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

Loss of T-antigen sequences allows SV40-transformed human cells in crisis to acquire a senescent-like phenotype.

The journals of gerontology. Series A, Biological sciences and medical sciences - 1 Sept 1997

Rubelj I, Venable S F, Lednicky J, Butel J S, Bilyeu T, Darlington G, Surmacz E, Campisi J, Pereira-Smith O M

Abstract excerpt

Normal human cells transfected with SV40 DNA exhibit an extended proliferative potential compared with controls, but they eventually enter a phase known as "crisis." During crisis, extensive cell death occurs and the cells exhibit some gene expression changes similar to senescent cells. This arti...

Read the complete abstract on PubMed

Topics

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

Share to Antigens, Polyomavirus Transforming
Share to Cells, Cultured

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cellular Senescence

Share to Microinjections

Share to Phenotype

Share to Promoter Regions, Genetic

Share to Simian virus 40

Share to Transfection

Source

Identifiers

PMID: 9310070
DOI: 10.1093/gerona/52a.5.b229

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-9310070-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of T-antigen sequences allows SV40-transformed human cells in crisis to acquire a senescent-like phenotype.PMID 9310070Read ↗

The helix-loop-helix protein Id-1 and a retinoblastoma protein binding mutant of SV40 T antigen synergize to reactivate DNA synthesis in senescent human fibroblasts.Semantic proximity Read ↗

Evidence that high telomerase activity may induce a senescent-like growth arrest in human fibroblasts.Semantic proximity Read ↗

SV40 T antigen <i>alone</i> drives karyotype instability that precedes neoplastic transformation of human diploid fibroblastsSemantic proximity Read ↗

The senescent microenvironment promotes the emergence of heterogeneous cancer stem-like cellsSemantic proximity Read ↗

A role for both RB and p53 in the regulation of human cellular senescence.Semantic proximity Read ↗

Origins of G<sub>1</sub> arrest in senescent human fibroblastsSemantic proximity Read ↗

Dissociation among <i>in vitro</i> telomerase activity, telomere maintenance, and cellular immortalizationSemantic proximity Read ↗

DNA methyltransferase inhibition in normal human fibroblasts induces a p21-dependent cell cycle withdrawal.Semantic proximity Read ↗

Human pulp‐derived cells immortalized with Simian Virus 40 T‐antigenSemantic proximity Read ↗

Phenotypic conversion of SV40-immortalized human diploid fibroblasts to senescing cells by introduction of an antisense gene for SV40-T antigen.Semantic proximity Read ↗

The Normal Response to RAS: Senescence or Transformation?Semantic proximity Read ↗

Expression of SV40 large T antigen, but not small t antigen, is required for the induction of chromosomal aberrations in transformed human cells.Semantic proximity Read ↗

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