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Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
The Hallmarks of Aging
Cellular senescence: from physiology to pathology
In cancer and during active tissue repair, pro-senescent therapies contribute to minimize the damage by limiting proliferation and fibrosis, respectively, and antisenescent therapies may help to eliminate accumulated senescent cells and to recover tissue function.
Role of the INK4a Locus in Tumor Suppression and Cell Mortality
Cellular Senescence in Cancer and Aging
Tumour biology: Senescence in premalignant tumours
It is shown that senescent cells exist in premalignant tumours but not in malignant ones, and that senescence is therefore a defining feature of premalign tumours that could prove valuable in the diagnosis and prognosis of cancer.
Sirt1 protects against high-fat diet-induced metabolic damage
- P. Pfluger, D. Herranz, S. Velasco-Miguel, M. Serrano, M. Tschöp
- BiologyProceedings of the National Academy of Sciences
- 15 July 2008
Data is presented indicating that beneficial effects of Sirt1 are due to at least two mechanisms: induction of antioxidant proteins MnSOD and Nrf1, possibly via stimulation of PGC1α, and lower activation of proinflammatory cytokines, such as TNFα and IL-6, via down-modulation of NFκB activity.
The Ink4/Arf locus is a barrier for iPS cell reprogramming
It is concluded that the silencing of Ink4/Arf locus is rate-limiting for reprogramming, and its transient inhibition may significantly improve the generation of iPS cells.
Cellular Senescence: Defining a Path Forward
Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.
- A. Lin, M. Barradas, J. Stone, L. Van Aelst, M. Serrano, S. Lowe
- Biology, MedicineGenes & development
- 1 October 1998
The precisely opposite response of normal and immortalized cells to constitutive activation of the MAPK cascade implies that premature senescence acts as a fail-safe mechanism to limit the transforming potential of excessive Ras mitogenic signaling.