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

Normal Human Fibroblasts Are Resistant to RAS-Induced Senescence

15 Mar 2004

Abstract excerpt

Oncogenic stimuli are thought to induce senescence in normal cells in order to protect against transformation and to induce proliferation in cells with altered p53 and/or retinoblastoma (Rb) pathways. In human fibroblasts, RAS initiates senescence through upregulation of the cyclin-dependent kinase inhibitor p16INK4A. We show here that in contrast to cultured fibroblast strains, freshly isolated normal...

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 Ocular Oncology and Treatments
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 15024073
DOI: 10.1128/mcb.24.7.2842-2852.2004

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Normal Human Fibroblasts Are Resistant to RAS-Induced SenescencePMID 15024073Read ↗

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

Single‐cell analysis of p16INK4a and p21WAF1 expression suggests distinct mechanisms of senescence in normal human and Li‐Fraumeni Syndrome fibroblastsSemantic proximity Read ↗

Replicative senescence of human fibroblasts: the role of Ras-dependent signaling and oxidative stressSemantic proximity Read ↗

Ras-Induced Senescence and its Physiological Relevance in CancerSemantic proximity Read ↗

High Intensity ras Signaling Induces Premature Senescence by Activating p38 Pathway in Primary Human FibroblastsSemantic proximity Read ↗

Real-time in vivo imaging of p16Ink4a gene expression: a new approach to study senescence stress signaling in living animalsSemantic proximity Read ↗

Efficient immortalization of primary human cells by p16<sup>INK4a</sup>‐specific short hairpin RNA or Bmi‐1, combined with introduction of hTERTSemantic proximity Read ↗

Cellular senescence in naevi and immortalisation in melanoma: a role for p16?Semantic proximity Read ↗

Stress-induced Premature Senescence in hTERT-expressing Ataxia Telangiectasia FibroblastsSemantic proximity Read ↗

The molecular scaffold kinase suppressor of Ras 1 is a modifier of RasV12-induced and replicative senescence.Semantic proximity Read ↗

Dissecting the senescence-like program in tumor cells activated by Ras signaling.Semantic proximity Read ↗

Gene expression profile associated with oncogenic ras-induced senescence, cell death, and transforming properties in human cells.Semantic proximity Read ↗

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