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

CENP-A reduction induces a p53-dependent cellular senescence response to protect cells from executing defective mitoses.

Molecular and cellular biology - 1 May 2010

Maehara Kayoko, Takahashi Kohta, Saitoh Shigeaki

Abstract excerpt

Cellular senescence is an irreversible growth arrest and is presumed to be a natural barrier to tumor development. Like telomere shortening, certain defects in chromosome integrity can trigger senescence; however, the roles of centromere proteins in regulating commitment to the senescent state remains to be established. We examined chromatin structure in senescent human primary fibroblasts and found that CENP-A...

Read the complete abstract on PubMed

Topics

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

Share to Autoantigens
Share to Cellular Senescence
Share to Chromosomal Proteins, Non-Histone

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Cytoprotection

Share to Heterochromatin

Share to Receptors, Retinoic Acid

Share to Retinoblastoma Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 20160010
DOI: 10.1128/MCB.01318-09
PMCID: PMC2863584

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

CENP-A reduction induces a p53-dependent cellular senescence response to protect cells from executing defective mitoses.PMID 20160010Read ↗

Interrogating the regulatory epigenome of cellular senescenceSemantic proximity Read ↗

Senescent Cells: A Novel Therapeutic Target for Aging and Age-Related DiseasesSemantic proximity Read ↗

Towards prevention of aneuploidy-associated cellular senescence and aging: more questions than answers?Semantic proximity Read ↗

DNA-SCARS: distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretionSemantic proximity Read ↗

Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseasesSemantic proximity Read ↗

Lysosome-mediated processing of chromatin in senescenceSemantic proximity Read ↗

Centromere inactivation during aging can be rescued in human cellsSemantic proximity Read ↗

Emerging role of NF-κB signaling in the induction of senescence-associated secretory phenotype (SASP).Semantic proximity Read ↗

Higher-order unfolding of satellite heterochromatin is a consistent and early event in cell senescenceSemantic proximity Read ↗

Lamin B1 loss is a senescence-associated biomarkerSemantic proximity Read ↗

Remodeling of chromatin structure in senescent cells and its potential impact on tumor suppression and agingSemantic proximity Read ↗

The NuA4 acetyltransferase and non-canonical chromatin-associated MRN/ATM activity temporally define senescence-associated secretory programsSemantic proximity Read ↗

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