Mechanisms of switching on p53: a role for covalent modification?

No abstract is available for this paper.

• Publication year

  1999

• Venue

  Oncogene

• Publication date

  1999-12-13

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/sj.onc.1202951PMID 10618706
• 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.

• DNA damage‐inducible phosphorylation of p53 at N‐terminal sites including a novel site, Ser20, requires tetramerization

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• ATM associates with and phosphorylates p53: mapping the region of interaction

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• Phosphorylation of p53 protein in response to ionizing radiation occurs at multiple sites in both normal and DNA-PK deficient cells

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• Association of p19ARF with Mdm2 inhibits ubiquitin ligase activity of Mdm2 for tumor suppressor p53

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• DNA damage induced p53 stabilization: no indication for an involvement of p53 phosphorylation

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• A role for ATR in the DNA damage-induced phosphorylation of p53.

  1999influential reference
• Regulation of p53 Function and Stability by Phosphorylation

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• Critical role for Ser20 of human p53 in the negative regulation of p53 by Mdm2

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• p53 Sites Acetylated In Vitro by PCAF and p300 Are Acetylated In Vivo in Response to DNA Damage

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• The p53 pathway

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• Comparative study of the p53-mdm2 and p53-MDMX interfaces

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• MEKK1/JNK signaling stabilizes and activates p53.

  1998cited by this paper
• Functional activation of p53 via phosphorylation following DNA damage by UV but not γ radiation

  1998cited by this paper
• ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways.

  1998influential reference
• Enhanced phosphorylation of p53 by ATM in response to DNA damage.

  1998cited by this paper
• Stabilization and activation of p53 are regulated independently by different phosphorylation events.

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• Protein kinase mutants of human ATR increase sensitivity to UV and ionizing radiation and abrogate cell cycle checkpoint control.

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• Phosphorylation of p53 Serine 15 Increases Interaction with CBP*

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• MAGNETIZATION CURVE OF A SQUARE-LATTICE HEISENBERG ANTIFERROMAGNET

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• The complexity of p53 modulation: emerging patterns from divergent signals.

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• Activation of the ATM kinase by ionizing radiation and phosphorylation of p53.

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• Functional activation of p53 via phosphorylation following DNA damage by UV but not gamma radiation.

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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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• Overexpression of a kinase‐inactive ATR protein causes sensitivity to DNA‐damaging agents and defects in cell cycle checkpoints

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

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• The p53 Network*

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

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• Ultraviolet radiation, but not gamma radiation or etoposide-induced DNA damage, results in the phosphorylation of the murine p53 protein at serine-389.

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• Mdm-2 phosphorylation by DNA-dependent protein kinase prevents interaction with p53.

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• Regulation of p53 stability by Mdm2

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• Mdm2 promotes the rapid degradation of p53

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• The CDK7-cycH-p36 complex of transcription factor IIH phosphorylates p53, enhancing its sequence-specific DNA binding activity in vitro

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• Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal forms

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• DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2.

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• Protein interactions at the carboxyl terminus of p53 result in the induction of its in vitro transactivation potential

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• Design of a synthetic Mdm2-binding mini protein that activates the p53 response in vivo.

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• Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.

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• DNA damage induces phosphorylation of the amino terminus of p53.

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• Conformation-dependent phosphorylation of p53.

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• JNK1, JNK2 and JNK3 are p53 N-terminal serine 34 kinases

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• Phosphorylation of serine 392 stabilizes the tetramer formation of tumor suppressor protein p53.

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• Reciprocal interference between the sequence-specific core and nonspecific C-terminal DNA binding domains of p53: implications for regulation

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• Genomic instability and apoptosis are frequent in p53 deficient young mice

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• V(D)J recombination activates a p53-dependent DNA damage checkpoint in scid lymphocyte precursors.

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• Somatic point mutations in the p53 gene of human tumors and cell lines: updated compilation

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• Mutations in the p53 and SCID genes cooperate in tumorigenesis.

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• The DNA damage response in DNA-dependent protein kinase-deficient SCID mouse cells: replication protein A hyperphosphorylation and p53 induction.

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• Mutation of Phosphoserine 389 Affects p53 Function in Vivo*

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• DNA double-strand break repair and V(D)J recombination: involvement of DNA-PK.

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• Increased and altered DNA binding of human p53 by S and G2/M but not Gl cyclin-dependent kinases

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• p53 Is Phosphorylated in Vitro and in Vivo by an Ultraviolet Radiation-induced Protein Kinase Characteristic of the c-Jun Kinase, JNK1 (*)

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