(Q28190064)

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The INK4a/ARF network in tumour suppression

scientific article (publication date: October 2001)

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Europe PubMed Central

The INK4a/ARF network in tumour suppression (English)

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C J Sherr

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publication date

October 2001

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Nature Reviews Molecular Cell Biology

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10

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731-7

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The retinoblastoma protein and cell cycle control

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The regulation of E2F by pRB-family proteins

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A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4

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Cancer cell cycles

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p53, the cellular gatekeeper for growth and division

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The complexity of p53 modulation: emerging patterns from divergent signals

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The cellular response to p53: the decision between life and death

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Mechanisms of p53-mediated apoptosis

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Nucleolar Arf sequesters Mdm2 and activates p53

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Association of p19(ARF) with Mdm2 inhibits ubiquitin ligase activity of Mdm2 for tumor suppressor p53.

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Stabilization of p53 by p14ARF without relocation of MDM2 to the nucleolus.

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Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest

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A cell cycle regulator potentially involved in genesis of many tumor types

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The p16INK4a/CDKN2A tumor suppressor and its relatives.

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The Rb/E2F pathway: expanding roles and emerging paradigms

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The INK4 family of cell cycle inhibitors in cancer

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Deregulated expression of E2F family members induces S-phase entry and overcomes p16INK4A-mediated growth suppression

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Distinct roles for E2F proteins in cell growth control and apoptosis

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E2Fs regulate the expression of genes involved in differentiation, development, proliferation, and apoptosis.

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E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos

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A common E2F-1 and p73 pathway mediates cell death induced by TCR activation.

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Role for the p53 homologue p73 in E2F-1-induced apoptosis

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Loss of E2F-1 reduces tumorigenesis and extends the lifespan of Rb1(+/-)mice

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Key roles for E2F1 in signaling p53-dependent apoptosis and in cell division within developing tumors

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Mutation of E2f-1 suppresses apoptosis and inappropriate S phase entry and extends survival of Rb-deficient mouse embryos

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The retinoblastoma gene family in differentiation and development.

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Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16

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Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition

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Growth suppression by p16ink4 requires functional retinoblastoma protein

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CDK inhibitors: positive and negative regulators of G1-phase progression

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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

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Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

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Limited overlapping roles of P15(INK4b) and P18(INK4c) cell cycle inhibitors in proliferation and tumorigenesis

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Control of spermatogenesis in mice by the cyclin D-dependent kinase inhibitors p18(Ink4c) and p19(Ink4d)

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Postnatal neuronal proliferation in mice lacking Ink4d and Kip1 inhibitors of cyclin-dependent kinases

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Functional collaboration between different cyclin-dependent kinase inhibitors suppresses tumor growth with distinct tissue specificity

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Role of the INK4a locus in tumor suppression and cell mortality.

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Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

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Cdkn2a, the cyclin-dependent kinase inhibitor encoding p16INK4a and p19ARF, is a candidate for the plasmacytoma susceptibility locus, Pctr1.

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Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis

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Multiple docking sites on substrate proteins form a modular system that mediates recognition by ERK MAP kinase

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INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53.

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p16INK4A and p19ARF act in overlapping pathways in cellular immortalization

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Cooperative effects of INK4a and ras in melanoma susceptibility in vivo

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Cellular senescence: mitotic clock or culture shock?

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Cellular senescence as a tumor-protection mechanism: the essential role of counting

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Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization

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Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions

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Escape from premature senescence is not sufficient for oncogenic transformation by Ras.

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Differential effects of p19(Arf) and p16(Ink4a) loss on senescence of murine bone marrow-derived preB cells and macrophages

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Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells.

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Increased p16 expression with first senescence arrest in human mammary epithelial cells and extended growth capacity with p16 inactivation

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Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

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E1A signaling to p53 involves the p19(ARF) tumor suppressor

1 reference

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p19ARF links the tumour suppressor p53 to Ras

1 reference

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p19(Arf) induces p53-dependent apoptosis during abelson virus-mediated pre-B cell transformation

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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

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Opposing effects of Ras on p53: transcriptional activation of mdm2 and induction of p19ARF.

1 reference

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p14ARF links the tumour suppressors RB and p53.

1 reference

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Myc requires distinct E2F activities to induce S phase and apoptosis

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The many substrates and functions of ATM

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ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage

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The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

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Twist is a potential oncogene that inhibits apoptosis

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Senescence bypass screen identifies TBX2, which represses Cdkn2a (p19(ARF)) and is amplified in a subset of human breast cancers.

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Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras.

1 reference

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Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2

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The alternative product from the human CDKN2A locus, p14(ARF), participates in a regulatory feedback loop with p53 and MDM2.

1 reference

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p53-independent functions of the p19(ARF) tumor suppressor

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