Description
Key facts
Cell type:A549,
Species or organism:Human,
Tissue:Lung,
Form:LiquidSee storage information,
Knockout validation:Next Generation Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Heterozygous: (+/-): 49 bp deletion in exon 3,
Disease:Carcinoma
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-ATR, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Next Generation Sequencing, Western blot, Zygosity-Heterozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°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.
