• Publications
  • Influence
Mdm2 promotes the rapid degradation of p53
TLDR
It is proposed that the Mdm2-promoted degradation of p53 provides a new mechanism to ensure effective termination of the p53 signal.
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
TLDR
An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
The first 30 years of p53: growing ever more complex
TLDR
Thirty years ago p53 was discovered as a cellular partner of simian virus 40 large T-antigen, the oncoprotein of this tumour virus, and new functions of this protein were revealed, including the regulation of metabolic pathways and cytokines that are required for embryo implantation.
Generation of oscillations by the p53-Mdm2 feedback loop: a theoretical and experimental study.
TLDR
A simple mathematical model is presented suggesting that, under certain circumstances, oscillations in p53 and Mdm2 protein levels can emerge in response to a stress signal, and oscillations may allow cells to repair their DNA without risking the irreversible consequences of continuous excessive p53 activation.
Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes
TLDR
A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
mdm2 expression is induced by wild type p53 activity.
TLDR
It is suggested that the mdm2 gene is a target for activation by wt p53, and the induction of mDM2 expression by t p53 activity is at the mRNA level, suggesting a direct involvement of p53 in the process.
Decision making by p53: life, death and cancer
  • M. Oren
  • Biology
    Cell Death and Differentiation
  • 1 April 2003
TLDR
How the functional balance between these different interactions might dictate the likelihood of a given cell to become cancerous or be eliminated from the replicative pool, resulting in suppression of cancer is discussed.
p53 Activates the CD95 (APO-1/Fas) Gene in Response to DNA Damage by Anticancer Drugs
TLDR
Observations provide a mechanistic explanation for the ability of p53 to contribute to tumor progression and to resistance of cancer cells to chemotherapy.
The p53-Mdm2 module and the ubiquitin system.
...
...