Tumor suppression by Ink4a-Arf: progress and puzzles.

By Scott W. Lowe, C. Sherr. Current Opinion in Genetics and Development, 2003

781 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1433cd1a3c93dfc632c866a8be905ee7095e4ee5

How researchers see this paper

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

In Immunology

1. J. Campisi
2. R. Weinberg
3. Arnold J. Levine
4. S. Morrison
5. Alec C. Kimmelman
6. R. DePinho
7. N. Bardeesy
8. M. Demaria

In Molecular Biology

1. K. Helin
2. J. Campisi
3. A. Bracken
4. S. Morrison
5. H. Ohgaki
6. P. Kleihues
7. Alec C. Kimmelman
8. Diego Pasini

In Oncology

1. J. Campisi
2. R. Weinberg
3. Alec C. Kimmelman
4. S. Harris
5. R. DePinho
6. S. Morrison
7. K. Helin
8. Arnold J. Levine

Citations in the corpus

• Hmga2 promotes neural stem cell self-renewal in young, but not old, mice by reducing p16Ink4a and p19Arf expression (2008, background): “…al., 2005; Molofsky et al., 2005). p16 Ink4a is a cyclin-dependent kinase inhibitor that promotes Rb activation, slowing cell-cycle progression or inducing cellular senescence (Lowe and Sherr, 2003). p19 Arf promotes p53 activity, also slowing cell-cycle progression or inducing cellular senescence.”
• Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “…or both. the cell cycle inhibitor p16. p16 is a positive regulator of pRB and tumor suppressor in its own right (Sherr and McCormick, 2002). p16 is induced by a variety of stressful stimuli, including overexpression of oncogenes such as RAS and suboptimal culture conditions (Lowe and Sherr, 2003).”
• The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells. (2007, background): “Both of these proteins are encoded by the INK4A-ARF locus and are tumor suppressors that act upstream of the pRB and p53 pathways, respectively (Lowe and Sherr 2003).”
• p53 represses c-Myc through induction of the tumor suppressor miR-145 (2009, background): “Moreover, c-Myc can enhance p53 expression through p19Arf (31).”
• Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas. (2005, background): “p16 binds to cyclin-dependent kinase 4 (CDK4) and inhibits the CDK4/cyclin D1 complex (44, 45).”