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1 hat p14(ARF) can control the activity of the E2F transcription factor.
2 or protein (Rb), which in turn regulates the E2F transcription factor.
3 hat can be bypassed by overexpression of the E2F transcription factor.
4 s transcriptional activation mediated by the E2F transcription factor.
5 he S phase by modulating the activity of the E2F transcription factor.
6 cell death, which is likely mediated by the E2F transcription factor.
7 sed genes that are likely coregulated by the E2F transcription factor.
8 dk inhibitors to Cdks, and downregulation of E2F transcription factor.
9 a tumor suppressor that binds and represses E2F transcription factors.
10 elial cells, that mouse DDB2 is regulated by E2F transcription factors.
11 sis through inhibitory interactions with the E2F transcription factors.
12 ar proliferation and apoptosis by regulating E2F transcription factors.
13 acterize the functional link between MIF and E2F transcription factors.
14 s its function through its interactions with E2F transcription factors.
15 lation of CCNE1 by miR-874 is independent of E2F transcription factors.
16 ediated by their ability to inhibit specific E2F transcription factors.
17 igenesis, in part, through interactions with E2F transcription factors.
18 nt fashion, likely through the pRB-dependent E2F transcription factors.
19 proliferation through the regulation of the E2F transcription factors.
20 (RB) regulates S-phase cell cycle entry via E2F transcription factors.
21 cell proliferation by binding and inhibiting E2F transcription factors.
22 of the cell cycle and which are regulated by E2F transcription factors.
23 inding to and regulating the activity of the E2F transcription factors.
24 ied as a downstream target gene of the c-myc/E2F transcription factors.
25 showed that MageB2 enhances the activity of E2F transcription factors.
26 ion, termed hypo-phosphorylation, to release E2F transcription factors.
27 ulated during cell cycle progression through E2F transcription factors.
28 a family members suggested the regulation of E2F transcription factors.
29 enic plants with altered levels of different E2F transcription factors.
30 ssion, principally through regulation of the E2f transcription factors.
31 sensitivity to apoptosis through binding to E2F transcription factors.
32 origenesis largely through regulation of the E2F transcription factors.
33 t in response to the activation of the other E2F transcription factors.
34 ed cell cycle progression, expression of the E2F transcription factor 1 (E2F1) and loss of retinoblas
37 ies utilizing MDM2 inhibitors, we noted that E2F transcription factor 1 (E2F1) was down regulated upo
38 iting cell cycle regulators Cyclin E (cycE), E2F transcription factor 1 (e2f1), and string (stg).
41 xpression, which inhibits Src, and increased E2F transcription factor 1 expression, which regulates b
43 for tumor progression and that it did so via E2F transcription factor 1-mediated regulation of androg
44 e homolog) and E2F1, E2F2 and E2F3 (encoding E2F transcription factors 1, 2 and 3, respectively).
45 ified a novel functional interaction between E2f Transcription Factor 2 (E2f2) and Brain Expressed X-
47 olved, we found here that HIV-1 Tat inhibits E2F transcription factor 3 (E2F3), CAMP-responsive eleme
51 oiesis highlights the nonredundant nature of E2f transcription factor activities in cell growth and d
52 kinase (CDK) in allowing the accumulation of E2F transcription factor activity and induction of the S
53 dy of evidence has shown that the control of E2F transcription factor activity is critical for determ
55 mbers, p107 and p130, function by repressing E2F transcription factor activity to limit the expressio
56 creases intracellular cAMP levels and boosts E2F transcription factor activity to promote cell prolif
59 ontaining a retinoblastoma family member, an E2F transcription factor and its dimerization partner, a
60 bladder cancer, including the activation of E2F transcription factor and subsequent Ezh2 expression
61 the early-expressed genes, we identified an E2F transcription factor and the RNA-binding protein Pum
62 ate specific activator and repressor MYB and E2F transcription factors and indicate the possibility o
63 t this site overlaps with a binding site for E2F transcription factors and is subtly distinct from a
64 tion through inhibition of Rb complexes with E2F transcription factors and other regulatory proteins.
68 lastoma (Rb) family members interacting with E2F transcription factors and recruiting heterochromatin
69 cycle progression, in part, by sequestering E2F transcription factors and repressing E2F-responsive
70 (pRb) mediates cell cycle control by binding E2F transcription factors and repressing expression from
71 pRb) restrains cell proliferation by binding E2f transcription factors and repressing the expression
72 tein (pRb), which normally functions to bind E2F transcription factors and restrict expression of gen
73 that Dnmt1 is transcriptionally regulated by E2F transcription factors and that retinoblastoma protei
74 s, resulting in the dissociation of pRb from E2F transcription factors and the premature cell progres
75 in noncycling cells by complexes between the E2F transcription factors and the retinoblastoma (Rb) tu
76 Much circumstantial evidence implicates both E2F transcription factors and the retinoblastoma protein
77 ls exit the cell cycle through the action of E2F transcription factors and the retinoblastoma tumor s
79 te cell-cycle exit through inhibition of the E2F transcription factors and the transcriptional repres
81 y dependent upon its capacity to inhibit the E2F transcription factors and thereby cell proliferation
82 ary for regulating binding interactions with E2F transcription factors and transcription repressors t
83 Rb and related proteins act as regulators of E2F transcription factors, and RbAp48 may act with such
93 en together, these data demonstrate that the E2F transcription factors are integral to HER2+ tumor de
111 line) raised cyclin D1 expression, increased E2F transcription factor binding to cyclin D1 promoter,
113 y abrogating the transcription repression of E2F transcription factors by the retinoblastoma suscepti
114 pic expression of Drosophila Cyclin E or the E2F transcription factor can drive quiescent endoreplica
117 ferating EC, which display repression of the E2F transcription factor coincident with TNF-induced apo
118 ry pathways (the Rb-like protein RBF and the E2F transcription factor complex components dE2F and dDP
122 t on Sp1 is specific, in that the Stat-3 and E2F transcription factors did not undergo degradation un
123 athway analyses predicted activation of E2F (E2F transcription factor), DNA damage response, TP53 (tu
124 RB family mutant TECs, increased activity of E2F transcription factors drives increased expression of
125 Thus we have uncovered new functions for E2F transcription factors during development, including
129 predicted miR-142 target genes, the atypical E2F transcription factors E2f7 and E2f8, were most highl
132 lock cell cycle progression by inhibition of E2F transcription factors, experiments were conducted to
134 e functional interaction between pRB and the E2F transcription factor family appears to be critical.
