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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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The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2’s inhibition of p53

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

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The alternative product from the human CDKN2A locus, p14ARF, participates in a regulatory feedback loop with p53 and MDM2

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Germline p16 mutations in familial melanoma

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Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

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p14ARF links the tumour suppressors RB and p53

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

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p53 and E2F-1 cooperate to mediate apoptosis.

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Senescence of human fibroblasts induced by oncogenic Raf

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Germline mutations in the p16INK4a binding domain of CDK4 in familial melanoma

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Deregulated transcription factor E2F-1 expression leads to S-phase entry and p53-mediated apoptosis.

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Tumor surveillance via the ARF–p53 pathwayPreprint

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Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function.Preprint

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Binding and modulation of p53 by p300/CBP coactivators

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Recruitment of p300/CBP in p53-Dependent Signal Pathways

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Stabilization of the p53 tumor suppressor is induced by adenovirus 5 E1A and accompanies apoptosis.Preprint

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Increased Risk of Pancreatic Cancer in Melanoma-Prone Kindreds withp16INK4Mutations

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p19ARF links the tumour suppressor p53 to Ras

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E1A signaling to p53 involves the p19ARFtumor suppressorPreprint

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Synergistic activation of transcription by CBP and p53

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

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p300/MDM2 complexes participate in MDM2-mediated p53 degradation

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Complex structure and regulation of the P16 (MTS1) locus.

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Inhibition of Ras-Induced Proliferation and Cellular Transformation by p16 INK4

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CDKN2AMutations in Multiple Primary Melanomas

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Mutation and altered expression of p16^ in human cancer

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Cancer-associated mutations at the INK4a locus cancel cell cycle arrest by p16 INK4a but not by the alternative reading frame protein p19 ARF

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CREB-binding protein and p300/CBP-associated factor are transcriptional coactivators of the p53 tumor suppressor protein.

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p16 INK4A Participates in a G 1 Arrest Checkpoint in Response to DNA Damage

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Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors

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Inactivation of multiple tumor-suppressor genes involved in negative regulation of the cell cycle, MTS1/p16INK4A/CDKN2, MTS2/p15INK4B, p53, and Rb genes in primary lymphoid malignancies

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Genetic evidence in melanoma and bladder cancers that p16 and p53 function in separate pathways of tumor suppression.

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Genomic Alterations of the p19ARF Encoding Exons in T-Cell Acute Lymphoblastic Leukemia

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Alterations of the p16 gene in head and neck cancer: frequency and association with p53, PRAD-1 and HPV

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Homozygous loss of the p15INK4B gene (and not the p16INK4 gene) during tumor progression in a sporadic melanoma patient.

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The INK4A Locus and the p16 INK4A and p19 ARF Genes

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