The signals and pathways activating cellular senescence.

By I. Ben-Porath, R. Weinberg. International Journal of Biochemistry and Cell Biology, 2005

1,070 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d1d033fcefc2538e5f278308a03e76a3963404a5

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In Aging

1. M. Demaria
2. D. Peeper
3. T. Kuilman
4. J. Campisi
5. P. Desprez
6. Jean-Philippe Coppé
7. Jesús Gil
8. Tao Lu

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. P. Desprez
5. Jean-Philippe Coppé
6. D. Peeper
7. T. Kuilman
8. A. Krtolica

In Physiology

1. J. Campisi
2. M. Demaria
3. Jesús Gil
4. P. Desprez
5. Jean-Philippe Coppé
6. D. Peeper
7. T. Kuilman
8. A. Krtolica

Citations in the corpus

• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “This has been referred to as premature senescence, as opposed to replicative or telomeredependent senescence (Ben-Porath and Weinberg, 2005).”
• The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “A plethora of stresses can provoke cellular senescence (22, 23).”
• DNA damage response and cellular senescence in tissues of aging mice (2009, background): “Whether senescence is simply an artefact of cell culture or whether it exists to any significant amount in vivo has been repeatedly and intensively debated (Ben-Porath & Weinberg, 2005).”
• Therapy-induced senescence in cancer. (2010, background): “Stress signaling through the p38 (mitogen-activated protein kinase 14, MAPK14), c-JUN N-terminal kinase (MAPK8), and extracellular signal-regulated kinase (MAPK1) pathways occurs in oncogene-induced senescence and replicative senescence, although this has not been widely investigated in TIS (42,55,5”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Many types of stresses can provoke cellular senescence [5, 29] (see Fig.”
• The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4 (2015, background): “5E), which suggests that the DNA damage response (DDR) acts upstream of this pathway (1, 2, 20, 54, 55).”
• Skin Wound Healing Process and New Emerging Technologies for Skin Wound Care and Regeneration (2020, background): “Inflammatory cells collected in the chronic wound bed rise to levels of reactive oxygen species (ROS), resulting in ECM protein injuries and premature cellular senescence [22].”
• Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “Their crucial roles in senescence are highlighted by their almost invariable inactivation in cance”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, neutral): “replicative and oncogene-induced senescence (reviewed in Ben-Porath and Weinberg, 2005 ).”
• Targeting the Mitogen-Activated Protein Kinase RAS-RAF Signaling Pathway in Cancer Therapy (2012, background): “, p27Kip1), and it is adopted by normal cells to overcome oncogene activation [40,41].”