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

Stress-induced premature senescence mediated by a novel gene, SENEX, results in an anti-inflammatory phenotype in endothelial cells.

Blood - 11 Nov 2010

Coleman Paul R, Hahn Christopher N, Grimshaw Matthew, Lu Ying, Li Xiaochun, Brautigan Peter J, Beck Konstanze, Stocker Roland, Vadas Mathew A, Gamble Jennifer R

Abstract excerpt

Cellular senescence is a mechanism to inhibit the growth of mammalian cells after oncogenic activation, or in response to damage or stress. We describe here the identification of a novel gene, SENEX, that regulates stress induced premature senescence pathways in endothelial cells (ECs) involving p16(INK4a) and retinoblastoma protein activation. Endogenous levels of SENEX remain unchanged during replicative...

Read the complete abstract on PubMed

Topics

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

Share to Cell Adhesion
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Endothelial Cells

Share to Hydrogen Peroxide

Share to Neovascularization, Physiologic

Share to RNA, Small Interfering

Share to Tumor Necrosis Factor-alpha

Source

Identifiers

PMID: 20664062
DOI: 10.1182/blood-2009-11-252700

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Stress-induced premature senescence mediated by a novel gene, SENEX, results in an anti-inflammatory phenotype in endothelial cells.PMID 20664062Read ↗

Age-associated stresses induce an anti-inflammatory senescent phenotype in endothelial cellsSemantic proximity Read ↗

miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stressSemantic proximity Read ↗

Premature senescence of endothelial cells: Methusaleh's dilemmaSemantic proximity Read ↗

Cellular senescence in the aging retina and developments of senotherapies for age-related macular degenerationSemantic proximity Read ↗

Connecting epigenetics and inflammation in vascular senescence: state of the art, biomarkers and senotherapeuticsSemantic proximity Read ↗

Senolytic-Resistant Senescent Cells Have a Distinct SASP Profile and Functional Impact: The Path to Developing SenosensitizersSemantic proximity Read ↗

The Achilles’ heel of senescent cells: from transcriptome to senolytic drugsSemantic proximity Read ↗

Vascular senescence and aging: mechanisms, clinical implications, and therapeutic prospectsSemantic proximity Read ↗

Senolytic treatment with fisetin reverses age-related endothelial dysfunction partially mediated by SASP factor CXCL12Semantic proximity Read ↗

Identifying specific functional roles for senescence across cell typesSemantic proximity Read ↗

Short- and Long-Term Endothelial Inflammation Have Distinct Effects and Overlap with Signatures of Cellular SenescenceSemantic proximity Read ↗

Senescence-induced endothelial phenotypes underpin immune-mediated senescence surveillance.Semantic proximity Read ↗

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