Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence

By Naoko Ohtani, Z. Zebedee, T. Huot, Julie A Stinson, M. Sugimoto, Y. Ohashi, Andrew D. Sharrocks, G. Peters, E. Hara. Nature, 2001

694 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/5fa318f16a15f0705e8e7c0f726bff0cf61f63da

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In Molecular Biology

1. J. Campisi
2. N. Sharpless
3. M. Demaria
4. R. DePinho
5. N. Bardeesy
6. A. Alimonti
7. J. Kohli
8. E. Zagato

In Oncology

1. J. Campisi
2. D. Tuveson
3. R. DePinho
4. N. Bardeesy
5. M. Demaria
6. Ralph Weissleder
7. M. Pittet
8. Rakesh K. Jain

In Physiology

1. J. Campisi
2. N. Sharpless
3. M. Demaria
4. A. Alimonti
5. J. Kohli
6. E. Zagato
7. L. Pellegrini
8. A. Calcinotto

Citations in the corpus

• Exosomes maintain cellular homeostasis by excreting harmful DNA from cells (2017, neutral): “( d ) Purified exosomes from pre-senescent TIG-3 cells were subjected to sucrose density-gradient separation followed by western blotting using antibodies shown right, NanoSight analysis (NTA) for quantitative measurement of isolated exosome particles and quantitative PCR analysis for detection of ge”
• The ETS-domain transcription factor family (2001, background): “and, more recently, in regulation of cellular senescenc”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “In addition, PTEN loss can induce p16INK4A through upregulation of the transcription factor Ets2 (248) and involves APC/CDH1 (301).”
• Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “In addition, expression of Ets-1, a transcriptional activator of p16 (Ohtani et al., 2001), correlated with p16 expression, although absolute levels of Ets-1 did not necessarily increase with age (Krishnamurthy et al., 2004).”
• Hallmarks of Cellular Senescence. (2018, neutral): “Transcription factors, such as Sp1, Ets, AP1 (particularly JunB subunit), and PPARg [26–29], bind to the p16 promoter and trigger its transcription, while repressor mechanisms, such as the INK4A transcription silence element (ITSE), YB1, ID1, and AP-1 (c-Jun subunit), balance the activation of p16 [”
• Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “2003) and mitogenic stimuli (Alani et al. 2001; Ohtani et al. 2001).”
• Ink4a/Arf expression is a biomarker of aging. (2004, background): “This observation is consistent with the finding that Ets-1 induces the expression of p16INK4a, but not Arf, in cultured cells (40, 41) and suggests that a significant component of the in vivo variance in p16INK4a expression with aging (r2 = 0.”