Skip to main content

DNA Damage-Mediated c-Myc Degradation Requires 14-3-3 Sigma

Buy Article:

$105.00 plus tax (Refund Policy)

14-3-3σ (sigma) is a gene product upregulated by p53 in response to DNA damage. DNA damage can also alter c-Myc protein levels, but the mechanism by which c-Myc is regulated after DNA damage remains unclear. Here, we discover that the expression of 14-3-3σ is essential to facilitate the degradation of c-Myc in response to DNA damage. 14-3-3σ targets c-Myc for degradation by mediating the interaction between c-Myc and Pin1, which facilitates subsequent ubiquitin-mediated degradation of c-Myc. 14-3-3σ-enhanced c-Myc degradation functionally antagonizes c-Myc-mediated DNA damage (genomic instability) and suppression of p53 transcriptional activity. These results define a novel mechanism for c-Myc inactivation after DNA damage and imply that 14-3-3σ and Pin1 collaborate in response to DNA damage to reduce c-Myc-mediated genomic instability and remove the braking effect of c-Myc on p53 transcriptional activity.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Data/Media
No Metrics

Keywords: 14-3-3 SIGMA; DNA DAMAGE; MYC; PIN1; UBIQUITINATION

Document Type: Research Article

Publication date: 2013-03-01

More about this publication?
  • World Journal of Cancer Research publishes original articles describing significant new findings in any area related to basic and clinical cancer research. These include studies of cancer related genes, molecules, drugs, cancer cell lines, tumorigenesis, cancer prevention, cancer progression and metastasis, cancer diagnosis, cancer treatment, cancer animal models, human cancer samples as well as cancer patients and all other cancer research related areas.
  • Editorial Board
  • Information for Authors
  • Subscribe to this Title
  • Aims and Scope
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more