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

Transcriptome Analysis of Cardiac Hypertrophic Growth in MYBPC3-Null Mice Suggests Early Responders in Hypertrophic Remodeling

25 Oct 2018

Abstract excerpt

Rationale– With a prevalence of 1 in 200 individuals, hypertrophic cardiomyopathy (HCM) is thought to be the most common genetic cardiac disease, with potential outcomes that include severe hypertrophy, heart failure, and sudden cardiac death. Though much research has furthered our understanding of how HCM-causing mutations in genes such as cardiac myosin binding protein C (MYBPC3) impair contractile function, it...

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 Cardiovascular Effects of Exercise
Share to Muscle Physiology and Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30410445
DOI: 10.3389/fphys.2018.01442

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

Transcriptome Analysis of Cardiac Hypertrophic Growth in MYBPC3-Null Mice Suggests Early Responders in Hypertrophic RemodelingPMID 30410445Read ↗

Cardiac myosin-binding protein C (MYBPC3) in cardiac pathophysiology.Semantic proximity Read ↗

Haploinsufficiency of MYBPC3 exacerbates the development of hypertrophic cardiomyopathy in heterozygous mice.Semantic proximity Read ↗

The impact of non-cardiomyocyte <i>MYBPC3</i> expression on the development of hypertrophic cardiomyopathySemantic proximity Read ↗

Cardiac myosin binding protein C regulates postnatal myocyte cytokinesisSemantic proximity Read ↗

The mechanics of the heart: zooming in on hypertrophic cardiomyopathy and cMyBP-C.Semantic proximity Read ↗

Abnormal ventricular wall patterning precedes and drives MYBPC3 hypertrophic cardiomyopathySemantic proximity Read ↗

Contractile dysfunction in a mouse model expressing a heterozygous MYBPC3 mutation associated with hypertrophic cardiomyopathy.Semantic proximity Read ↗

Increased myofilament Ca2+ sensitivity and diastolic dysfunction as early consequences of Mybpc3 mutation in heterozygous knock-in mice.Semantic proximity Read ↗

Hypertrophic cardiomyopathy in MYBPC3 carriers in agingSemantic proximity Read ↗

Transcriptome Profile Identifies Actin as an Essential Regulator of Cardiac Myosin Binding Protein C3 Hypertrophic Cardiomyopathy in a Zebrafish Model.Semantic proximity Read ↗

Multi-omics integration identifies key upstream regulators of pathomechanisms in hypertrophic cardiomyopathy due to truncating MYBPC3 mutations.Semantic proximity Read ↗

Proteomic profiling identifies molecular subtypes and unveils mechanistic insights into clinical features of hypertrophic cardiomyopathy.Semantic proximity Read ↗

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