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

Senescence Delay of Human Diploid Fibroblast Induced by Anti-sense p16INK4a Expression

1 Dec 2001

Abstract excerpt

p16(INK4a), a tumor suppressor gene that inhibits cyclin-dependent kinase 4 and cyclin-dependent kinase 6, is also implicated in the mechanisms underlying replicative senescence, because its RNA and protein accumulate as cells approach their finite number of population doublings in tissue culture. To further explore the involvement of p16(INK4a) in replicative senescence, we constructed a retroviral vector...

Read the complete abstract on PubMed

Topics

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

Share to Advanced biosensing and bioanalysis techniques
Share to Cancer-related Molecular Pathways
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 11606567
DOI: 10.1074/jbc.m104814200

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

Senescence Delay of Human Diploid Fibroblast Induced by Anti-sense p16INK4a ExpressionPMID 11606567Read ↗

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 ↗

A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status.Semantic proximity Read ↗

Contribution of p16(INK4a) to replicative senescence of human fibroblasts.Semantic proximity Read ↗

Features of replicative senescence induced by direct addition of antennapedia-p16INK4A fusion protein to human diploid fibroblasts.Semantic proximity Read ↗

Direct evidence from siRNA-directed "knock down" that p16(INK4a) is required for human fibroblast senescence and for limiting ras-induced epithelial cell proliferation.Semantic proximity Read ↗

p16INK4a and the control of cellular proliferative life spanSemantic proximity Read ↗

CDK4 and CDK6 delay senescence by kinase-dependent and p16INK4a-independent mechanisms.Semantic proximity Read ↗

Telomere-based proliferative lifespan barriers in Werner-syndrome fibroblasts involve both p53-dependent and p53-independent mechanismsSemantic 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 ↗

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

Replicative senescence of human fibroblast-like cells in cultureSemantic proximity Read ↗

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