Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks

By Arkady Celeste, O. Fernández-Capetillo, M. Kruhlak, D. Pilch, David W. Staudt, Alicia Lee, R. Bonner, W. Bonner, A. Nussenzweig. Nature Cell Biology, 2003

1,078 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/bdfc56ecb53e857a34653f9b8e93eea22df93410

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

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. Ryuji Hamamoto
5. S. Polo
6. Yusuke Nakamura
7. P. Jeggo
8. C. Lukas

In Oncology

1. J. Bartek
2. Stephen P. Jackson
3. J. Lukas
4. P. Jeggo
5. S. Polo
6. M. Löbrich
7. T. Halazonetis
8. C. Lukas

Citations in the corpus

• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “…are viable and show only partial DDR defects, they are growth-retarded and display increased cancer predisposition in the context of oncogenic mutations (Bassing et al. 2002, 2003; Celeste et al. 2002, 2003a), and H2AX-deficient cells show increased error-prone repair of DSBs (Xie et al. 2004).”
• Checking on DNA damage in S phase (2004, background): “Although this is not required for the initial recruitment of the checkpoint sensor (or sensors”
• ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation (2004, background): “Interestingly, a recent study has suggested that H2AX is not required for the recruitment of these proteins to the DSB but is required for their retention (22).”
• Cell-cycle checkpoints and cancer (2004, background): “Exciting insights into these highly dynamic events have recently been obtained using new technologies for real-time imaging of fluorescently labelled checkpoint proteins in live cells, and phospho-specific antibodies that recognize proteins modified in response to DNA damag”
• Surviving the breakup: the DNA damage checkpoint. (2006, background): “A major role for γ-H2AX is the recruitment of chromatin remodelers, including the Ino80, Rvb1, NuA4, and Swr1 complexes to the DSB (12, 17, 35, 97, 110, 147).”
• γ-H2AX Dephosphorylation by Protein Phosphatase 2A Facilitates DNA Double-Strand Break Repair (2005, background): “Upon genotoxic stress, PP2A dissociates, at which point ATM is activated by S1981 autophosphorylation ( Bakkenist and Kastan, 2003; Goodarzi et al., 2004).”
• The γ‐H2A.X: Is it just a surrogate marker of double‐strand breaks or much more? (2008, background): “X and p53 functions in suppressing tumors [Bassing et al., 2003; Celeste et al., 2003a].”
• Mechanism and regulation of class switch recombination. (2008, background): “Rogakou EP, Pilch DR, Orr AH, Ivanova VS, Bonner WM. DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139.”
• γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “Also, laser-aided generation of DSBs in defined subnuclear volumes indicate that the initial distribution of NBS1, BRCA1 and 53BP1 to sites of DSBs does not require H2AX (86).”
• Methylated lysine 79 of histone H3 targets 53BP1 to DNA double-strand breaks (2004, background): “, and retention of 53BP1 at sites of DSBs requires histone H2A”