Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence

By R. Kortlever, P. Higgins, René Bernards. Nature Cell Biology, 2006

630 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/2f85cf740f1006b6a4b0515ca5aa4f7ff50f7d66

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Citations in the corpus

Senescence and apoptosis: dueling or complementary cell fates? (2014, positive): “First, the SASP can reinforce and maintain the senescent state in cell culture models of senescence [21,129–131].”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “The plasminogen activator inhibitor (PAI)-1 is necessary and sufficient for the induction of senescence (Kortlever et al., 2006).”
cGAS is essential for cellular senescence (2017, background): “Components of SASP not only serve as a marker of senescence, but also participate in the senescence process (13).”
The essence of senescence. (2010, background): “Likewise, the ECM regulator PAI-1 has been shown to mediate senescence (Kortlever et al. 2006), although clinical data seem to point to a more complex picture (Kuilman and Peeper 2009).”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “As with other p53 responses, senescence is likely to result from changes in the expression of a number of proteins such as the plasminogen activator inhibitor 1 (PAI-1) (Kortlever et al., 2006; Leal et al., 2008).”
Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “Importantly, a second, independent shRNA knocking down PTEN expression (Kortlever et al., 2006) also conferred resistance to trastuzumab, effectively ruling out the possibility that ‘‘off target’’ effects of the shRNA vectors caused the resistance phenotype (Figure 2A).”
Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “demonstrated that it does have a fundamental role in replicative senescenc”
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.”
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (2015, background): “p21 and PAI-1, both regulated by p53, are implicated in protection of cancer and other cell types from apoptosis (Gartel & Radhakrishnan, 2005; Kortlever et al., 2006; Schneider et al., 2008; Vousden & Prives, 2009).”
Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “Depending on the biological context, this process can facilitate tumor regression or the resolution of wound healing responses (Xue et al. 2007; Krizhanovsky et al. 2008).”
Aging, Cellular Senescence, and Cancer (2012, background): “In mouse cells, the SASP factor PAI-1 (plasminogen activator inhibitor 1) reinforces replicative senescence (137).”
Cellular senescence and its effector programs (2014, background): “Early studies showed that late passage human fibroblasts or fibroblasts derived from subjects with premature aging syndromes produce secretory proteins, including plasminogen activator inhibitor type-1 (PAI-1), which later became a functional marker of senescence (Murano et al. 1991; Goldstein et al”
Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Secreted factors such as PAI-1 (Kortlever et al., 2006) and IGFBP7 (Wajapeyee et al., 2008) also contribute to senescent growth arrest.”