Skip to content

Advertisement

We’re sorry, something doesn't seem to be working properly.

Please try refreshing the page. If that doesn't work, please contact us so we can address the problem.

Id and aging

  • Jonathan B Weitzman
Genome Biology20012:spotlight-20010629-01

https://doi.org/10.1186/gb-spotlight-20010629-01

Published: 29 June 2001

Keywords

Cell GrowthCellular AgingCell AgingGenetic EvidencePremature Senescence

Id1 is one of a family of helix-loop-helix (HLH) proteins that inhibits transcription by sequestering other HLH factors. It has been implicated in the regulation of cell growth and cellular aging. In the July 3 Proceedings of the National Academy of Sciences, Alani et al. provide genetic evidence supporting a role for Id1 in preventing cell aging (Proc Natl Acad Sci USA 2001, 98:7812-7816). They found that fibroblasts from Id1-null mice display premature senescence with increased expression of the cell-cycle regulators p16/INK4a, cyclin D1 and cyclin E. They show that Id1 specifically inhibits transcription of the p16/INK4a promoter, but does not affect p19/Arf regulation (although p19 is transcribed from the same locus as p16). Two E-box motifs in the p16/INK4a promoter are essential for Id1 repression. Finally, they report increased expression of p16/INK4a in vivo, in the ventral telencephalon of Id1-null embryos. The authors speculate that Id1 repression may be responsible for deregulation of p16 expression in the early stages of tumorigenesis.

References

  1. ID helix-loop-helix proteins in cell growth, differentiation and tumorigenesisGoogle Scholar
  2. Proceedings of the National Academy of Sciences , [http://www.pnas.org]
  3. High incidence of T-cell tumors in E2A-null mice and E2A/Id1 double-knockout mice.Google Scholar

Copyright

© BioMed Central Ltd 2001

Advertisement