-Cell cycle genes Homology Region) region of cyclin A pro
191 uencing in mouse and rat OPCs, we identified cell cycle genes (i.e., Cdc2) and chromatin components (
193 t TEAD4 directly regulates expression of key cell cycle genes in both mouse and human TSCs and establ
194 ssociated with significant downregulation of cell cycle genes in both OE21 (P<0.0001) and OE33 (P=0.0
196 To explore the mechanism of repression of cell cycle genes in cervical carcinoma cells following E
197 n contrast, expression was lower in 40 of 44 cell cycle genes in eNOS-KO mice, in association with im
198 M complex that mediates global repression of cell cycle genes in G0/G1, including a subset of MMB tar
200 ing domain, CHT7 modulates the expression of cell cycle genes in response to N availability, which is
203 rofluidic device, we tracked the dynamics of cell cycle genes in single yeast with subminute exposure
204 the expression of several growth factors and cell cycle genes in the aromatase transgenic mammary gla
205 in transcript abundance of cell division and cell cycle genes in the drought-stressed ovary only.
208 rough transcriptional regulation of specific cell-cycle genes in a cell-type- and developmental-stage
209 nt cells, AR selectively upregulates M-phase cell-cycle genes in androgen-independent cells, includin
211 ing genes, there was increased expression of cell cycle genes including an A-type cyclin and a subuni
212 ma cells in the levels of expression of many cell cycle genes including cyclin A, B and E, cdk 2,4 an
213 Etv2 ES/EB system showed increased levels of cell cycle genes including E2f4 and Ccne1 as early as 6
214 -195 regulates the expression of a number of cell cycle genes, including checkpoint kinase 1 (Chek1),
215 88 target the upstream regions especially of cell cycle genes, including cyclins, cyclin-dependent ki
216 nfection results in dysregulation of several cell cycle genes, including inhibition of cyclin A trans
217 amming in this setting activated a subset of cell-cycle genes, including CENPE, a centromere binding
219 ered expression of developmental factors and cell cycle genes is associated with a higher degree of e
223 ndividual REST target ribosome biogenesis or cell cycle genes is sufficient to induce activation of Q
224 t increase and the expression of an array of cell cycle genes is virtually unchanged in Dp1-deficient
225 Most strikingly, p53-dependent repression of cell-cycle genes is completely abrogated in LIN37-/-;RB-
226 t while Chd8 stimulates the transcription of cell cycle genes, it also precludes the induction of neu
227 revealed downregulation of ion transport and cell cycle genes, leading to altered calcium handling an
228 arly G2 had increased RNA levels, while core cell cycle genes linked to early G1 and late G2 had redu
229 atform enables a detailed exploration of the cell cycle gene lists generated using the Boolean logic
230 selectively regulating H3K9 demethylation at cell cycle gene loci, thereby representing a key player
232 LL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression o
234 ne expression studies point to regulation of cell cycle genes, muscle myosins, NotchR and Wnt pathway
236 he KEN box as a template, we have identified cell cycle genes Nek2 and B99 as additional Cdh1-APC sub
238 is encoded within the promoter region of the cell cycle gene POLR3D in the antisense orientation.
239 ow broadly CMV alters the regulation of host cell cycle gene products and highlight the establishment
240 immortalized rat-1 fibroblasts by monitoring cell-cycle gene promoter-driven luciferase activity.
241 kdown, p107 compensated for p130 loss at all cell cycle gene promoters examined, allowing cells to re
242 this manner, SCIRT induced transcription at cell-cycle gene promoters by recruiting FOXM1 through EZ
243 tor homeobox Protein (ADNP) and located near cell-cycle genes recruits TFIIIC, which alters their chr
244 r the DREAM complex finds that a set of core cell cycle genes regulated in both U2OS and HeLa cells a
247 ically disrupted, chromatin accessibility at cell cycle genes remains unaffected, and the closing of
249 is critical for regulating the expression of cell cycle genes required for hepatocyte proliferation.
252 and specifically expresses the regulator of cell cycle gene (RGCC), a gene that responds to compleme
253 hanges in alternative polyadenylation (APA), cell cycle genes showed mostly alternative splicing (AS)
255 gous neonatal hearts identified a network of cell cycle genes significantly up-regulated and down-reg
256 nd that, rapidly after BET displacement, key cell-cycle genes (SKP2, ERK1, and c-MYC) were downregula
259 inhibited the E2-induced expression of early cell cycle genes such as cyclins D1, D3, E1, E2, and B2.
260 ding p38 MAPK-regulated or ERK-1/2-regulated cell-cycle genes such as FOS, MAPK8, MYC, various cyclin
263 er many cells), some, but not all, canonical cell cycle genes tend to be co-expressed in groups in si
266 right ventricle, and we identified numerous cell cycle genes that are dependent on Gata4 by microarr
267 ethylation analysis shows hypomethylation of cell cycle genes that are Myc targets in islets from you
268 n of transcriptional, signalling, growth and cell cycle genes that probably play a role in the atroph
269 patocyte proliferation through expression of cell cycle genes that stimulate cyclin-dependent kinase
270 s transcription of the CCNB2, KIF23 and PLK4 cell cycle genes through the recently discovered p53-p21
272 of expression of transcriptionally regulated cell cycle genes to an accuracy of 2 min (approximately
273 from embryonically dysregulated synaptic and cell cycle genes to disrupted adult glia, inhibitory syn
275 g hepatocyte proliferation and expression of cell cycle genes to levels found in young regenerating m
276 density array that tiles the promoters of 56 cell-cycle genes to interrogate 108 samples representing
277 e promoters, interfering with progression of cell cycle, gene transcription, initiation of apoptotic
279 eta/SMAD signaling, which directly regulates cell-cycle gene transcription to control a reversible G1
281 oherence of the relative activation times of cell-cycling genes under different experimental conditio
282 1, Fibronectin, Heparan Sulfate, LOX, FAK1), cell cycle genes (USP16, S1P complexes), and DNA damage
285 ed expression of miR-221, expression of many cell cycle genes was altered and pathways promoting epit
286 our data showed that expression of the core cell-cycle genes was coordinately regulated during polli
288 wed a decrease in total heterochromatin, and cell cycle genes were derepressed, leading to proliferat
291 onfirmed at the protein level, revealed that cell cycle genes were upregulated in trkB.T1(+/+) but no
292 GSIS), and expression of differentiation and cell-cycle genes were analyzed in human islets transduce
293 feration, survival, and induction of several cell cycle genes, whereas expression of antisense TR3 ab
294 th distant CTCF sites near promoter of other cell-cycle genes, which also become hyperacetylated at H
295 analyses revealed that low dox downregulated cell cycle genes while high dox upregulated DNA damage r
296 fibroblasts and decreased binding to target cell cycle genes, while a phosphomimetic substitution (S
297 only a practical tool for identifying novel cell cycle genes with high accuracy, but also new insigh
299 a distinct expression signature enriched for cell-cycle genes without requiring the presence of AR-FL