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Musculoskeletal model predicted paraspinal loading may quick estimate the effect of exercise on spine BMD.
Front Bioeng Biotechnol
December 2024
Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, China.
Purpose: Spine is the most commonly found fracture site due to osteoporosis. Combined exercise including high-impact and resistance exercise shows the potential to improve bone mineral density (BMD) in the spine. However, the mechanical loading introduced by exercise, which is the mechanism of BMD changes, has not been investigated.
View Article and Find Full Text PDFThe C-terminal 4CXXC-type zinc finger domain of CDCA7 recognizes hemimethylated DNA and modulates activities of chromatin remodeling enzyme HELLS.
Nucleic Acids Res
September 2024
Cellular Memory Laboratory, RIKEN Cluster for Pioneering Research, Wako City, Saitama 351-0198, Japan.
The chromatin-remodeling enzyme helicase lymphoid-specific (HELLS) interacts with cell division cycle-associated 7 (CDCA7) on nucleosomes and is involved in the regulation of DNA methylation in higher organisms. Mutations in these genes cause immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome, which also results in DNA hypomethylation of satellite repeat regions. We investigated the functional domains of human CDCA7 in HELLS using several mutant CDCA7 proteins.
View Article and Find Full Text PDFCDCA7 is a hemimethylated DNA adaptor for the nucleosome remodeler HELLS.
bioRxiv
December 2023
Laboratory of Chromosome and Cell Biology, The Rockefeller University, New York, NY 10065, USA.
Mutations of the SNF2 family ATPase HELLS and its activator CDCA7 cause immunodeficiency-centromeric instability-facial anomalies (ICF) syndrome, characterized by hypomethylation at heterochromatin. The unique zinc-finger domain, zf-4CXXC_R1, of CDCA7 is widely conserved across eukaryotes but is absent from species that lack HELLS and DNA methyltransferases, implying its specialized relation with methylated DNA. Here we demonstrate that zf-4CXXC_R1 acts as a hemimethylated DNA sensor.
View Article and Find Full Text PDFAP-1 signaling modulates cardiac fibroblast stress responses.
J Cell Sci
December 2023
Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA.
Matrix remodeling outcomes largely dictate patient survival post myocardial infarction. Moreover, human-restricted noncoding regulatory elements have been shown to worsen fibrosis, but their mechanism of action remains elusive. Here, we demonstrate, using induced pluripotent stem cell-derived cardiac fibroblasts (iCFs), that inflammatory ligands abundant in the remodeling heart after infarction activate AP-1 transcription factor signaling pathways resulting in fibrotic responses.
View Article and Find Full Text PDFCoevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.
Elife
September 2023
Bioinformatics Resource Center, The Rockefeller University, New York, United States.
Article Synopsis
- 5-Methylcytosine (5mC) and DNA methyltransferases (DNMTs) play essential roles in maintaining DNA methylation across eukaryotes, but these mechanisms can be lost through evolution.
- Mutations in genes like HELLS and CDCA7, along with the DNA methyltransferase DNMT3B, are linked to ICF syndrome, which results in reduced DNA methylation.
- The study explores the coevolution of CDCA7, HELLS, and DNMTs, showing that their presence tends to be conserved in certain species while frequently lost in others, hinting at their critical interdependence in maintaining DNA methylation.
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