PUBLICATION

Fam83F induces p53 stabilisation and promotes its activity

Authors
Salama, M., Benitez-Riquelme, D., Elabd, S., Munoz, L., Zhang, P., Glanemann, M., Mione, M.C., Goldin, R., Soussi, T., Davidson, G., Blattner, C.
ID
ZDB-PUB-190130-5
Date
2019
Source
Cell death and differentiation   26(10): 2125-2138 (Journal)
Registered Authors
Blattner, Christine, Mione, Marina
Keywords
none
MeSH Terms
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Intracellular Signaling Peptides and Proteins/genetics*
  • Neoplasm Proteins/genetics*
  • Tumor Suppressor Protein p53/metabolism*
PubMed
30692643 Full text @ Cell Death Differ.
Abstract
p53 is one of the most important tumour suppressor proteins currently known. It is activated in response to DNA damage and this activation leads to proliferation arrest and cell death. The abundance and activity of p53 are tightly controlled and reductions in p53's activity can contribute to the development of cancer. Here, we show that Fam83F increases p53 protein levels by protein stabilisation. Fam83F interacts with p53 and decreases its ubiquitination and degradation. Fam83F is induced in response to DNA damage and its overexpression also increases p53 activity in cell culture experiments and in zebrafish embryos. Downregulation of Fam83F decreases transcription of p53 target genes in response to DNA damage and increases cell proliferation, identifying Fam83F as an important regulator of the DNA damage response. Overexpression of Fam83F also enhances migration of cells harbouring mutant p53 demonstrating that it can also activate mutant forms of p53.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping