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

A High Throughput Phenotypic Screening reveals compounds that counteract premature osteogenic differentiation of HGPS iPS-derived mesenchymal stem cells

14 Oct 2016

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is a rare fatal genetic disorder that causes systemic accelerated aging in children. Thanks to the pluripotency and self-renewal properties of induced pluripotent stem cells (iPSC), HGPS iPSC-based modeling opens up the possibility of access to different relevant cell types for pharmacological approaches. In this study, 2800 small molecules were explored using...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Nuclear Structure and Function
Share to Retinoids in leukemia and cellular processes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 27739443
DOI: 10.1038/srep34798

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

A High Throughput Phenotypic Screening reveals compounds that counteract premature osteogenic differentiation of HGPS iPS-derived mesenchymal stem cellsPMID 27739443Read ↗

Pluripotent stem cells to model Hutchinson-Gilford progeria syndrome (HGPS): Current trends and future perspectives for drug discovery.Semantic proximity Read ↗

Metabolic Dysfunction in Hutchinson–Gilford Progeria SyndromeSemantic proximity Read ↗

Improved Arterial Stiffness and Bone Mineral Density in Hutchinson–Gilford Progeria Treated with Bone Marrow-Derived Mesenchymal Stem Cells: A Case Study and Literature ReviewSemantic proximity Read ↗

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

Hutchinson-Gilford progeria syndrome: Rejuvenating old drugs to fight accelerated ageingSemantic proximity Read ↗

Small-Molecule Therapeutic Perspectives for the Treatment of Progeria.Semantic proximity Read ↗

Rapid and robust derivation of mesenchymal stem cells from human pluripotent stem cells via temporal induction of neuralized ectodermSemantic proximity Read ↗

Diminished Canonical β-Catenin Signaling During Osteoblast Differentiation Contributes to Osteopenia in Progeria.Semantic proximity Read ↗

Progress and trends in the development of therapies for Hutchinson–Gilford progeria syndromeSemantic proximity Read ↗

Pharmacologic activation of Δ133p53α reduces cellular senescence in progeria patients-derived cellsSemantic proximity Read ↗

A multiparametric anti-aging CRISPR screen uncovers a role for BAF in protein translationSemantic proximity Read ↗

Differential stem cell aging kinetics in Hutchinson-Gilford progeria syndrome and Werner syndrome.Semantic proximity Read ↗

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