Splicing into senescence: the curious case of p16 and p19ARF. (Q41657944)

6 October 2017

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title

Splicing into senescence: the curious case of p16 and p19ARF. (English)

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6 October 2017

Haber DA

1

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6 October 2017

language of work or name

English

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publication date

1 November 1997

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6 October 2017

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6 October 2017

volume

91

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6 October 2017

issue

5

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6 October 2017

page(s)

555-558

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Prevalence of germ-line mutations in p16, p19ARF, and CDK4 in familial melanoma: analysis of a clinic-based population

6 October 2017

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Regulation of p16CDKN2 expression and its implications for cell immortalization and senescence

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Germline p16 mutations in familial melanoma

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

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5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers

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7 January 2021

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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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7 January 2021

Cancer-associated mutations at the INK4a locus cancel cell cycle arrest by p16INK4a but not by the alternative reading frame protein p19ARF.

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

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

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

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Inhibitors of mammalian G1 cyclin-dependent kinases

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The retinoblastoma protein and cell cycle control

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

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Identifiers

DOI

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6 October 2017

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