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

Modulation of survival motor neuron pre-mRNA splicing by inhibition of alternative 3' splice site pairing.

The Journal of biological chemistry - 30 Nov 2001

Lim S R, Hertel K J

Abstract excerpt

Spinal muscular atrophy is caused by the loss of functional survival motor neuron (SMN1) alleles. A translationally silent nucleotide transition in the duplicated copy of the gene (SMN2) leads to exon 7 skipping and expression of a nonfunctional gene product. It has been suggested that differential SMN2 splicing is caused by the disruption of an exonic splicing enhancer. Here we show that the single nucleotide...

Read the complete abstract on PubMed

Topics

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

Share to Cyclic AMP Response Element-Binding Protein
Share to Oligonucleotides, Antisense

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Protein Biosynthesis

Share to RNA-Binding Proteins

Share to RNA Splicing

Share to SMN Complex Proteins

Share to Survival of Motor Neuron 1 Protein

Share to Survival of Motor Neuron 2 Protein

Source

Identifiers

PMID: 11584013
DOI: 10.1074/jbc.M107632200

Genes

SMN2
SMN1

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

Modulation of survival motor neuron pre-mRNA splicing by inhibition of alternative 3' splice site pairing.PMID 11584013Read ↗

Splicing of the Survival Motor Neuron genes and implications for treatment of SMASemantic proximity Read ↗

Enhancement of SMN2 Exon 7 Inclusion by Antisense Oligonucleotides Targeting the ExonSemantic proximity Read ↗

Dual Masking of Specific Negative Splicing Regulatory Elements Resulted in Maximal Exon 7 Inclusion of SMN2 GeneSemantic proximity Read ↗

Evolving concepts on human SMN pre-mRNA splicing.Semantic proximity Read ↗

Splicing of a Critical Exon of Human <i>Survival Motor Neuron</i> Is Regulated by a Unique Silencer Element Located in the Last IntronSemantic proximity Read ↗

Antisense Oligonucleotides for the Treatment of Spinal Muscular AtrophySemantic proximity Read ↗

Targeting the 5′ untranslated region of SMN2 as a therapeutic strategy for spinal muscular atrophySemantic proximity Read ↗

Determinants of exon 7 splicing in the spinal muscular atrophy genes, SMN1 and SMN2.Semantic proximity Read ↗

Correction of SMN2 Pre-mRNA splicing by antisense U7 small nuclear RNAs.Semantic proximity Read ↗

A single nucleotide in the SMN gene regulates splicing and is responsible for spinal muscular atrophy.Semantic proximity Read ↗

An Intronic Splicing Enhancer Element in Survival Motor Neuron (SMN) Pre-mRNASemantic proximity Read ↗

Bifunctional antisense oligonucleotides provide a trans-acting splicing enhancer that stimulates <i>SMN2</i> gene expression in patient fibroblastsSemantic proximity Read ↗

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