Control of cellular senescence by CPEB

Student Author(s)

Maria Ivshina

Academic Program

Interdisciplinary Graduate Program

UMMS Affiliation

Program in Molecular Medicine

Publication Date


Document Type



Biochemistry, Biophysics, and Structural Biology | Cell and Developmental Biology | Life Sciences | Medicine and Health Sciences


Cytoplasmic polyadenylation element-binding protein (CPEB) is a sequence-specific RNA-binding protein that promotes polyadenylation-induced translation. While a CPEB knockout (KO) mouse is sterile but overtly normal, embryo fibroblasts derived from this mouse (MEFs) do not enter senescence in culture as do wild-type MEFs, but instead are immortal. Exogenous CPEB restores senescence in the KO MEFs and also induces precocious senescence in wild-type MEFs. CPEB cannot stimulate senescence in MEFs lacking the tumor suppressors p53, p19ARF, or p16(INK4A); however, the mRNAs encoding these proteins are unlikely targets of CPEB since their expression is the same in wild-type and KO MEFs. Conversely, Ras cannot induce senescence in MEFs lacking CPEB, suggesting that it may lie upstream of CPEB. One target of CPEB regulation is myc mRNA, whose unregulated translation in the KO MEFs may cause them to bypass senescence. Thus, CPEB appears to act as a translational repressor protein to control myc translation and resulting cellular senescence.

DOI of Published Version



Genes Dev. 2006 Oct 1;20(19):2701-12. Link to article on publisher's site

Journal/Book/Conference Title

Genes and development

Related Resources

Link to article in PubMed

PubMed ID