Atm P53 Interaction
Atm P53 Interaction - Related Videos
17:59
Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice
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Cited by 11 •
2011
In this video we demonstrate a protocol to establish mouse thymic lymphoma cell lines. By following this protocol, we have successfully established several T-cell lines from Atm-/- and p53-/- mice with thymic lymphoma.
04:56
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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2025
Hs578T breast cancer cells harboring the p53 V157F mutation exhibit significantly higher Thioflavin T fluorescence compared to MCF7 cells, indicating enhanced protein aggregation. Multipoint fluorescence measurements improve detection accuracy and reliability in identifying β-sheet-rich aggregates, underscoring the importance of aggregation-prone p53 mutations in cancer research and the development of therapeutic strategies.
10:55
Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Cited by 1 •
2022
The protocol describes a step-by-step method to purify ubiquitinated proteins from mammalian cells using the p53 tumor suppressor protein as an example. Ubiquitinated p53 proteins were purified from cells under stringent nondenaturing and denaturing conditions.
13:10
Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
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Cited by 3 •
2017
Here, it is demonstrated how the in situ Proximity Ligation Assay (PLA) can be used to detect and visualize the direct protein-protein interactions between ATM and p53 in suspension cell cultures exposed to genotoxic stress.
14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Cited by 16 •
2019
Presented here are four protocols to construct and exploit yeast Saccharomyces cerevisiae reporter strains to study human P53 transactivation potential, impacts of its various cancer-associated mutations, co-expressed interacting proteins, and the effects of specific small molecules.
FAQs
Phosphorylation changes the regulatory balance surrounding p53. After double-strand breaks activate ATM, the kinase modifies both p53 and MDM2, a regulatory protein that normally inhibits p53. These modifications reduce MDM2-mediated inhibition, allowing p53 to become more stable and accumulate. This shift converts a damage signal into a stronger tumor-suppressor response.
The p53 response can produce different outcomes depending on damage severity. A repairable signal can promote cell-cycle arrest, giving the cell time to support DNA repair. When damage is severe, p53 can instead activate apoptosis, eliminating a cell that may threaten genomic stability. Thus, the pathway links damage assessment with distinct protective outcomes.
ATM functions primarily as a damage-responsive kinase that transmits information from DNA double-strand breaks. p53 acts downstream as a transcriptional regulator that activates genes affecting cell-cycle arrest, DNA repair, or apoptosis. Their interaction therefore connects signal detection with changes in cellular behavior, rather than representing two interchangeable components of the response.
A focused analysis can follow the sequence from ATM activation to phosphorylation of p53 and MDM2, followed by p53 stabilization and accumulation. The downstream assessment should then consider activation of genes associated with cell-cycle arrest, DNA repair, or apoptosis. Tracking these linked events helps determine whether damage signaling reaches its expected functional outcomes.
Defects in ATM or p53 can weaken the mechanisms that preserve genomic stability after DNA damage, helping explain their association with cancer. Comparing pathway activity or failure may support identification of biomarkers that reflect DNA-damage responses. The same information can guide research into therapies designed to target or exploit altered damage-response signaling.
This interaction provides a molecular framework for connecting DNA damage with regulated changes in protein activity, stability, and gene expression. In biochemistry, it highlights how phosphorylation and inhibitory regulation reshape signaling pathways. In cancer research, the pathway helps explain how impaired damage responses affect genomic stability and supports investigation of diagnostic biomarkers and targeted therapeutic strategies.