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

Altered stoichiometry and nuclear delocalization of NonO and PSF promote cellular senescence.

Aging - 13 Dec 2016

Huang Ching-Jung, Das Utsab, Xie Weijun, Ducasse Miryam, Tucker Haley O

Abstract excerpt

While cellular senescence is a critical mechanism to prevent malignant transformation of potentially mutated cells, persistence of senescent cells can also promote cancer and aging phenotypes. NonO/p54nrb and PSF are multifunctional hnRNPs typically found as a complex exclusively within the nuclei of all mammalian cells. We demonstrate here that either increase or reduction of expression of either factor results...

Read the complete abstract on PubMed

Topics

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

Share to Cellular Senescence
Share to Cytoplasm
Share to Mitosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Nuclear Matrix-Associated Proteins

Share to Protein Processing, Post-Translational

Share to RNA-Binding Proteins

Share to Telomere Shortening

Share to Transformation, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 27992859
DOI: 10.18632/aging.101125
PMCID: PMC5270673

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

Altered stoichiometry and nuclear delocalization of NonO and PSF promote cellular senescence.PMID 27992859Read ↗

Silencing nuclear pore protein Tpr elicits a senescent-like phenotype in cancer cells.Semantic proximity Read ↗

Autophagy-mediated degradation of nuclear envelope proteins during oncogene-induced senescenceSemantic proximity Read ↗

A prototypical non-malignant epithelial model to study genome dynamics and concurrently monitor micro-RNAs and proteins in situ during oncogene-induced senescenceSemantic proximity Read ↗

Dynamic PML protein nucleolar associations with persistent DNA damage lesions in response to nucleolar stress and senescence-inducing stimuliSemantic proximity Read ↗

CRISPR-based screening identifies XPO7 as a positive regulator of senescenceSemantic proximity Read ↗

The transcription factor <scp>S</scp>p1 is responsible for aging‐dependent altered nucleocytoplasmic traffickingSemantic proximity Read ↗

Nek4 Regulates Entry into Replicative Senescence and the Response to DNA Damage in Human FibroblastsSemantic proximity Read ↗

Higher-order unfolding of satellite heterochromatin is a consistent and early event in cell senescenceSemantic proximity Read ↗

MYCN-induced nucleolar stress drives an early senescence-like transcriptional program in hTERT-immortalized RPE cellsSemantic proximity Read ↗

SON and SRRM2 form nuclear speckles in human cellsSemantic proximity Read ↗

Sequences in PSF/SFPQ mediate radioresistance and recruitment of PSF/SFPQ-containing complexes to DNA damage sites in human cells.Semantic proximity Read ↗

Nesprin-1 impact on tumorigenic cell phenotypes.Semantic proximity Read ↗

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