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SAB4300213

Sigma-Aldrich

Anti-phospho-H2AFX (pSer139) antibody produced in rabbit

affinity isolated antibody

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Synonym(s):
Anti-H2A histone family, member X antibody produced in rabbit, Anti-H2A.X antibody produced in rabbit, Anti-H2A/X antibody produced in rabbit, Anti-H2AX antibody produced in rabbit
MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~15 kDa

species reactivity

human

concentration

1 mg/mL

technique(s)

indirect immunofluorescence: 1:100-1:200
western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(Q-A-SP-Q-E)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pSer139)

Gene Information

human ... H2AFX(3014)

Immunogen

Peptide sequence around phosphorylation site of serine 139 (Q-A-S(p)-Q-E), according to the protein H2AFX.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

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.

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Eva Pagáčová et al.
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Diverse stresses including genotoxic therapy can induce proliferating cancer cells to undergo cellular senescence and take on the characteristic phenotypes of replicative cellular aging. This accelerated or therapy-induced senescence has been alternatively proposed to contribute to therapeutic efficacy or resistance.
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Cell death & disease, 10(3), 199-199 (2019-03-01)
Senescence is a tumor-suppressive mechanism induced by telomere shortening, oncogenes, or chemotherapy treatment. Although it is clear that this suppressive pathway leads to a permanent arrest in primary cells, this might not be the case in cancer cells that have

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