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

Nuclear import pathway key to rescuing dominant progerin phenotypes.

Science signaling - 3 Jul 2018

Wilson Katherine L

Abstract excerpt

In this issue of Science Signaling, Larrieu et al show that an acetyltransferase inhibitor that rescues many dominant nuclear phenotypes caused by progerin, a truncated form of lamin A, does so by releasing the specialized nuclear import receptor TNPO1 from sequestration by microtubules. This release enables TNPO1-dependent import of specific cargoes, including the nuclear pore protein Nup153 and the...

Read the complete abstract on PubMed

Topics

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

Share to Acetyltransferases
Share to Active Transport, Cell Nucleus
Share to beta Karyopherins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Nucleus

Share to Karyopherins

Share to Nuclear Pore Complex Proteins

Share to Phenotype

Share to Progeria

Source

Open in PubMed Open full text

Identifiers

PMID: 29970604
DOI: 10.1126/scisignal.aat9448
PMCID: PMC6504936

Genes

TNPO1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Nuclear import pathway key to rescuing dominant progerin phenotypes.PMID 29970604Read ↗

Inhibition of the acetyltransferase NAT10 normalizes progeric and aging cells by rebalancing the Transportin-1 nuclear import pathway.Semantic proximity Read ↗

Defective nuclear import of Tpr in Progeria reflects the Ran sensitivity of large cargo transport.Semantic proximity Read ↗

Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome.Semantic proximity Read ↗

Progerin-Induced Nuclear Envelope Remodeling is Shaped by Cell Division and NUP153Semantic proximity Read ↗

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

Targeting SerpinE1 reverses cellular features of Hutchinson-Gilford progeria syndromeSemantic proximity Read ↗

SUMOylation of nuclear receptor Nor1/NR4A3 coordinates microtubule cytoskeletal dynamics and stability in neuronal cellsSemantic proximity Read ↗

Overexpression of ATase1 and ATase2 disrupts the secretome and causes a progeria phenotype.Semantic proximity Read ↗

The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B.Semantic proximity Read ↗

Lamin A and microtubules collaborate to maintain nuclear morphology.Semantic proximity Read ↗

ZC3HC1 has many functions distinct from TPR and is dispensable for TPR localisation to the nuclear basketSemantic proximity Read ↗

Depletion of nuclear import protein karyopherin alpha 7 (KPNA7) induces mitotic defects and deformation of nuclei in cancer cellsSemantic proximity Read ↗

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