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

The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.

Aging cell - 1 Apr 2020

Griveau Audrey, Wiel Clotilde, Ziegler Dorian V, Bergo Martin O, Bernard David

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is caused by an LMNA mutation that results in the production of the abnormal progerin protein. Children with HGPS display phenotypes of premature aging and have an average lifespan of 13 years. We found earlier that the targeting of the transmembrane protein PLA2R1 overcomes senescence and improves phenotypes in a mouse model of progeria. PLA2R1 is regulating the...

Read the complete abstract on PubMed

Topics

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

Share to Aging, Premature
Share to Cell Cycle Checkpoints
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Janus Kinase 1

Share to Janus Kinase 2

Share to Nitriles

Share to Pyrazoles

Share to Pyrimidines

Source

Open in PubMed Open full text

Identifiers

PMID: 32196928
DOI: 10.1111/acel.13122
PMCID: PMC7189991

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.PMID 32196928Read ↗

Targeting the phospholipase A2 receptor ameliorates premature aging phenotypes.Semantic proximity Read ↗

Hutchinson-Gilford Progeria Syndrome: A Literature ReviewSemantic proximity Read ↗

Molecular insights into the premature aging disease progeria.Semantic proximity Read ↗

Hutchinson-Gilford Progeria Syndrome—Current Status and Prospects for Gene Therapy TreatmentSemantic proximity Read ↗

Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype.Semantic proximity Read ↗

Unraveling the mysteries of Hutchinson-Gilford progeria syndrome: a comprehensive review of LMNA gene mutations.Semantic proximity Read ↗

Isoprenylcysteine Carboxylmethyltransferase-Based Therapy for Hutchinson–Gilford Progeria SyndromeSemantic proximity Read ↗

Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease.Semantic proximity Read ↗

Hutchinson-Gilford Progeria Syndrome: An Overview of the Molecular Mechanism, Pathophysiology and Therapeutic Approach.Semantic proximity Read ↗

Progerin, an Aberrant Spliced form of Lamin A, is a Potential Therapeutic Target for HGPSSemantic proximity Read ↗

Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome.Semantic proximity Read ↗

Hutchinson-Gilford Progeria paves the way for novel targeted anti-aging therapies.Semantic proximity Read ↗

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