Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7.

By N. Wajapeyee, Ryan W Serra, Xiaochun Zhu, M. Mahalingam, Michael R. Green. Cell, 2008

927 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2eb493866c9a27e929df2cc8e759219620e63322

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. J. Campisi
2. Jesús Gil
3. F. Rodier
4. Peter W. Laird
5. Charles M. Perou
6. Scott W. Lowe
7. P. Jat
8. S. Baylin

In Immunology

1. J. Campisi
2. M. Demaria
3. Adam Freund
4. C. Patil
5. Jesús Gil
6. P. Jat
7. R. Kumari
8. F. Rodier

In Molecular Biology

1. J. Campisi
2. M. Demaria
3. Jesús Gil
4. Peter W. Laird
5. Adam Freund
6. S. Baylin
7. Hui Shen
8. F. Rodier

Citations in the corpus

• The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “Recently, activation of the BRAF oncogene in primary fibroblasts was shown to lead to the secretion of IGFBP-7, which acts through autocrine/paracrine pathways to induce senescence and apoptosis in neighboring cells (72).”
• p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “Among the benefits, some SASP components reinforce the senescence growth arrest (Kortlever et al, 2006; Acosta et al, 2008; Kuilman et al, 2008; Wajapeyee et al, 2008).”
• Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “First, the SASP can reinforce and maintain the senescent state in cell culture models of senescence [21,129–131].”
• Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Whether secreted CXCR2 ligands contribute to senescence in normal cells by acting in a paracrine way, as it has been described for IGFBP7, will require further investigation.”
• Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury (2013, background): “Importantly, both TIMP-2 and IGFBP7 appear to be able to signal in autocrine and paracrine fashions [24,27-30] thus spreading the ‘alarm’ from the site of injury.”
• Alzheimer's disease risk genes and mechanisms of disease pathogenesis (2014, neutral): “BIN1 also plays an important role in senescence and apoptosis (116,117).”
• Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “…factors, and stress stimuli, kinases catalyze the phosphorylation of IkB and the p65 subunit, triggering p65 release and the translocation of p65/p50 transcription factors into the nucleus, where they activate a range of genes involved in immune and inflammatory responses (Wan and Lenardo 2009).”
• 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).”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “shown to mediate senescence induced by oncogenic BRAF (Wajapeyee et al., 2008).”