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

Partial loss of TDP-43 function causes phenotypes of amyotrophic lateral sclerosis.

Proceedings of the National Academy of Sciences of the United States of America - 25 Mar 2014

Yang Chunxing, Wang Hongyan, Qiao Tao, Yang Bin, Aliaga Leonardo, Qiu Linghua, Tan Weijia, Salameh Johnny, McKenna-Yasek Diane M, Smith Thomas, Peng Lingtao, Moore Melissa J, Brown Robert H, Cai Huaibin, Xu Zuoshang

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurological disease that causes motor neuron degeneration, progressive motor dysfunction, paralysis, and death. Although multiple causes have been identified for this disease, >95% of ALS cases show aggregation of transactive response DNA binding protein (TDP-43) accompanied by its nuclear depletion. Therefore, the TDP-43 pathology may be a converging point in the...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Amyotrophic Lateral Sclerosis Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Animals, Genetically Modified

Share to Central Nervous System

Share to Disease Models, Animal

Share to DNA-Binding Proteins

Share to Phenotype

Source

Open in PubMed Open full text

Identifiers

PMID: 24616503
DOI: 10.1073/pnas.1322641111
PMCID: PMC3970502

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

Partial loss of TDP-43 function causes phenotypes of amyotrophic lateral sclerosis.PMID 24616503Read ↗

TDP-43—The key to understanding amyotrophic lateral sclerosisSemantic proximity Read ↗

Rapid and Inducible Mislocalization of Endogenous TDP43 in a Novel Human Model of Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Loss of TDP-43 causes age-dependent progressive motor neuron degenerationSemantic proximity Read ↗

Motor neurons and glia exhibit specific individualized responses to TDP-43 expression in a Drosophila model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in miceSemantic proximity Read ↗

TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration.Semantic proximity Read ↗

Cytoplasmic mislocalization of TDP-43 is toxic to neurons and enhanced by a mutation associated with familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Skeletal muscle TDP-43 aggregation drives progressive motor dysfunction and neurodegeneration with potential for functional recovery after clearanceSemantic proximity Read ↗

Low-level overexpression of wild type TDP-43 causes late-onset, progressive neurodegeneration and paralysis in miceSemantic proximity Read ↗

Wild type human TDP-43 potentiates ALS-linked mutant TDP-43 driven progressive motor and cortical neuron degeneration with pathological features of ALS.Semantic proximity Read ↗

Low-level overexpression of wild type TDP-43 causes late-onset, progressive neurodegeneration and paralysis in miceSemantic proximity Read ↗

TDP-43 proteinopathies: a new wave of neurodegenerative diseasesSemantic proximity Read ↗

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