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

Epigenetic Study of Cohort of Monozygotic Twins With Hypertrophic Cardiomyopathy Due to MYBPC3 (Cardiac Myosin-Binding Protein C).

Journal of the American Heart Association - 5 Nov 2024

Peñarroya Alfonso, Lorca Rebeca, Rodríguez Reguero José Julián, Gómez Juan, Avanzas Pablo, Tejedor Juan Ramon, Fernandez Agustín F, Fraga Mario F

Abstract excerpt

BACKGROUND: Hypertrophic cardiomyopathy is an autosomal dominant cardiac disease. The mechanisms that determine its variable expressivity are poorly understood. Epigenetics could play a crucial role in bridging the gap between genotype and phenotype by orchestrating the interplay between the environment and the genome regulation. In this study we aimed to establish a possible correlation between the peripheral...

Read the complete abstract on PubMed

Topics

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

Share to Cardiomyopathy, Hypertrophic
Share to Carrier Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Diseases in Twins

Share to DNA Methylation

Share to Epigenesis, Genetic

Share to Hypertrophy, Left Ventricular

Share to Severity of Illness Index

Share to Twins, Monozygotic

Source

Open in PubMed Open full text

Identifiers

PMID: 39470061
DOI: 10.1161/JAHA.124.035777
PMCID: PMC11935665

Genes

MYBPC3
HOXA5
PLSCR2
TRPC3
UCN3

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Epigenetic Study of Cohort of Monozygotic Twins With Hypertrophic Cardiomyopathy Due to MYBPC3 (Cardiac Myosin-Binding Protein C).PMID 39470061Read ↗

Differential methylation of CpG sites in two isoforms of myosin binding protein C, an important hypertrophic cardiomyopathy geneSemantic proximity Read ↗

Genome-wide mapping of modifier chromosomal loci for human hypertrophic cardiomyopathy.Semantic proximity Read ↗

Epigenome-wide association study for dilated cardiomyopathy in left ventricular heart tissue identifies putative gene sets associated with cardiac development and early indicators of cardiac riskSemantic proximity Read ↗

Epigenome-wide association study for dilated cardiomyopathy in left ventricular heart tissue identifies putative gene sets associated with cardiac development and early indicators of cardiac riskSemantic proximity Read ↗

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

A homozygous MYBPC3 gene mutation associated with a severe phenotype and a high risk of sudden death in a family with hypertrophic cardiomyopathy.Semantic proximity Read ↗

MYBPC3 polymorphism is a modifier for expression of cardiac hypertrophy in patients with hypertrophic cardiomyopathy.Semantic proximity Read ↗

Epigenome-Wide Association Study Identifies Cardiac Gene Patterning and a Novel Class of Biomarkers for Heart Failure.Semantic proximity Read ↗

Genome-wide DNA methylation analysis of discordant monozygotic twins reveals consistent sites of differential methylation associated with congenital heart diseaseSemantic proximity Read ↗

Demographic Model for Inheritable Cardiac DiseaseSemantic proximity Read ↗

Discordant clinical features of identical hypertrophic cardiomyopathy twinsSemantic proximity Read ↗

Clinical Features and Prognostic Implications of Familial Hypertrophic Cardiomyopathy Related to the Cardiac Myosin-Binding Protein C GeneSemantic proximity Read ↗

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