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Proteomic profiling of ATM kinase proficient and deficient cell lines upon blockage of proteasome activity

Valeria Marzano1, Simonetta Santini, Claudia Rossi

  • 1Proteomic and Metabonomic Laboratory, Fondazione Santa Lucia, 00143 Rome, Italy.

Journal of Proteomics
|May 30, 2012
PubMed

Insights

Ataxia Telangiectasia Mutated (ATM) deficiency impacts cellular stress responses and protein stability. This study reveals ATM

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Ataxia Telangiectasia Mutated (ATM) protein kinase is crucial for DNA damage and oxidative stress responses.
  • ATM deficiency characterizes Ataxia Telangiectasia (A-T), a rare genetic disorder.
  • ATM regulates hundreds of proteins, balancing cell proliferation and death.

Purpose of the Study:

  • To investigate phenotypic adaptations at the protein level in ATM-deficient versus ATM-proficient cells.
  • To identify proteins affected by ATM expression under basal and proteasome-inhibited conditions.
  • To explore the role of ATM in cellular carbohydrate metabolism regulation.

Main Methods:

  • Comparative proteomic analysis using label-free shotgun experiments on lymphoblastoid cells.
  • Bioinformatic analysis to identify differentially expressed proteins and functional pathways.
  • Targeted metabolic fingerprint analysis using Selected Reaction Monitoring (SRM) for glycolysis checkpoints.

Main Results:

  • Proteomic analysis revealed differentially expressed proteins between ATM-deficient and proficient cells.
  • Bioinformatic analysis suggested ATM deficiency influences cellular carbohydrate metabolism.
  • SRM analysis confirmed alterations in key glycolysis regulatory points.

Conclusions:

  • ATM deficiency leads to significant protein level changes and impacts cellular metabolism.
  • ATM plays a role in regulating glycolysis, suggesting a link between DNA damage response and metabolic pathways.
  • These findings contribute to understanding the molecular basis of A-T and potential therapeutic targets.

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