Rabbit anti-ATR Antibody, Affinity Purified

Ataxia-telangiectasia and Rad3-related protein (ATR) plays a key role in maintaining the integrity of the genome. It participates in stabilizing replication forks and modulates the cell cycle progression and DNA repair. ATR plays a vital role in cell viability. It sends out signals to control replication origin firing, replication fork repair, and mitotic entry prematurely. Lack of ATR affects normal development, aging, and tissue homeostasis. Mutation in the ATR gene is associated with Seckel syndrome.

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Ataxia telangiectasia and Rad3-related protein (ATR), a serine/threonine kinase, is a member of the phosphoinositide 3- kinase-related protein kinase s (PIKKs) family mainly to ataxia telangiectasia mutated (ATM) subfamily. It has a phosphatidylinositol 3/4 (PI3/4) kinase catalytic domain, 1 focal adhesion kinase, targeting (FAT) domain, 1 FATC domain, 1 UME domain, and 2 HEAT repeats. ATR has ATR-201 and ATR-202 isoforms. Isoform 1 is expressed at a high level in the testis. Isoform 2 is expressed in the pancreas, liver and, placenta. The ATR gene is located on human chromosome 3q23.

The epitope recognized by PLA0046 maps to a region between residues 1675 and 1725 of human Ataxia Telangiectasia and Rad3-related using the numbering given in entry NP_001175.1 (GeneID 545).

ATR (ATM and Rad3 related) is closely related to ATM (Ataxia telangiectasia, mutated) and is a member of the phosphatidylinositol 3 kinase (PI-3) family that is an early sensor of DNA damage. ATR is a serine-threonine kinase that reacts to UV damage and interruptions in replication. ATR may be able to sense DNA damage through interaction with Rad17 and 1as well as components of nucleosome remodeling complexes. In response to DNA damage, ATR has been shown to phosphorylate a multitude of substrates which include BRCA1, p53, Chk2, Rad 17, and E2F transcription factor 1.

Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide