Home | Impressum | Sitemap | KIT

Stem cells - p53 - DNA damage

     Group Leader: Christine Blattner

     tel.: +49 721 608 22634 (office) or -22714 (lab)
     fax: +49 721 608 23354
     email: christine blattnerBlb5∂kit edu

Blattner Lab Members
Blattner Publications
ITG Home

 

P53 is one of the most important tumour suppressor proteins. In resting cells, p53 is in a latent state. In the presence of DNA damage or upon other conditions with oncogenic potential, p53 becomes rapidly activated and slows down proliferation and/or eliminates cells with damaged DNA from the population. The importance of these activities becomes particularly clear in patients with Li-Fraumeni Syndrome. Carriers of this disease have inactivating mutations of p53 in the germ line which leads to tumourigenesis at a particular early age.

In addition, p53 is increasingly recognized as a DNA repair factor and it also has some, although as yet poorly characterized,
functions during embryonic development.

While maintaining genomic integrity is important for differentiated cells, it is absolutely fundamental for stem cells since this cell type provides the proliferative pool of a whole organism. Stem cells therefore should respond very efficiently to lesions in the DNA. In contrast to differentiated cells, p53, one of the key factors of the DNA damage response, is primarily localised in the cytoplasm of this cell type, while it is nuclear in differentiated cells. This aberrant localisation of p53 raises several questions that we are investigating.

We are particularly focussing on the following issues:

  • Why is p53 cytoplasmic in stem cells ?
  • How do stem cells respond to DNA damage and what is the role of p53 ?
  • What is the function of cytoplasmic p53 ?
  • What alters the cellular localisation of p53 during development ?
  • Is p53 important forl development and if yes, what is its function ?

p53 expression in stem cells

p53 expression in stem
cells.
The p53 protein is
stained in green while nuclei
are stained in blue.

 

 

Updated: January 29, 2010