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Histone H2AX is a variant of histone H2A, a nuclear protein and a component of the nucleosome core.1,2 It is a globular protein containing unstructured N- and C-terminal tails that extend outside of the nucleosome core that are subject to a variety of post-translational modifications (PTMs), including phosphorylation, acetylation, methylation, and ubiquitination, which function as epigenetic regulators of transcription.3,4 H2AX has a key role in the DNA damage response.1,3,4,5 Ionizing radiation induces acetylation of lysine 5 on H2AX (H2AXK5Ac) by TIP60, which is recognized by a bromodomain-like module in DNA protein kinase (DNA-PK).6,7 DNA-PK and other PI3K-like kinases ataxia-telangiectasia mutated kinase (ATM) and ataxia-telangiectasia and Rad3-related protein/kinase (ATR) phosphorylate serine 139 on H2AX (γH2AX) in response to DNA damage, leading to changes in chromatin structure at the damaged site that promote DNA repair.1,3,4,5 H2AX has additional roles in chromatin inactivation during meiosis and mitosis, as well as neural stem cell development and cellular senescence.5 Decreased tumor H2AX levels are associated with increased progression-free survival in patients with triple-negative breast cancer.8 Cayman’s Histone H2AXK5Ac Rabbit Monoclonal Antibody (Clone RM445) can be used for multiplex-based assay and Western blot (WB) applications. The antibody recognizes H2AXK5Ac at 15 kDa from human and other vertebrate samples.
WARNING This product is not for human or veterinary use.
1. Histone H2A variants in nucleosomes and chromatin: More or less stable? Nucleic Acids Res. 40(21), 10719-10741 (2012).
2. Writing, erasing and reading histone lysine methylations. Exp. Mol. Med. 49(4), e324 (2017).
3. H2AX: Functional roles and potential applications. Chromosoma 118(6), 683-692 (2009).
4. Post-
5. Multiple facets of histone variant H2AX: A DNA double-
6. DNA damage-
7. Non-
8. Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients. EMBO Mol. Med. 8(5), 527-549 (2016).