INK4a/ARF: a multifunctional tumor suppressor locus.

No abstract is available for this paper.

• Publication year

  2005

• Venue

  Mutation research

• Publication date

  2005-08-25

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.MRFMMM.2004.08.021PMID 15878778
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• p18(INK4c) collaborates with other CDK‐inhibitory proteins in the regenerating liver

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• Both products of the mouse Ink4a/Arf locus suppress melanoma formation in vivo

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• p16(INK4a) and p53 deficiency cooperate in tumorigenesis.

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• p14ARF regulates E2F activity

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• ARF Function Does Not Require p53 Stabilization or Mdm2 Relocalization

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• Biallelic Mutations in p16INK4a Confer Resistance to Ras- and Ets-Induced Senescence in Human Diploid Fibroblasts

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• Adenovirus-mediated gene transfer of P16INK4/CDKN2 into bax-negative colon cancer cells induces apoptosis and tumor regression in vivo

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• Epidermal growth factor receptor and Ink4a/Arf: convergent mechanisms governing terminal differentiation and transformation along the neural stem cell to astrocyte axis.

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• Human ARF protein interacts with Topoisomerase I and stimulates its activity

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• MdmX Binding to ARF Affects Mdm2 Protein Stability and p53 Transactivation*

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• Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions.

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• The Human Tumor Suppressor ARF Interacts with Spinophilin/Neurabin II, a Type 1 Protein-phosphatase-binding Protein*

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