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

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

Life science alliance - 1 Apr 2020

Williams Jack L, Paudyal Anju, Awad Sherine, Nicholson James, Grzesik Dominika, Botta Joaquin, Meimaridou Eirini, Maharaj Avinaash V, Stewart Michelle, Tinker Andrew, Cox Roger D, Metherell Lou A

Abstract excerpt

The C57BL/6J and C57BL/6N mice have well-documented phenotypic and genotypic differences, including the infamous nicotinamide nucleotide transhydrogenase (Nnt) null mutation in the C57BL/6J substrain, which has been linked to cardiovascular traits in mice and cardiomyopathy in humans. To assess whether Nnt loss alone causes a cardiovascular phenotype, we investigated the C57BL/6N, C57BL/6J mice and a C57BL/6J-BAC...

Read the complete abstract on PubMed

Topics

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

Share to Cardiomyopathies
Share to Disease Models, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genotype

Share to Mice, Inbred C57BL

Share to Mice, Transgenic

Share to Mitochondrial Proteins

Share to Myosin-Light-Chain Kinase

Source

Open in PubMed Open full text

Identifiers

PMID: 32213617
DOI: 10.26508/lsa.201900593
PMCID: PMC7103425

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

Mylk3 null C57BL/6N mice develop cardiomyopathy, whereas Nnt null C57BL/6J mice do not.PMID 32213617Read ↗

Loss of Nnt Increases Expression of Oxidative Phosphorylation Complexes in C57BL/6J Hearts.Semantic proximity Read ↗

The prevalent I686T human variant and loss-of-function mutations in the cardiomyocyte-specific kinase gene TNNI3K cause adverse contractility and concentric remodeling in mice.Semantic proximity Read ↗

Comparative phenotypic assessment of cardiac pathology, physiology, and gene expression in C3H/HeJ, C57BL/6J, and B6C3F1/J mice.Semantic proximity Read ↗

Genetic differences among C57BL/6 substrains.Semantic proximity Read ↗

A genetic and physiological study of impaired glucose homeostasis control in C57BL/6J mice.Semantic proximity Read ↗

Tnni3k modifies disease progression in murine models of cardiomyopathy.Semantic proximity Read ↗

Tnni3k alleles influence ventricular mononuclear diploid cardiomyocyte frequencySemantic proximity Read ↗

Molecular insights from a novel cardiac troponin I mouse model of familial hypertrophic cardiomyopathy.Semantic proximity Read ↗

Substrain-Dependent Differences in Doxorubicin-Induced Cardiotoxicity in Adult C57BL/6 Mice.Semantic proximity Read ↗

Genetic Loss of Nicotinamide Nucleotide Transhydrogenase Prevents from Cardiometabolic Heart Failure with Preserved Ejection FractionSemantic proximity Read ↗

Ventricular arrhythmia vulnerability in cardiomyopathic mice with homozygous mutant Myosin-binding protein C gene.Semantic proximity Read ↗

A Murine Hypertrophic Cardiomyopathy Model: The DBA/2J Strain.Semantic proximity Read ↗

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