Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Posttranslational Modifications of p53 in Replicative Senescence Overlapping but Distinct from Those Induced by DNA Damage

1 Apr 2000

Abstract excerpt

Replicative senescence in human fibroblasts is absolutely dependent on the function of the phosphoprotein p53 and correlates with activation of p53-dependent transcription. However, no evidence for posttranslational modification of p53 in senescence has been presented, raising the possibility that changes in transcriptional activity result from upregulation of a coactivator. Using a series of antibodies with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer-related Molecular Pathways
Share to DNA Repair Mechanisms
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 10733583
DOI: 10.1128/mcb.20.8.2803-2808.2000

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Posttranslational Modifications of p53 in Replicative Senescence Overlapping but Distinct from Those Induced by DNA DamagePMID 10733583Read ↗

p53 is preferentially recruited to the promoters of growth arrest genes p21 and GADD45 during replicative senescence of normal human fibroblasts.Semantic proximity Read ↗

Radiation-Induced Senescence-like Growth Arrest Requires TP53 Function but not Telomere ShorteningSemantic proximity Read ↗

Loss of proliferative capacity and induction of senescence in oxidatively stressed human fibroblasts.Semantic proximity Read ↗

Signal transduction in H2O2-induced senescence-like phenotype in human diploid fibroblasts.Semantic proximity Read ↗

Regulation of p53 during senescence in normal human keratinocytesSemantic proximity Read ↗

The cellular oncogene p53 can be activated by mutagenesis.Semantic proximity Read ↗

The catalytic subunit of DNA-dependent protein kinase is downstream of ATM and feeds forward oxidative stress in the selenium-induced senescence response.Semantic proximity Read ↗

Control of fibroblast senescence and activation of programmed cell death.Semantic proximity Read ↗

Phosphorylation of serines 15 and 37 is necessary for efficient accumulation of p53 following irradiation with UV.Semantic proximity Read ↗

Downregulation of PEA-15 reverses G1 arrest, and nuclear and chromatin changes of senescence phenotype via pErk1/2 translocation to nuclei.Semantic proximity Read ↗

Characterization of the p53 response to oncogene-induced senescence.Semantic proximity Read ↗

Double-stranded-RNA-activated protein kinase PKR enhances transcriptional activation by tumor suppressor p53.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.