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1 icantly with those bound by the S-phase gene transcription factor E2F1.
2 ating myoblasts by the cell cycle-associated transcription factor E2F1.
3 n of AMP kinase and the proapoptotic nuclear transcription factor E2F1.
4 53, but also on its ability to signal to the transcription factor E2F1.
5 B1 and upstream of the cell cycle regulatory transcription factor E2F1.
6 r suppressors p53 and retinoblastoma and the transcription factor E2F1.
7 inhibits the EC cycle and downregulates the transcription factor E2F1.
8 ed the activity of the cell cycle regulatory transcription factor E2F1.
9 actor PCNA and of the proliferation-specific transcription factor E2F1.
10 t of rapamycin complex 1-S6K pathway and the transcription factor E2F1.
11 e NAD(+)-dependent deacetylase SIRT1 and the transcription factor E2F1.
14 s directly and specifically activated by the transcription factor E2F1--a factor perturbed in the maj
15 es indicated that DDB can associate with the transcription factor E2F1 and can function as a transcri
16 restored RB1 function and downstream targets transcription factor E2F1 and cycling-dependent kinase 2
17 The A-, E-, and D-type cyclins as well as transcription factor E2F1 and the E1A viral oncoprotein
19 d protein levels of cyclins A, B, and E, the transcription factor E2F1, and the cyclin-dependent kina
20 mice are not dependent on either p53 or the transcription factor E2F1, as mice null for these genes
21 ained induction of NF-kappaB signaling and a transcription factor E2F1-dependent metabolic pathway by
22 ivation of AMP kinase (AMPK) and the nuclear transcription factor E2F1, detailed auditory pathology w
24 of ChIP-seq data from a panel of cell cycle transcription factors (E2F1, E2F4, E2F6, and GABPA) from
26 astoma susceptibility gene product (pRb) and transcription factor E2F1, exhibit altered immunostainin
35 is mechanistically linked to suppression of transcription factor E2F1-mediated cell cycle regulation
37 n p130 and increased the Rb family-regulated transcription factor E2F1, overexpression of which inhib
42 hanistic studies showed that PELP1 modulates transcription factor E2F1 transactivation functions, tha
43 s have also shown that downregulation of the transcription factor E2F1 was a key mechanism of TNF's e
44 rubicin-induced upregulation mediated by the transcription factor E2F1, was enhanced by Cry1/Cry2 dou
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