138 pRB-independent, noncanonical member of the E2F transcription factor family that acts as a transcrip
139 tify E2F7 as a novel member of the mammalian E2F transcription factor family that has properties of a
141 s p105RB (retinoblastoma, acting through the E2F transcription factor family) and p53 regulate cell p
142 the RB1 gene product, pRB, is to repress the E2F transcription factor family, but pRB also functions
143 l as that of the DNA-bending capacity of the E2F transcription factor family, in the activation of tr
149 ylate the retinoblastoma protein and release E2F transcription factors for progression through cell c
150 een suggested that the subsequent release of E2F transcription factors from inhibitory complexes may
151 cell transformation, in part, by displacing E2F transcription factors from the retinoblastoma protei
152 myocytes and other cell types by displacing E2F transcription factors from tumor suppressor "pocket"
156 ammals, a large number of proteins including E2F transcription factors have been shown to interact wi
159 the pRB family and its principal target, the E2F transcription factor, have focused on cells that hav
160 best-known target of RB protein (pRB) is the E2F transcription factor; however, many other chromatin-
161 horylation prevents its association with the E2F transcription factor; however, the molecular basis f
163 stand whether Rb function can be mediated by E2F transcription factors in a BM-derived hematopoietic
164 le entry and quiescence are regulated by the E2F transcription factors in association with RETINOBLAS
165 , we found that lipid overload activates the E2F transcription factors in BECs, which drive cell cycl
166 ress this and to further analyze the role of E2F transcription factors in development we have phenoty
171 thods, we predicted a role for the activator E2F transcription factors in the mouse mammary tumor vir
172 hematopoietic-specific miR-142 and atypical E2F transcription factors in the regulation of mature T
175 environment lead to an activation of Myc and E2F transcription factors, induce senescence, and suppre
177 dependent expression of an antagonist of the E2F transcription factor inhibits viral replication in n
187 o-oncoprotein, is cell-cycle regulated by an E2F transcription factor-mediated repression mechanism o
196 aken together, these results reveal that the E2F transcription factors play key roles in mediating tu
200 atypical E2F family member E2F7 as the only E2F transcription factor potently up-regulated during on
201 ons, in part, by binding to and inactivating E2F transcription factors, preventing expression of E2F-
209 o the human pRb tumor suppressor protein and E2F transcription factors, resulting in the dissociation
210 th RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of
211 ression, activation of the Notch pathway via E2F transcription factors serves as a negative feedback
213 ith peak expression in G1/S, is activated by E2F transcription factors (TFs) and is required for DNA
214 ed the expression of genes including p53 and E2F transcription factors that regulate the cell cycle i
215 long been known to target regulation of the E2F transcription factors, the downstream target of the
216 oblastoma (pRB) family proteins regulate the E2F transcription factors; their complexes regulate crit
217 additional roles of this pathway, especially E2F transcription factors themselves, in tumor progressi
219 CR2 binds RB family members, de-repressing E2F transcription factors, thus activating genes require
220 e Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and D
221 l its growth-inhibitory effects and enabling E2F transcription factors to activate genes required for
222 , p107, and p130 pocket proteins bind to the E2F transcription factors to control gene expression.
223 (Rb) through phosphorylation, which releases E2F transcription factors to drive cell-cycle progressio
225 a hypophosphorylated state, associates with E2F transcription factors to prevent the activation of g
226 ation by G1-CDK of Whi5/Rb inhibitors of SBF/E2F transcription factors triggers irreversible S-phase
227 ulates the G1-S transition by binding to the E2F transcription factors, until cyclin-dependent kinase
228 ists to support the tenet that activation of E2F transcription factors, via alterations in the p16-cy
229 N-MYC promoter in cycling cells required the E2F transcription factor, we show that E2F-1 and HBP1 re
230 specificity of function within the family of E2F transcription factors, we have identified proteins t
232 sphorylated pRb binds to and inactivates the E2F transcription factor, which controls the expression
234 GF signaling regulated the expression of the E2F transcription factors, which directly bound to and a
235 n proliferating cells include members of the E2F transcription factors, which mediate the expression
236 ly proteins binds to distinct members of the E2F transcription factors, which regulate the expression
237 ssing adenovirus E2 promoter binding factor (E2F) transcription factors, which drive the expression o
238 wn that prohibitin represses the activity of E2F transcription factors while enhancing p53-mediated t