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

Knockout of MYOM1 in human cardiomyocytes leads to myocardial atrophy via impairing calcium homeostasis.

Journal of cellular and molecular medicine - 1 Feb 2021

Hang Chengwen, Song Yuanxiu, Li Ya'nan, Zhang Siyao, Chang Yun, Bai Rui, Saleem Amina, Jiang Mengqi, Lu Wenjing, Lan Feng, Cui Ming

Abstract excerpt

Myomesin-1 (encoded by MYOM1 gene) is expressed in almost all cross-striated muscles, whose family (together with myomesin-2 and myomesin-3) helps to cross-link adjacent myosin to form the M-line in myofibrils. However, little is known about its biological function, causal relationship and mechanisms underlying the MYOM1-related myopathies (especially in the heart). Regrettably, there is no MYMO1 knockout model...

Read the complete abstract on PubMed

Topics

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

Share to Connectin
Share to Embryonic Stem Cells

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Editing

Share to Gene Knockout Techniques

Share to Molecular Imaging

Share to Muscular Atrophy

Share to Myocytes, Cardiac

Share to Sarcomeres

Source

Open in PubMed Open full text

Identifiers

PMID: 33452765
DOI: 10.1111/jcmm.16268
PMCID: PMC7875908

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Knockout of MYOM1 in human cardiomyocytes leads to myocardial atrophy via impairing calcium homeostasis.PMID 33452765Read ↗

MLP-deficient human pluripotent stem cell derived cardiomyocytes develop hypertrophic cardiomyopathy and heart failure phenotypes due to abnormal calcium handlingSemantic proximity Read ↗

Generation of a heterozygous TPM1-E192K knock-in human induced pluripotent stem cell line using CRISPR/Cas9 system.Semantic proximity Read ↗

Identification of <i>MYOM2</i> as a candidate gene in hypertrophic cardiomyopathy and Tetralogy of Fallot and its functional evaluation in the <i>Drosophila</i> heartSemantic proximity Read ↗

cMyBP-C ablation in human engineered cardiac tissue causes progressive Ca2+-handling abnormalities.Semantic proximity Read ↗

Conditionally targeted deletion of PSEN1 leads to diastolic heart dysfunction.Semantic proximity Read ↗

CRISPR/Cas9 editing in human pluripotent stem cell-cardiomyocytes highlights arrhythmias, hypocontractility, and energy depletion as potential therapeutic targets for hypertrophic cardiomyopathySemantic proximity Read ↗

The role of the M-band myomesin proteins in muscle integrity and cardiac diseaseSemantic proximity Read ↗

Enhanced myofilament calcium sensitivity aggravates abnormal calcium handling and diastolic dysfunction in patient-specific induced pluripotent stem cell-derived cardiomyocytes with MYH7 mutation.Semantic proximity Read ↗

A straightforward guide to the sarcomeric basis of cardiomyopathies.Semantic proximity Read ↗

Functional and transcriptomic insights into pathogenesis of R9C phospholamban mutation using human induced pluripotent stem cell-derived cardiomyocytes.Semantic proximity Read ↗

Histone demethylase KDM5 regulates cardiomyocyte maturation by promoting fatty acid oxidation, oxidative phosphorylation, and myofibrillar organizationSemantic proximity Read ↗

Myocardial YBX1 is dispensable for cardiac development and function.Semantic proximity Read ↗

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