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

Exploiting the CRISPR/Cas9 system to study alternative splicing<i>in vivo</i>: application to titin

23 Aug 2016

Abstract excerpt

The giant protein titin is the third most abundant protein in striated muscle. Mutations in its gene are responsible for diseases affecting the cardiac and/or the skeletal muscle. Titin has been reported to be expressed in multiple isoforms with considerable variability in the I-band, ensuring the modulation of the passive mechanical properties of the sarcomere. In the M-line, only the penultimate Mex5 exon...

Read the complete abstract on PubMed

Topics

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

Share to Cardiomyopathy and Myosin Studies
Share to CRISPR and Genetic Engineering
Share to RNA and protein synthesis mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 28173117
DOI: 10.1093/hmg/ddw280

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Exploiting the CRISPR/Cas9 system to study alternative splicing<i>in vivo</i>: application to titinPMID 28173117Read ↗

Knock-in Mouse Model of Hereditary Myopathy with Early Respiratory Failure Carrying the Titin Variant Corresponding to Human p.N31786KSemantic proximity Read ↗

Functional benefit of CRISPR/Cas9-induced allele deletion for <i>RYR1</i> dominant mutationSemantic proximity Read ↗

The role of <i>Limch1</i> alternative splicing in skeletal muscle functionSemantic proximity Read ↗

CRISPR-induced deletion with SaCas9 restores dystrophin expression in dystrophic models <i>in vitro</i> and <i>in vivo</i>Semantic proximity Read ↗

The role of titin in muscular disorders.Semantic proximity Read ↗

Efficient Generation of Myostatin Gene Mutated Rabbit by CRISPR/Cas9.Semantic proximity Read ↗

CRISPR/Cas9-mediated elimination of the <i>LMNA</i> c.745C>G pathogenic mutation enhances survival and cardiac function in <i>LMNA</i> -associated congenital muscular dystrophySemantic proximity Read ↗

A Titin Knock-in model for Hereditary Myopathy with Early Respiratory FailureSemantic proximity Read ↗

Efficient and Specific Generation of MSTN-Edited Hu Sheep Using C-CRISPR.Semantic proximity Read ↗

Cas13b-mediated RNA targeted therapy alleviates genetic dilated cardiomyopathy in miceSemantic proximity Read ↗

A <i>MSTN</i> <sup>Del273C</sup> mutation with <i>FGF5</i> knockout sheep by CRISPR/Cas9 promotes skeletal muscle myofiber hyperplasiaSemantic proximity Read ↗

Gene Editing for <i>ATXN3</i> Inactivation in Machado-Joseph disease: CRISPR-Cas9 as a Therapeutic Alternative to TALEN-Induced ToxicitySemantic proximity Read ↗

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