Zobrazeno 1 - 10
of 30
pro vyhledávání: '"Charis L, Himeda"'
Publikováno v:
Molecular Therapy: Methods & Clinical Development, Vol 20, Iss , Pp 298-311 (2021)
Facioscapulohumeral muscular dystrophy (FSHD) is caused by incomplete silencing of the disease locus, leading to pathogenic misexpression of DUX4 in skeletal muscle. Previously, we showed that CRISPR inhibition could successfully target and repress D
Externí odkaz:
https://doaj.org/article/3cd3d9dd12634bd680d39f32a431065f
Autor:
Charis L. Himeda, Peter L. Jones
Publikováno v:
Annual Review of Genomics and Human Genetics. 20:265-291
Facioscapulohumeral muscular dystrophy (FSHD), a progressive myopathy that afflicts individuals of all ages, provides a powerful model of the complex interplay between genetic and epigenetic mechanisms of chromatin regulation. FSHD is caused by dysre
Autor:
Charis L, Himeda, Peter L, Jones
Publikováno v:
Journal of Personalized Medicine. 12:865
Facioscapulohumeral muscular dystrophy (FSHD) is arguably one of the most challenging genetic diseases to understand and treat. The disease is caused by epigenetic dysregulation of a macrosatellite repeat, either by contraction of the repeat or by mu
Publikováno v:
Neuromuscular Disorders. 27:221-238
Facioscapulohumeral muscular dystrophy (FSHD) is associated with aberrant epigenetic regulation of the chromosome 4q35 D4Z4 macrosatellite repeat. The resulting DNA hypomethylation and relaxation of epigenetic repression leads to increased expression
Autor:
Peter L. Jones, Charis L. Himeda, Takako I. Jones, Mary Lou Beermann, Céline Debarnot, Sachiko Homma, Jeffrey Boone Miller
Publikováno v:
Molecular and Cellular Biology. 34:1942-1955
Facioscapulohumeral muscular dystrophy (FSHD) is linked to epigenetic dysregulation of the chromosome 4q35 D4Z4 macrosatellite. However, this does not account for the tissue specificity of FSHD pathology, which requires stable expression of an altern
Publikováno v:
Developmental Biology. 383:7-14
Both Glis, the downstream effectors of hedgehog signaling, and Zic transcription factors are required for Myf5 expression in the epaxial somite. Here we demonstrate a novel synergistic interaction between members of both families and Pax3, a paired-d
Versatility of CRISPR/Cas9-based platforms makes them promising tools for the correction of diverse genetic/epigenetic disorders. Here we contrast the use of these genome editing tools in two myopathies with very different molecular origins: Duchenne
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a5eb48e92b873461448a3dc830f91ce
https://europepmc.org/articles/PMC5193161/
https://europepmc.org/articles/PMC5193161/
Autor:
Charis L. Himeda, Merlin Crossley, Stephen D. Hauschka, Richard C. M. Pearson, Jeffrey A. Ranish
Publikováno v:
Molecular and Cellular Biology. 30:3430-3443
This study identifies KLF3 as a transcriptional regulator of muscle genes and reveals a novel synergistic interaction between KLF3 and serum response factor (SRF). Using quantitative proteomics, KLF3 was identified as one of several candidate factors
Publikováno v:
Molecular and Cellular Biology. 28:6521-6535
We identified a conserved sequence within the Muscle creatine kinase (MCK) promoter that is critical for high-level activity in skeletal and cardiac myocytes (MCK Promoter Element X [MPEX]). After selectively enriching for MPEX-binding factor(s) (MPE
Publikováno v:
Molecular therapy : the journal of the American Society of Gene Therapy. 24(3)
Facioscapulohumeral muscular dystrophy (FSHD) is one of the most prevalent myopathies, affecting males and females of all ages. Both forms of the disease are linked by epigenetic derepression of the D4Z4 macrosatellite repeat array at chromosome 4q35