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

Insertional Mutagenesis Confounds the Mechanism of the Morbid Phenotype of a PLNR9C Transgenic Mouse Line.

Journal of cardiac failure - 1 Feb 2018

Kraev Alexander

Abstract excerpt

BACKGROUND: A mouse line with heterozygous transgenic expression of phospholamban carrying a substitution of cysteine for arginine 9 (TgPLNR9C) under the control of α-myosin heavy chain (αMHC) promoter features dilated cardiomyopathy, heart failure, and premature death. METHODS AND RESULTS: Determination of transgene chromosomal localization by conventional methods shows that in this line the transgenic array of...

Read the complete abstract on PubMed

Topics

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

Share to Cardiomyopathy, Dilated
Share to Disease Models, Animal
Share to Mice, Transgenic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutagenesis, Insertional

Share to Myocardium

Share to Myosin Heavy Chains

Share to Reverse Transcriptase Polymerase Chain Reaction

Source

Identifiers

PMID: 29325795
DOI: 10.1016/j.cardfail.2017.12.009

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 11 closest

Insertional Mutagenesis Confounds the Mechanism of the Morbid Phenotype of a PLNR9C Transgenic Mouse Line.PMID 29325795Read ↗

Insertional mutagenesis in PLN <sup>R9C</sup> transgenic mouse: a case report and a review of the literature on cardiac-specific transgenic expressionSemantic proximity Read ↗

Human phospholamban null results in lethal dilated cardiomyopathy revealing a critical difference between mouse and humanSemantic proximity Read ↗

Human phospholamban null results in lethal dilated cardiomyopathy revealing a critical difference between mouse and human.Semantic proximity Read ↗

Prolonged Cre expression driven by the α-myosin heavy chain promoter can be cardiotoxic.Semantic proximity Read ↗

A truncated cardiac troponin T molecule in transgenic mice suggests multiple cellular mechanisms for familial hypertrophic cardiomyopathy.Semantic proximity Read ↗

Gene editing reverses arrhythmia susceptibility in humanized PLN-R14del mice: modelling a European cardiomyopathy with global impactSemantic proximity Read ↗

Cardiac phenotype induced by a dysfunctional α 1C transgene: a general problem for the transgenic approach.Semantic proximity Read ↗

Mylk3 null C57BL/6N mice develop cardiomyopathy, whereas Nnt null C57BL/6J mice do not.Semantic proximity Read ↗

A mouse model for adult cardiac-specific gene deletion with CRISPR/Cas9Semantic proximity Read ↗

MATR3 disruption in human and mouse associated with bicuspid aortic valve, aortic coarctation and patent ductus arteriosusSemantic proximity Read ↗

Construction of transgenic mice with tissue-specific acceleration of mitochondrial DNA mutagenesis.Semantic proximity Read ↗

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