home   genetic news   bioinformatics   biotechnology   literature   journals   ethics   positions   events   sitemap
 
  HUM-MOLGEN -> Genetic News | search  
 

p53 as a Barrier to Pluripotency

 
  August, 13 2009 14:49
your information resource in human molecular genetics
 
     
The well known molecule p53 serves not only as a tumour suppressor, but also acts as a barrier to the generation of induced pluripotent stem (iPS) cells. Five papers online in Nature show that when p53 is removed from cell populations that often fail to reprogram there is a higher degree of success.

The iPS cell field is fast moving -- just three years ago stem cells were created from fibroblasts thanks to the insertion of four viral factors. Teams have tweaked the method, removing one or more of those factors.

Shinya Yamanaka and colleagues managed to induce pluripotency in cells lacking p53 even without one of the four factors, and using a method that avoids genome integration of the factors.

Juan Carlos Izpisua Belmonte and co-workers also demonstrate that reprogramming in the absence of oncogenes such as c-Myc and Klf4 occurs more efficiently when inactivating both p53 and another tumour suppressor.

Another team led by Konrad Hochedlinger show that deletion of p53 in populations that do not reprogram rescues their ability to produce iPS cells, and that very high efficiencies can be achieved using immortalized cell lines that lack p53.

Maria Blasco and colleagues show that p53 is critically involved in preventing the reprogramming of cells carrying various types of DNA damage, including short telomeres. They go on to demonstrate that eliminating p53 allows efficient reprogramming even when there is DNA damage.

Meanwhile Manuel Serrano and his team look at a tumour suppressor locus and report that the locus limits reprogramming. Furthermore, ageing has an effect on this locus, which means reprogramming is less efficient in cells from older organisms.

Authors contacts:

Shinya Yamanaka (Kyoto University, Japan)(DOI: nature08235)
E-mail: yamanaka@frontier.kyoto-u.ac.jp

Juan Carlos Izpisua Belmonte (The Salk Institute, La Jolla, CA, USA)(DOI: nature08311)
E-mail: belmonte@salk.edu

Konrad Hochedlinger (Massachusetts General Hospital, Boston, MA, USA)(DOI: nature08285)
E-mail: khochedlinger@helix.mgh.harvard.edu

Maria Blasco Spanish (National Cancer Research Centre, Madrid, Spain)(DOI: nature08287)
E-mail: mblasco@cnio.es

Manuel Serrano (Spanish National Cancer Research Center, Madrid, Spain)(DOI: nature08290)
E-mail: mserrano@cnio.es

Abstracts available online:
Abstract of Paper 1.
Abstract of Paper 2.
Abstract of Paper 3.
Abstract of Paper 4.
Abstract of Paper 5.

(C) Nature press release.


Message posted by: Trevor M. D'Souza

print this article mail this article
Bookmark and Share this page (what is this?)

Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.

Use the links below to share this article on the social bookmarking site of your choice.

Read more about social bookmarking at Wikipedia - Social Bookmarking

Latest News
Variants Associated with Pediatric Allergic Disorder

Mutations in PHF6 Found in T-Cell Leukemia

Genetic Risk Variant for Urinary Bladder Cancer

Antibody Has Therapeutic Effect on Mice with ALS

Regulating P53 Activity in Cancer Cells

Anti-RNA Therapy Counters Breast Cancer Spread

Mitochondrial DNA Diversity

The Power of RNA Sequencing

‘Pro-Ageing' Therapy for Cancer?

Niche Genetics Influence Leukaemia

Molecular Biology: Clinical Promise for RNA Interference

Chemoprevention Cocktail for Colon Cancer

more news ...

Generated by News Editor 2.0 by Kai Garlipp
WWW: Kai Garlipp, Frank S. Zollmann.
7.0 © 1995-2017 HUM-MOLGEN. All rights reserved. Liability, Copyright and Imprint.