Regulation of E2F1 activity by acetylation
By M. Martínez-Balbás, U. Bauer, S. Nielsen, A. Brehm, Tony Kouzarides. EMBO Journal, 2000
714 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/7c74a50d4eb9d830cc5789994f657a19081ae1ba
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Tony Kouzarides
- Andrew J. Bannister
- E. Verdin
- Carlos Caldas
- N. Iyer
- H. Özdağ
- Jessica E. Bolden
- M. Peart
In Oncology
Citations in the corpus
- The Rb/E2F pathway: expanding roles and emerging paradigms. (2000, background): “Therefore, recruitment of HDAC to E2F via Rb may inhibit E2F activity by deacetylation of the protein, thereby inhibiting its binding to DNA (Fig.”
- Structure of a -TrCP1-Skp1--Catenin Complex (2003, background): “sampling the vicinity of the E2 through random diffusion, transcription factor (Li and Verma, 2002; Martinez-Balbas et al., 2000).”
- CBP/p300 in cell growth, transformation, and development. (2000, background): “This group has recently extended this model by showing that E2F1 can be acetylated by P/CAF, a CBP/ p300-associated factor, and to a lessor degree by CBP/ p300 itself (Martinez-Balbas et al. 2000).”
- The NAD+-Dependent Deacetylase SIRT1 Modulates CLOCK-Mediated Chromatin Remodeling and Circadian Control (2008, neutral): “HDACs have also been implicated in the reversible acetylation of nonhistone proteins, including p53 (Luo et al., 2001; Vaziri et al., 2001), Hsp90 (Kovacs et al., 2005), MyoD (Mal et al., 2001), and E2F1 (Martinez-Balbas et al., 2000).”
- p300/CBP and cancer (2004, background): “…(Eckner et al., 1994; Bannister and Kouzarides, 1995; Bannister et al., 1995; Avantaggiati et al., 1997; Lill et al., 1997; Pouponnot et al., 1998; Patel et al., 1999; Ghosh et al., 2000; Martinez-Balbas et al., 2000; Marzio et al., 2000; Pao et al., 2000; Tomita et al., 2000; Chan et al., 2001).”
- Histone Deacetylase Inhibitors: Overview and Perspectives (2007, neutral): “Protein Substrates of HDACs (Partial List) Functional Group Protein HDAC Implicated References Structural protein a-Tubulin HDAC6 (19) Chaperone protein Hsp90 HDAC6 (84) DNA binding nuclear receptors Androgen receptor HDAC1 (85) Glucocorticoid receptor HDAC2 (86) Estrogen receptor a ND (87) SHP HDAC”
- Sirtuins: critical regulators at the crossroads between cancer and aging (2007, background): “E2F1 is acetylated by p300/CBP-associated factor (PCAF), which enhances its DNA-binding, transactivation activity, and stability, and transforms E2F1 into an activator of transcription (Martinez-Balbas et al., 2000).”
- Anticancer activities of histone deacetylase inhibitors (2006, background): “For example, the gene regulatory activity of transcription factors such as E2F1, p53, STAT1, STAT3 and NF-κB can be modulated through direct acetylation and deacetylation of the factors themselves, and all of these proteins are hyperacetylated in response to HDAC”
- Acetylation: a regulatory modification to rival phosphorylation? (2000, background): “Many of these substrates are involved in the regulation of transcription and include p53, E2F1, EKLF, TFIIEβ, TFIIF, TCF, GATA1, HMGI(Y) and ACTR (Gu and Roeder, 1997; Imhof et al., 1997; Boyes et al., 1998; Munshi et al., 1998; Waltzer and Bienz, 1998; Zhang and Bieker et al., 1998; Chen et al., 19”