p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype

By Adam Freund, C. Patil, J. Campisi. EMBO Journal, 2011

983 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/59fbe4359578b6f7c6c1ef9498cf4b24f0503a77

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. Jesús Gil
2. J. Campisi
3. Adam Freund
4. Claudio Franceschi
5. E. Verdin
6. Nicolás Herranz
7. Jodie Birch
8. Masashi Narita

In Oncology

1. J. Campisi
2. Jesús Gil
3. Adam Freund
4. E. Verdin
5. J. Rehwinkel
6. Jan H. J. Hoeijmakers
7. M. F. Gulen
8. Nicolás Herranz

In Physiology

1. Jesús Gil
2. J. Campisi
3. Adam Freund
4. Nicolás Herranz
5. Claudio Franceschi
6. Jodie Birch
7. E. Verdin
8. Domhnall McHugh

Citations in the corpus

• Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging (2017, background): “, 2015), and we have previously observed similar effects for NFkB and p53 inhibition (Freund et al., 2011; Rodier et al., 2009).”
• Senescence and the SASP: many therapeutic avenues (2020, background): “Glucocorticoid treatment decreases the production of selected components of the SASP, namely, proinflammatory cytokines like IL-6, across different inducers of senescence by inhibiting NF-κB (Laberge et al. 2012).”
• Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, neutral): “61–64 , 92– 94 ).”
• The senescence-associated secretory phenotype and its physiological and pathological implications (2024, neutral): “These data suggest that the DDR-independent and p53-associated SASP might be essential for senescence-mediated immune surveillance, although more studies are needed to validate this function.”
• Mechanisms of Vascular Aging (2018, background): “age response pathway, and GATA4 (transcription factor GATA-4).(82,83) There is growing evidence that the presence”
• Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence (2017, positive): “On a molecular level, several transcription factors have been implicated in the up-regulation of SASP-genes including NF-κ B, C/EBP-β , p38 MAPK and GATA4 12, 13, 14, 15, 16.”
• Cellular senescence and its effector programs (2014, background): “Of note, DDR-independent senescence has also been reported in some experimental conditions where p16, p38MAPK, or ATR is constitutively activated or tumor suppressor Pten is completely lost (Toledo et al. 2008; Rodier et al. 2009; Alimonti et al. 2010; Freund et al. 2011).”
• Aging, Cellular Senescence, and Cancer (2012, background): “This plasma membrane–associated cytokine binds its plasma membrane–associated receptor (IL1R), ARI 10 January 2013 17:40 MMP: matrix metalloproteinase which in turn initiates a signaling cascade that ultimately activates NF-κB (116, 117).”
• Mechanisms and functions of cellular senescence. (2018, neutral): “Multiple signaling pathways, including the DDR (81, 82), p38 MAP kinase (33), and cGAS/STING (83–85), have been linked with the regulation of the SASP.”