Reversal of human cellular senescence: roles of the p53 and p16 pathways

By C. Beauséjour, A. Krtolica, F. Galimi, Masashi Narita, Scott W. Lowe, P. Yaswen, J. Campisi. EMBO Journal, 2003

1,448 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3227e8459bc6436a72add9365fc876983707f00b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Campisi
2. Adam Freund
3. F. Rodier
4. D. Peeper
5. T. Kuilman
6. C. Patil
7. P. Desprez
8. Jiandong Chen

In Physiology

1. J. Campisi
2. Adam Freund
3. F. Rodier
4. P. Desprez
5. C. Patil
6. Jean-Philippe Coppé
7. M. Demaria
8. D. Peeper

Citations in the corpus

• Four faces of cellular senescence (2011, neutral): “However, some senescent cells that do not express the CDKi p16INK4a can resume growth after genetic interventions that inactivate the p53 tumor suppressor (Beauséjour et al., 2003).”
• Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “Although largely irreversible, upon acute inactivation of Rb or p53 genes senescence can be reversed (Beausejour et al., 2003; Dirac and Bernards, 2003; Sage et al., 2003).”
• Metabolic regulation of hematopoietic stem cells in the hypoxic niche. (2011, background): “However, once p16Ink4a is highly expressed, cell cycle arrest becomes irreversible by p53 downregulation, indicating that activation of the p53 pathway plays an important role in the initiation of senescence (Campisi, 2005; Beauséjour et al., 2003).”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, neutral): “There have been several previous reports that loss of TP53 does not enable escape from oncogene-induced senescence (see, for example, Beausejour et al., 2003; Narita et al., 2006; Zhu et al., 1998).”
• The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Despite the general perception that senescence is irreversible, inactivation of p53 can cause cell-cycle reentry in senescent cells (Beausejour et al. 2003).”
• An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “These signaling responses subsequently stimulate pathways related to cell senescence and death (20).”
• Aging, Cellular Senescence, and Cancer (2012, background): “However, molecular biological manipulations, for example, the sequential inactivation of certain tumor suppressor genes, can cause senescent cells to proliferate (10).”
• Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion (2009, neutral): “dtd" [ ]> Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cell”
• Cellular senescence and its effector programs (2014, background): “Compared with senescent BJ cells, which tend to have relatively low expression of p16, attempts to reverse senescence in WI38 lung embryonic fibroblasts in which the p16–Rb pathway is intact are less successful (Beauséjour et al. 2003).”
• p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, methodology): “Lentiviral vectors encoding ATM shRNAs, CHK2 shRNAs, p53 shRNA (Rodier et al, 2009) and virus production were as described (Naldini et al, 1996; Beausejour et al, 2003).”
• Modulation of mammalian life span by the short isoform of p53. (2004, result): “Pharmacological reversal of replicative senescence by blocking the expression of p21Cip1 is similar to a result with presenescent human fibroblasts in which senescence could be reversed in cells expressing p21, but not in cells expressing p16 (Beausejour et al. 2003).”