Genomic Instability in Mice Lacking Histone H2AX

By Arkady Celeste, Simone Petersen, P. Romanienko, O. Fernández-Capetillo, H. Chen, O. Sedelnikova, B. Reina-San-Martin, V. Coppola, E. Meffre, M. Difilippantonio and 11 more. Science, 2002

1,477 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4f052ee4869b06a863ca68142c7a85d97df7e7ab

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “While 53BP1 can be targeted to damaged chromatin by the above mechanism, its efficient accumulation and sustained retention withinDSB-containing chromatin requires g-H2AX andMDC1 (64,65,72,77,83).”
Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL) (2015, background): “Phosphorylated histone H2AX (γ-H2AX) is associated with activation of DNA-damage repair pathways and enhanced radio and chemoresistance of cancer cells [21–25].”
The role of double-strand break repair — insights from human genetics (2006, background): “During V(D)J recombination, Artemis-mediated cleavage of coding-junction hairpins does not require ATM, the MRN complex, TP53BP1 or H2AFX, as mice or patients that lack these components do not show a SCID phenotyp”
Surviving the breakup: the DNA damage checkpoint. (2006, background): “both fungal and animal cells and is required for full viability of yeast and animal cells in the presence of DNA damaging agents (17, 18, 36, 102, 116).”
Mechanism and regulation of class switch recombination. (2008, background): “The antigenspecific IgG1 response to immunization is reduced to about 30% of wild-type mice, and nonimmune serum levels of IgG1, IgG3, and IgA are all reduced to 15%–50% of wild-type (43, 113, 142, 169).”
A Probabilistic Classification Tool for Genetic Subtypes of Diffuse Large B Cell Lymphoma with Therapeutic Implications (2020, background): “A53 tumors also acquire homozygous deletions and mutations targeting 53BP1 (TP53BP1), a DNA-damage sensor that prevents aneuploidy (Celeste et al., 2002), consistent with the recurrent gains and losses of chromosome arms in A53.”
ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation (2004, background): “More recently, another aspect of the DNA damage response has been described in which the role of ATM appears to be redundant, namely, the recruitment of proteins that form as foci that overlap with -H2AX foci (4, 6, 21, 22).”
Cellular response to hyperosmotic stresses. (2007, background): “Thus Mre11 exonuclease is a nuclear protein that normally binds rapidly to DNA breaks, beginning the process of repair (64), and histone H2AX becomes phosphorylated at DNA doublestranded breaks caused by a number of agents (90, 250, 309), both being prerequisite for successful DNA repair (45, 229).”
Role of RAD52 Epistasis Group Genes in Homologous Recombination and Double-Strand Break Repair (2002, background): “The phosphorylated form of H2AX ( -H2AX), a nonessential member of the histone H2A family (48), associated with the sites of damage within 30 min, and HsRad50 was found to colocalize extensively with -H2AX.”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “…lacking H2AX, RNF8, or 53BP1, and, to a lesser extent, MDC1, have class switch recombination defects that would have profound impacts on animal viability in natural environments (Petersen et al. 2001; Celeste et al. 2002; Ward et al. 2004; Lou et al. 2006; L Li et al. 2010; Santos et al. 2010).”