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

Suppression of the DHX9 Helicase Induces Premature Senescence in Human Diploid Fibroblasts in a p53-dependent Manner

3 Jul 2014

Abstract excerpt

DHX9 is an ATP-dependent DEXH box helicase with a multitude of cellular functions. Its ability to unwind both DNA and RNA, as well as aberrant, noncanonical polynucleotide structures, has implicated it in transcriptional and translational regulation, DNA replication and repair, and maintenance of genome stability. We report that loss of DHX9 in primary human fibroblasts results in premature senescence, a state of...

Read the complete abstract on PubMed

Topics

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

Share to DNA Repair Mechanisms
Share to Genomics and Chromatin Dynamics
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 24990949
DOI: 10.1074/jbc.m114.568535

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Suppression of the DHX9 Helicase Induces Premature Senescence in Human Diploid Fibroblasts in a p53-dependent MannerPMID 24990949Read ↗

DHX9 helicase promotes R-loop formation in cells with impaired RNA splicingSemantic proximity Read ↗

RNA/DNA Hybrid Interactome Identifies DXH9 as a Molecular Player in Transcriptional Termination and R-Loop-Associated DNA DamageSemantic proximity Read ↗

Requirement of DDX39 DEAD box RNA helicase for genome integrity and telomere protectionSemantic proximity Read ↗

Human RAD9 checkpoint control/proapoptotic protein can activate transcription of p21Semantic proximity Read ↗

DDX11 loss causes replication stress and pharmacologically exploitable DNA repair defectsSemantic proximity Read ↗

DDK has a primary role in processing stalled replication forks to initiate downstream checkpoint signalingSemantic proximity Read ↗

A Potent, Selective, Small-Molecule Inhibitor of DHX9 Abrogates Proliferation of Microsatellite Instable Cancers with Deficient Mismatch RepairSemantic proximity Read ↗

RNA Helicase DDX3: A Double-Edged Sword for Viral Replication and Immune SignalingSemantic proximity Read ↗

DDX5 Regulates DNA Replication and Is Required for Cell Proliferation in a Subset of Breast Cancer CellsSemantic proximity Read ↗

Werner syndrome helicase modulates G4 DNA-dependent transcription and opposes mechanistically distinct senescence-associated gene expression programsSemantic proximity Read ↗

Functional role of the Werner syndrome RecQ helicase in human fibroblasts.Semantic proximity Read ↗

ATRX promotes heterochromatin formation to protect cells from G-quadruplex DNA-mediated stressSemantic proximity Read ↗

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