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Article

The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis.

Oncogene - 15 Jan 2004

Sharpless Norman E, Ramsey Matthew R, Balasubramanian Periasamy, Castrillon Diego H, DePinho Ronald A

Abstract excerpt

Mounting genetic evidence suggests that each product of the Ink4a/Arf locus, p16(INK4a) and p19(ARF), possesses tumor-suppressor activity (Kamijo et al., 1997; Krimpenfort et al., 2001; Sharpless et al., 2001a). We report the generation and characterization of a p19(ARF)-specific knockout allele (p19(ARF)-/-) and direct comparison with mice and derivative cells deficient for p16(INK4a), both p16(INK4a) and...

Topics

Alleles
Animals
Cell Division
Cell Transformation, Neoplastic
Cells, Cultured
Cyclin-Dependent Kinase Inhibitor p16
Embryo, Mammalian
Fibroblasts
Gene Deletion
Genotype
Mice

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Neoplasms

Phenotype

Tumor Suppressor Protein p14ARF

Tumor Suppressor Protein p53

Source

Identifiers

PMID: 14724566
DOI: 10.1038/sj.onc.1207074

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-14724566-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis.PMID 14724566Read ↗

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