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

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

Cancer research - 1 Sept 2006

Jackson James G, Pereira-Smith Olivia M

Abstract excerpt

Replicative senescence is the terminal growth arrest that most normal human cells enter into after a fixed number of divisions in vitro, limiting the proliferative potential of a cell and preventing genomic instability caused by critically short telomeres. Thus, senescence presents a tumor-suppressive mechanism and a barrier to tumor formation. However, senescent cells are inherently resistant to apoptosis and,...

Read the complete abstract on PubMed

Topics

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

Share to Cellular Senescence
Share to Diploidy
Share to DNA Replication

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Doxorubicin

Share to Fibroblasts

Share to Genes, p53

Share to Oncogene Protein p21(ras)

Share to Protein Processing, Post-Translational

Source

Identifiers

PMID: 16951143
DOI: 10.1158/0008-5472.CAN-06-1752

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

p53 is preferentially recruited to the promoters of growth arrest genes p21 and GADD45 during replicative senescence of normal human fibroblasts.PMID 16951143Read ↗

Identification of cellular senescence-specific genes by comparative transcriptomicsSemantic proximity Read ↗

A genomics approach identifies senescence‐specific gene expression regulationSemantic proximity Read ↗

Induction of Cellular Senescence by Doxorubicin Is Associated with Upregulated miR-375 and Induction of Autophagy in K562 CellsSemantic proximity Read ↗

Effects of p21 <sup>Waf1/Cip1/Sdi1</sup> on cellular gene expression: Implications for carcinogenesis, senescence, and age-related diseasesSemantic proximity Read ↗

Differential Roles for Cyclin-Dependent Kinase Inhibitors p21 and p16 in the Mechanisms of Senescence and Differentiation in Human FibroblastsSemantic proximity Read ↗

Real‐time imaging of transcriptional activation in live cells reveals rapid up‐regulation of the cyclin‐dependent kinase inhibitor gene CDKN1A in replicative cellular senescenceSemantic proximity Read ↗

A senescence-like phenotype distinguishes tumor cells that undergo terminal proliferation arrest after exposure to anticancer agents.Semantic proximity Read ↗

Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblastsSemantic proximity Read ↗

Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblastsSemantic proximity Read ↗

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

Histone Modifications in Senescence-Associated Resistance to Apoptosis by Oxidative StressSemantic proximity Read ↗

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

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