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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 cell death, which is likely mediated by the E2F transcription factor.
6 he S phase by modulating the activity of 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 lation of CCNE1 by miR-874 is independent of E2F transcription factors.
10 ar proliferation and apoptosis by regulating E2F transcription factors.
11 acterize the functional link between MIF and E2F transcription factors.
12 s its function through its interactions with E2F transcription factors.
13 ediated by their ability to inhibit specific E2F transcription factors.
14 igenesis, in part, through interactions with E2F transcription factors.
15 nt fashion, likely through the pRB-dependent E2F transcription factors.
16 proliferation through the regulation of the E2F transcription factors.
17 cell proliferation by binding and inhibiting E2F transcription factors.
18 of the cell cycle and which are regulated by E2F transcription factors.
19 inding to and regulating the activity of the E2F transcription factors.
20 showed that MageB2 enhances the activity of E2F transcription factors.
21 ion, termed hypo-phosphorylation, to release E2F transcription factors.
22 ulated during cell cycle progression through E2F transcription factors.
23 a family members suggested the regulation of E2F transcription factors.
24 enic plants with altered levels of different E2F transcription factors.
25 ssion, principally through regulation of the E2f transcription factors.
26 (RB) regulates S-phase cell cycle entry via E2F transcription factors.
27 sensitivity to apoptosis through binding to E2F transcription factors.
28 origenesis largely through regulation of the E2F transcription factors.
29 t in response to the activation of the other E2F transcription factors.
30 elial cells, that mouse DDB2 is regulated by E2F transcription factors.
31 sis through inhibitory interactions with the E2F transcription factors.
32 ed cell cycle progression, expression of the E2F transcription factor 1 (E2F1) and loss of retinoblas
35 ies utilizing MDM2 inhibitors, we noted that E2F transcription factor 1 (E2F1) was down regulated upo
37 xpression, which inhibits Src, and increased E2F transcription factor 1 expression, which regulates b
39 for tumor progression and that it did so via E2F transcription factor 1-mediated regulation of androg
40 e homolog) and E2F1, E2F2 and E2F3 (encoding E2F transcription factors 1, 2 and 3, respectively).
44 oiesis highlights the nonredundant nature of E2f transcription factor activities in cell growth and d
45 kinase (CDK) in allowing the accumulation of E2F transcription factor activity and induction of the S
46 dy of evidence has shown that the control of E2F transcription factor activity is critical for determ
48 mbers, p107 and p130, function by repressing E2F transcription factor activity to limit the expressio
51 bladder cancer, including the activation of E2F transcription factor and subsequent Ezh2 expression
52 ate specific activator and repressor MYB and E2F transcription factors and indicate the possibility o
53 t this site overlaps with a binding site for E2F transcription factors and is subtly distinct from a
54 tion through inhibition of Rb complexes with E2F transcription factors and other regulatory proteins.
58 lastoma (Rb) family members interacting with E2F transcription factors and recruiting heterochromatin
59 cycle progression, in part, by sequestering E2F transcription factors and repressing E2F-responsive
60 (pRb) mediates cell cycle control by binding E2F transcription factors and repressing expression from
61 pRb) restrains cell proliferation by binding E2f transcription factors and repressing the expression
62 tein (pRb), which normally functions to bind E2F transcription factors and restrict expression of gen
63 that Dnmt1 is transcriptionally regulated by E2F transcription factors and that retinoblastoma protei
64 s, resulting in the dissociation of pRb from E2F transcription factors and the premature cell progres
65 in noncycling cells by complexes between the E2F transcription factors and the retinoblastoma (Rb) tu
66 Much circumstantial evidence implicates both E2F transcription factors and the retinoblastoma protein
67 ls exit the cell cycle through the action of E2F transcription factors and the retinoblastoma tumor s
68 te cell-cycle exit through inhibition of the E2F transcription factors and the transcriptional repres
70 y dependent upon its capacity to inhibit the E2F transcription factors and thereby cell proliferation
71 Rb and related proteins act as regulators of E2F transcription factors, and RbAp48 may act with such
80 en together, these data demonstrate that the E2F transcription factors are integral to HER2+ tumor de
96 line) raised cyclin D1 expression, increased E2F transcription factor binding to cyclin D1 promoter,
98 y abrogating the transcription repression of E2F transcription factors by the retinoblastoma suscepti
99 pic expression of Drosophila Cyclin E or the E2F transcription factor can drive quiescent endoreplica
102 ferating EC, which display repression of the E2F transcription factor coincident with TNF-induced apo
103 ry pathways (the Rb-like protein RBF and the E2F transcription factor complex components dE2F and dDP
107 t on Sp1 is specific, in that the Stat-3 and E2F transcription factors did not undergo degradation un
108 RB family mutant TECs, increased activity of E2F transcription factors drives increased expression of
109 Thus we have uncovered new functions for E2F transcription factors during development, including
112 predicted miR-142 target genes, the atypical E2F transcription factors E2f7 and E2f8, were most highl
115 lock cell cycle progression by inhibition of E2F transcription factors, experiments were conducted to
117 e functional interaction between pRB and the E2F transcription factor family appears to be critical.
