Abcam, ab289363, Anti-ATR (phospho T1989) antibody [HL132] - BSA and Azide free

Size: 100µL
Rabbit Recombinant Monoclonal ATR phospho T1989 antibody. Carrier free. Suitable for WB, IHC-P, ICC/IF and reacts with Human, Mouse, Rat samples. Cited in 3 publications. Immunogen corresponding to Synthetic Peptide within Human ATR phospho T1989.
Key facts
Host species:Rabbit,
Clonality:Monoclonal,
Clone number:HL132,
Isotype:IgG,
Carrier free:Yes,
Reacts with:Mouse, Human, Rat,
Applications:IHC-P, WB, ICC/IFSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Synthetic Peptide within Human ATR phospho T1989. The exact immunogen used to generate this antibody is proprietary information.Q13535

Product details:
What are the advantages of a recombinant monoclonal antibody?
This product is a recombinant monoclonal antibody, which offers several advantages including:
- High batch-to-batch consistency and reproducibility
- Improved sensitivity and specificity
- Long-term security of supply
- Animal-free batch production
For more information, read more on
recombinant antibodies
Conjugation ready
Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications.
Use our
conjugation kits
for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein A, Storage buffer-pH: 7.4Constituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
ATR also known as Ataxia Telangiectasia and Rad3-related protein is a serine/threonine kinase with a molecular weight of approximately 301 kDa. This protein localizes mainly in the nucleus where it functions as an important component in the cellular response to DNA damage and replication stress. ATR detects DNA strand breaks and ssDNA coated with RPA and becomes activated to phosphorylate several downstream targets initiating the DNA damage response. High expression of ATR occurs in proliferative tissues emphasizing its role in cell cycle regulation.
Biological function summary
ATR plays an essential role in maintaining genomic stability. It is part of a larger protein complex that includes ATRIP (ATR-interacting protein) which helps in localizing ATR to sites of DNA damage. Once activated ATR phosphorylates various substrates including CHK1 a critical checkpoint kinase involved in cell cycle arrest during DNA repair processes. The ability of ATR to coordinate with these proteins helps cells manage DNA damage effectively and prevent genomic instability.
Pathways
ATR functions centrally in the DNA damage response and repair mechanisms particularly the ATR-Chk1 pathway. This pathway interacts closely with the ATM (Ataxia Telangiectasia Mutated) pathway which also responds to DNA damage but usually to double-strand breaks. ATR primarily acts in response to replication stress and its activation leads to the arrest of the cell cycle allowing DNA repair to occur. This cooperation between ATR and ATM highlights their complementary roles in safeguarding genomic integrity under stress.
ATR mutations and dysregulation have strong associations with cancer and Seckel syndrome. In the context of cancer ATR often works in concert with ATM to manage DNA repair and cancer cells frequently overexpress ATR to cope with high levels of replication stress. This makes ATR a potential target for cancer therapy where its inhibition could sensitize tumor cells to chemotherapy. In Seckel syndrome ATR mutations result in developmental anomalies showcasing the important role ATR plays in cellular replication and repair processes.