Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all

By J. Gil, G. Peters. Nature reviews. Molecular cell biology, 2006

891 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7d89100165f2f5b379ee5297398c681de295e7d9

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Citations in the corpus

Cellular senescence in cancer and aging. (2007, positive): “Whereas p16INK4a is an inhibitor of the cyclin-dependent kinases CDK4 and CDK6 and acts by imposing a G1 cell cycle arrest, ARF regulates p53 stability through inactivation of the p53-degrading ubiquitin ligase MDM2 (Gil and Peters, 2006; Kim and Sharpless, 2006).”
2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. (2010, neutral): “3 associaion with CHD remain unclear, although the variants are djacent to CDKN2A, ARF, and CDKN2B, which are enes thought to regulate senescence and apoptosis (88).”
The Nucleolus under Stress (2010, background): “While long-term upregulation of p14ARF involves increased synthesis at the transcriptional level (Gil and Peters, 2006 ), short-term p14ARF stabilization is achieved by promoting its nucleolar localization via interactions with B23/NPM, which in turn prevents its association with ubiquitin ligases, ”
Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15INK4B tumor suppressor gene (2010, background): “All the three genes are expressed at a barely detectable low level in young and normal cells, and are accumulated during cell aging or in cells insulted by hyperproliferative oncogenic stimuli (Zindy et al., 1997; Krishnamurthy et al., 2004; Gil and Peters, 2006), suggesting a common cellular mechan”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “Epigenetic regulation of the INK4a/ARF locus during RIS The INK4a/ARF locus is normally subjected to strong epigenetic repression mediated by H3K27 methylation and recruitment of Polycomb-repressive complexes (Gil and Peters, 2006).”
Expression of Linear and Novel Circular Forms of an INK4/ARF-Associated Non-Coding RNA Correlates with Atherosclerosis Risk (2010, background): “Until recently little progress was made in understanding the biochemical basis for PcG-mediated INK4/ARF silencing, however two independent groups have since shown that the PcG complexes, PRC-1 and PRC-2, localize to the INK4/ARF locus and repress its activity through the establishment of repressive”
Divorcing ARF and p53: an unsettled case (2006, background): “Because it is difficult to understand how exon 2 of INK4a and ARF evolved to serve the functions of two distinct proteins, others have suggested that the structure of the locus highlights a need, at least in some biological settings, for the coordinated regulation of the gene product”
Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer. (2010, positive): “Overexpression of Bmi1, Cbx7, Ezh2, and Cbx8 extends the replicative lifespan of cells by bypassing senescence in a pRB-p16INK4A/p19ARF-dependent manner (Gil and Peters, 2006).”
Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Given this unusual concentration of three tumor suppressors in barely 35 kb, this locus plays a key regulatory role and is frequently mutated in cancer (Gil and Peters, 2006; Kim and Sharpless, 2006).”
Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Further, virtually all cancers harbor mutations in the p53 and/or p16/ pRB pathways, which, among other activities, are crucial for the senescence response [8, 9].”
Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, neutral): “both of these pathways [14,15].”