120 pRB-independent, noncanonical member of the E2F transcription factor family that acts as a transcrip
121 tify E2F7 as a novel member of the mammalian E2F transcription factor family that has properties of a
122 s p105RB (retinoblastoma, acting through the E2F transcription factor family) and p53 regulate cell p
123 l as that of the DNA-bending capacity of the E2F transcription factor family, in the activation of tr
127 ylate the retinoblastoma protein and release E2F transcription factors for progression through cell c
128 een suggested that the subsequent release of E2F transcription factors from inhibitory complexes may
129 cell transformation, in part, by displacing E2F transcription factors from the retinoblastoma protei
130 myocytes and other cell types by displacing E2F transcription factors from tumor suppressor "pocket"
134 ammals, a large number of proteins including E2F transcription factors have been shown to interact wi
137 the pRB family and its principal target, the E2F transcription factor, have focused on cells that hav
138 best-known target of RB protein (pRB) is the E2F transcription factor; however, many other chromatin-
139 horylation prevents its association with the E2F transcription factor; however, the molecular basis f
141 stand whether Rb function can be mediated by E2F transcription factors in a BM-derived hematopoietic
142 ress this and to further analyze the role of E2F transcription factors in development we have phenoty
146 thods, we predicted a role for the activator E2F transcription factors in the mouse mammary tumor vir
147 hematopoietic-specific miR-142 and atypical E2F transcription factors in the regulation of mature T
151 dependent expression of an antagonist of the E2F transcription factor inhibits viral replication in n
160 o-oncoprotein, is cell-cycle regulated by an E2F transcription factor-mediated repression mechanism o
169 aken together, these results reveal that the E2F transcription factors play key roles in mediating tu
173 atypical E2F family member E2F7 as the only E2F transcription factor potently up-regulated during on
174 ons, in part, by binding to and inactivating E2F transcription factors, preventing expression of E2F-
181 o the human pRb tumor suppressor protein and E2F transcription factors, resulting in the dissociation
182 th RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of
183 ression, activation of the Notch pathway via E2F transcription factors serves as a negative feedback
185 long been known to target regulation of the E2F transcription factors, the downstream target of the
186 oblastoma (pRB) family proteins regulate the E2F transcription factors; their complexes regulate crit
187 additional roles of this pathway, especially E2F transcription factors themselves, in tumor progressi
189 CR2 binds RB family members, de-repressing E2F transcription factors, thus activating genes require
190 e Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and D
191 l its growth-inhibitory effects and enabling E2F transcription factors to activate genes required for
192 , p107, and p130 pocket proteins bind to the E2F transcription factors to control gene expression.
194 a hypophosphorylated state, associates with E2F transcription factors to prevent the activation of g
195 ation by G1-CDK of Whi5/Rb inhibitors of SBF/E2F transcription factors triggers irreversible S-phase
196 ulates the G1-S transition by binding to the E2F transcription factors, until cyclin-dependent kinase
197 ists to support the tenet that activation of E2F transcription factors, via alterations in the p16-cy
198 N-MYC promoter in cycling cells required the E2F transcription factor, we show that E2F-1 and HBP1 re
199 specificity of function within the family of E2F transcription factors, we have identified proteins t
201 sphorylated pRb binds to and inactivates the E2F transcription factor, which controls the expression
203 GF signaling regulated the expression of the E2F transcription factors, which directly bound to and a
204 n proliferating cells include members of the E2F transcription factors, which mediate the expression
205 ly proteins binds to distinct members of the E2F transcription factors, which regulate the expression
206 ssing adenovirus E2 promoter binding factor (E2F) transcription factors, which drive the expression o
207 wn that prohibitin represses the activity of E2F transcription factors while enhancing p53-mediated t
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