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

Mechanism of STMN2 cryptic splice-polyadenylation and its correction for TDP-43 proteinopathies

16 Mar 2023

Abstract excerpt

Loss of nuclear TDP-43 is a hallmark of neurodegeneration in TDP-43 proteinopathies, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). TDP-43 mislocalization results in cryptic splicing and polyadenylation of pre–messenger RNAs (pre-mRNAs) encoding stathmin-2 (also known as SCG10), a protein that is required for axonal regeneration. We found that TDP-43 binding to a GU-rich region...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis Research
Share to Neurogenetic and Muscular Disorders Research
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36927019
DOI: 10.1126/science.abq5622

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mechanism of STMN2 cryptic splice-polyadenylation and its correction for TDP-43 proteinopathiesPMID 36927019Read ↗

Cryptic splicing of stathmin-2 and UNC13A mRNAs is a pathological hallmark of TDP-43-associated Alzheimer’s diseaseSemantic proximity Read ↗

Cracking the cryptic code in amyotrophic lateral sclerosis and frontotemporal dementia: Towards therapeutic targets and biomarkersSemantic proximity Read ↗

TDP-43 regulates LC3ylation in neural tissue through ATG4B cryptic splicing inhibitionSemantic proximity Read ↗

The era of cryptic exons: implications for ALS-FTDSemantic proximity Read ↗

Generation and validation of a human iPSC-derived TDP-43 knockout model for ALS disease modelingSemantic proximity Read ↗

U7 small nuclear RNA splice-switching therapeutics for STMN2 and UNC13A in Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Stathmin-2: adding another piece to the puzzle of TDP-43 proteinopathies and neurodegenerationSemantic proximity Read ↗

Inhibition of nonsense-mediated decay in TDP-43 deficient neurons reveals novel cryptic exonsSemantic proximity Read ↗

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunctionSemantic proximity Read ↗

TDP-43 loss induces extensive cryptic polyadenylation in ALS/FTDSemantic proximity Read ↗

RNA aptamer reveals nuclear TDP-43 pathology is an early aggregation event that coincides with <i>STMN-2</i> cryptic splicing and precedes clinical manifestation in ALSSemantic proximity Read ↗

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunctionSemantic proximity Read ↗

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