Chemokine signaling via the CXCR2 receptor reinforces senescence.
By J. Acosta, A. O’Loghlen, Ana Banito, M. Guijarro, A. Augert, S. Raguz, M. Fumagalli, Marco da Costa, C. Brown, N. Popov and 6 more. Cell, 2008
1,732 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/fd0463827cdf6b621badb016c65d6b64e029ecff
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Citations in the corpus
- Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (2013, background): “An emerging hallmark feature of senescent cells is the senescence-associated secretory phenotype (SASP) that allows extensive signaling from the nonproliferating cells to the external environment (Acosta et al., 2008; Coppé et al., 2010; Kuilman et al., 2008, 2010).”
- Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, neutral): “The SASP cytokines, IL-6 and IL-8, also reinforce the senescence growth arrest, at least in some senescent cells (62, 63), which is beneficial in defense against cancer.”
- Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, background): “The SASP can be beneficial because some SASP components reinforce the senescent growth arrest by an autocrine cytokine network [37,38,40,41], thereby contributing to maintenance of the senescence growth arrest.”
- Mesenchymal Differentiation Mediated by NF-κB Promotes Radiation Resistance in Glioblastoma (2013, result): “The interdependency of NF-kB and C/EBPb has also been previously reported in other studies (Acosta et al., 2008; Kuilman et al., 2008).”
- mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype (2015, positive): “In contrast, the SASP can induce senescence 4,6,7 and activate the immune system to keep neoplastic cells in check 8 .”
- 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.”
- The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “Some of these cytokines, namely IL-8 and IL-6, are known to feedback to the secreting cells to reinforce senescence signaling (Acosta et al., 2008; Kuilman et al., 2008).”
- A proteomic atlas of senescence-associated secretomes for aging biomarker development (2019, background): “The SASP was originally characterized by antibody arrays, which are necessarily biased, to measure the secretion of a small set of pro-inflammatory cytokines, proteases and protease inhibitors, and growth factors [1,2,4,22].”
- Senescence impairs successful reprogramming to pluripotent stem cells. (2009, methodology): “, 2004), as well as E6, E7, E6/E7, plasmids; HRAS V12, and plasmid for expression of a shRNA targeting p53 (pRS-shp53) have been described before (Acosta et al., 2008; Brummelkamp et al., 2002).”
- Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, result): “Similar results are reported in an accompanying paper by Gil and colleagues (Acosta et al., 2008), showing that CXCR2-binding chemokines expressed by senescent cells regulate growth arrest.”
- CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma (2016, positive): “Of particular relevance to PDAC, are the elegant studies that show that CXCR2 reinforces RAS-mediated senescence in culture, and regulates the senescence-associated secretory phenotype (Acosta et al., 2008).”
- Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “IL-8, GROα, IL-6, and IGBP-7 are among the specific SASP components reinforcing senescence (Acosta et al., 2008; Kuilman et al., 2008; Wajapeyee et al., 2008).”