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

Early growth response 2 (EGR2) is a novel regulator of the senescence programme

6 Feb 2021

Abstract excerpt

Senescence, a state of stable growth arrest, plays an important role in ageing and age-related diseases in vivo. Although the INK4/ARF locus is known to be essential for senescence programmes, the key regulators driving p16 and ARF transcription remain largely underexplored. Using siRNA screening for modulators of the p16/pRB and ARF/p53/p21 pathways in deeply senescent human mammary epithelial cells (DS HMECs)...

Topics

Join the communities discussing this publication.

Cancer-related Molecular Pathways
MicroRNA in disease regulation
Telomeres, Telomerase, and Senescence

Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 33547862
DOI: 10.1111/acel.13318

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Early growth response 2 (EGR2) is a novel regulator of the senescence programmePMID 33547862Read ↗

Early growth response 2 (EGR2) is a novel regulator of the senescence programSemantic proximity Read ↗

CREG1 enhances p16 INK4a -induced cellular senescenceSemantic proximity Read ↗

Transcriptional repression of DNA repair genes is a hallmark and a cause of cellular senescenceSemantic proximity Read ↗

Regulation of a Senescence Checkpoint Response by the E2F1 Transcription Factor and p14 <sup>ARF</sup> Tumor SuppressorSemantic proximity Read ↗

Cellular senescence mediated by p16INK4A-coupled miRNA pathwaysSemantic proximity Read ↗

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

Modulation of the expression of p16<sup>INK4a</sup>and p14<sup>ARF</sup>by hnRNP A1 and A2 RNA binding proteins: Implications for cellular senescenceSemantic proximity Read ↗

Involvement of the INK4a/Arf gene locus in senescence.Semantic proximity Read ↗

Ink4a/Arf expression is a biomarker of agingSemantic proximity Read ↗

Tumor Suppressor and Aging Biomarker p16INK4a Induces Cellular Senescence without the Associated Inflammatory Secretory PhenotypeSemantic proximity Read ↗

An Arf-Egr-C/EBPβ pathway linked to ras-induced senescence and cancer.Semantic proximity Read ↗

Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.Semantic proximity Read ↗

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