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Histone H2A.X (Phospho Tyr142) Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | P16104 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 15145 Da |
| Gene ID | 3014 |
|---|---|
| Other Names | H2AFX; H2AX; Histone H2A.x; H2a/x |
| Dilution | WB~~WB: 1:1000-2000 |
| Format | PBS, pH 7.4, containing 0.09% (W/V) sodium azide as Preservative and 50% Glycerol. |
| Storage Conditions | -20℃ |
| Name | H2AX (HGNC:4739) |
|---|---|
| Function | Variant histone H2A which replaces conventional H2A in a subset of nucleosomes. Nucleosomes wrap and compact DNA into chromatin, limiting DNA accessibility to the cellular machineries which require DNA as a template. Histones thereby play a central role in transcription regulation, DNA repair, DNA replication and chromosomal stability. DNA accessibility is regulated via a complex set of post- translational modifications of histones, also called histone code, and nucleosome remodeling. Required for checkpoint-mediated arrest of cell cycle progression in response to low doses of ionizing radiation and for efficient repair of DNA double strand breaks (DSBs) specifically when modified by C-terminal phosphorylation. |
| Cellular Location | Nucleus. Chromosome |
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Provided below are standard protocols that you may find useful for product applications.
Background
Variant histone H2A which replaces conventional H2A in a subset of nucleosomes. Nucleosomes wrap and compact DNA into chromatin, limiting DNA accessibility to the cellular machineries which require DNA as a template. Histones thereby play a central role in transcription regulation, DNA repair, DNA replication and chromosomal stability. DNA accessibility is regulated via a complex set of post-translational modifications of histones, also called histone code, and nucleosome remodeling. Required for checkpoint-mediated arrest of cell cycle progression in response to low doses of ionizing radiation and for efficient repair of DNA double strand breaks (DSBs) specifically when modified by C- terminal phosphorylation.
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