Description
Key facts
Cell type:MCF7,
Species or organism:Human,
Tissue:Breast,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Disease:Adenocarcinoma
Product details:
Recommended control:
Human wild-type MCF7 cell line (ab277916). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
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-ATM, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
ATM also known as Ataxia Telangiectasia Mutated is a protein kinase with a molecular weight of approximately 370 kDa. ATM protein primarily resides in the cell nucleus and functions as a critical regulator of the cell cycle. It plays a significant role in the detection of DNA damage and initiation of repair processes. As part of its mechanical functions ATM phosphorylates serine and threonine residues on various substrates most notably in response to double-strand breaks in DNA. This activity is important for maintaining genomic stability.
Biological function summary
ATM acts as a coordinator in cellular response to DNA damage highly interacting with multiple components of the DNA repair machinery. It forms a complex with proteins like NBS1 and MRN complex facilitating repair by recruiting and activating other proteins involved in homologous recombination and non-homologous end joining pathways. ATM also modulates p53 activity a primary response factor in cellular stress management linking ATM to control of cell cycle arrest and apoptosis. This positions ATM as an integral part of maintaining cellular integrity in face of genomic insult.
Pathways
ATM integrates neatly within the DNA damage response and cell cycle control pathways. ATM's operative relationship with the MRN complex and its role in the PI3K-related protein kinase family helps initiate appropriate repair processes upon DNA damage detection. Additionally ATM regulates the activity of proteins such as Chk2 which further propagates signals to p53 influencing decisions between cell cycle arrest and apoptosis. These interactions link ATM closely to essential processes like DNA repair and cell survival highlighting its role in genomic maintenance.
ATM mutations or dysregulation leads to Ataxia Telangiectasia an autosomal recessive disorder characterized by neurodegeneration immune deficiencies and cancer predisposition. ATM dysfunction also connects to cancer development particularly breast cancer where it transmits signals involving BRCA1 contributing to DNA repair through homologous recombination. Understanding ATM dynamics and related pathways has important implications for developing therapeutic strategies to manage or mitigate effects associated with its dysfunction.
