ArticleHuman molecular genetics2017
Lamina-associated polypeptide 1 is dispensable for embryonic myogenesis but required for postnatal skeletal muscle growth.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Nuclear envelope and chromatin choreography direct cellular differentiation.Nucleus (Austin, Tex.) · 2025Review
- Quantitative proteome analysis of LAP1-deficient human fibroblasts: A pilot approach for predicting the signaling pathways deregulated in LAP1-associated diseases.Biochemistry and biophysics reports · 2024Article
- Review
- Loss of the Nuclear Envelope Protein LAP1B Disrupts the Myogenic Differentiation of Patient-Derived Fibroblasts.International journal of molecular sciences · 2022Article
- Hepatocytes Deficient in Nuclear Envelope Protein Lamina-associated Polypeptide 1 are an Ideal Mammalian System to Study Intranuclear Lipid Droplets.Journal of lipid research · 2022Article
- Molecular Pathology of Laminopathies.Annual review of pathology · 2022Review
- Review
- LINCing Nuclear Mechanobiology With Skeletal Muscle Mass and Function.Frontiers in cell and developmental biology · 2021Review
- Review
- The intragenic microRNAThe Journal of biological chemistry · 2020Article
- Congenital myasthenic syndrome due to aBrain communications · 2020Article
- Postnatal development of mice with combined genetic depletions of lamin A/C, emerin and lamina-associated polypeptide 1.Human molecular genetics · 2019Article
- Combined loss of LAP1B and LAP1C results in an early onset multisystemic nuclear envelopathy.Nature communications · 2019Article
- Descriptive Analysis of LAP1 Distribution and That of Associated Proteins throughout Spermatogenesis.Membranes · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Lamina-associated polypeptide 1 (LAP1) is an integral protein of the inner nuclear membrane that has been implicated in striated muscle maintenance. Mutations in its gene have been linked to muscular dystrophy and cardiomyopathy. As germline deletion of the gene encoding LAP1 is perinatal lethal, we explored its potential role in myogenic differentiation and development by generating a conditional knockout mouse in which the protein is depleted from muscle progenitors at embryonic day 8.5 (Myf5-Lap1CKO mice). Although cultured myoblasts lacking LAP1 demonstrated defective terminal differentiation and altered expression of muscle regulatory factors, embryonic myogenesis and formation of skeletal muscle occurred in both mice with a Lap1 germline deletion and Myf5-Lap1CKO mice. However, skeletal muscle fibres were hypotrophic and their nuclei were morphologically abnormal with a wider perinuclear space than normal myonuclei. Myf5-Lap1CKO mouse skeletal muscle contained fewer satellite cells than normal and these cells had evidence of reduced myogenic potential. Abnormalities in signalling pathways required for postnatal hypertrophic growth were also observed in skeletal muscles of these mice. Our results demonstrate that early embryonic depletion of LAP1 does not impair myogenesis but that it is necessary for postnatal skeletal muscle growth.
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Registered trials
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